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As far my knowledge, in body parts generally **acetacholine ** is the neurotransmitter. Which is responsible for most nervous impulses.
Consider a body part, say, foot. Only one nerve reaches here. When ant bites there, the impulse of pain and irritation moves from there ;
Secondly, when some soothing agent comes there the impulse of comfortness moves from there
Now, neurotransmitter is the same, nerve is the same, but different impacts are observed.
My teacher said that the impulse moves to different parts of the brain.
But how are the impacts really understood, analysed and sent to different regions ( as entrance of all stimuli enter through the same brain stem,)
My question is that how does our brain analyses two different stimuli when neurotransmitter is the same, nerve is the same and enter the brain through the same brain stem. They must be going to different regions of the brain but how is that decided
Studying the Brain and Behavior in Biopsychology
Andrea Rice is an award-winning journalist and a freelance writer, editor, and fact checker specializing in health and wellness.
Biopsychology is a branch of psychology that analyzes how the brain, neurotransmitters, and other aspects of our biology influence our behaviors, thoughts, and feelings. This field of psychology is often referred to by a variety of names including biopsychology, physiological psychology, behavioral neuroscience, and psychobiology.
Biopsychologists often look at how biological processes interact with emotions, cognitions, and other mental processes. The field of biopsychology is related to several other areas, including comparative psychology and evolutionary psychology.
Neurotransmitters: Functions and Impact on Behavior
1. Describe neurotransmitters, their function, and impact on behavior.
2. Discuss one neurotransmitter in detail describing the effect it has on our bodies and connection with disease.
3. Discuss the importance of biology for understanding behavior.
Please help me with these questions. Thank you.
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1. Describe neurotransmitters, their function, and impact on behavior.
Neurotransmitters are chemicals whose main function is to relay, amplify and modulate electrical signals between a neuron and another cell. According to the prevailing beliefs of the 1960s, a chemical can be classified as a neurotransmitter if it meets the following conditions:
• It is synthesized endogenously, that is, within the presynaptic neuron
• It is available in sufficient quantity in the presynaptic neuron to exert an effect on the postsynaptic neuron
• Externally administered, it must mimic the endogenously-released substance and
• A biochemical mechanism for inactivation must be present. http://en.wikipedia.org/wiki/Neurotransmitters
The link with behavior is complicated. These chemicals and hormones need to be balance in order for us to think "normally" which impacts how we act. It also relays messages to our muscles to respond in a balanced way, until our chemicals and hormones become imbalanced (implicated in depression). Why are there so many brain neurotransmitters? Because the functions performed by brain neurotransmitters are not as uniform as they might superficially appear. Some (like glutamate) are excitatory, whereas others (like GABA) are primarily inhibitory. In many cases (as with dopamine) it is the receptor, which determines whether the transmitter is excitatory or inhibitory. Receptors can also determine whether a transmitter acts rapidly by direct action on an ion channel (e.g., nicotinic acetylcholine receptors) or slowly, by a second-messenger system that allows for synaptic plasticity (e.g., muscarinic acetylcholine receptors). Speed & mechanism of transmitter inactivation after the signal has been sent is also a factor. There are probably also costs & benefits involved in synthesizing, transporting and recycling various neurotransmitters in the differing chemical mileus of the brain. http://www.benbest.com/science/anatmind/anatmd10.html#intro
See http://www.benbest.com/science/anatmind/anatmd10.html#intro for more detail on function by type of neurotransmitter (amino acids peptides monoamines - norepinephrine, dopamine & serotonin plus acetylcholine) [For a well-organized categorization of neurotransmitters, see Neurotransmitter (Wikipedia).]
2. Discuss one neurotransmitter in detail describing the effect it has on our bodies and connection with disease.
Serotonin (5-hydroxytryptamine, or .
Describes neurotransmitters, their function, and impact on behavior. It also discusses one specific neurotransmitter in detail describing the effect it has on our bodies and the connection with disease. Finally, it discusses the importance of biology for understanding behavior.
Neurobiology of alcoholism
Alcohol addiction takes place primarily through two means. The first is a positive reinforcement method and the second is a negative reinforcement method. Positive reinforcement represents an environmental situation in which a rewarding stimulus or experience (e.g., alcohol-induced euphoria) increases the chances that the individual displays a certain response (e.g., alcohol-seeking behavior). Negative reinforcement refers to an increase in behavioural patterns, such as alcohol ingestion, if the behavior facilitates the individual to circumvent or avoid an aversive stimulus. An alcoholic trying to abstain from drinking may experience a range of aversive stimuli in the form of alcohol withdrawal symptoms: irritability, anxiety and dysphoria. It is precisely such symptoms which make abstinence difficult and a relapse possible.
Hence, what begins as a mild way to seek pleasure, soon turns into a full-fledged addiction as the alcohol begins to cause widespread neuroadaptations in the brain, causing the person to convert from an alcohol non-addict to an alcohol addict. Such changes in the reinforcing value of alcohol during the transition from alcohol use to dependence reflect adaptive neural changes resulting from chronic exposure to high alcohol quantities. Thus, while on one hand, the early stages of nondependent alcohol use is largely motivated by alcohol's positive reinforcing effects, the drinking behavior in the dependent state is likely driven by both the positive and negative reinforcing effects of the drug. Neuroadaptations leading to dependence are driven by a constellation of processes which heighten motivation for alcohol consumption. Such neuroadaptations cause alcohol withdrawal symptoms upon cessation of drinking.
It has been posited by that the negative-affective state induced by alcohol withdrawal and especially the increase in anxiety is a major driving force in the propensity for relapse to alcohol-seeking behavior. The mechanisms involved behind alcohol sensitization, tolerance, withdrawal and dependence are discussed in the following sections.
The reward pathways
Underlying the brain changes and neuroadaptations are the reward and stress circuits of the brain. A neural circuit comprises of a series of neurons which send electro chemical signals to one another. An activated neuron sends chemical signaling molecules called neurotransmitters through the neural circuit which bind to specific molecules called the receptors. Depending upon the circuit involved, the binding of these neurotransmitters may cause excitatory or inhibitory signals to be passed further along the circuit.
Alcohol interacts with several neurotransmitter systems in the brain's reward and stress circuits. These interactions result in alcohol's acute reinforcing effects. Following chronic exposure, these interactions in turn cause changes in neuronal function that underlie the development of alcoholism. The following text introduces some of the neural circuits relevant to AD, categorized by neurotransmitter systems. These neural circuits include the dopaminergic, serotoninergic, glutamatergic and GABAergic neural circuits.
Dopamine is a neurotransmitter primarily involved in a circuit called the mesolimbic system, which projects from the brain's ventral tegmental area to the nucleus accumbens. This circuit affects incentive motivation, i.e., how an organism reacts to incentive changes in the environment.
Studies have shown that dopamine has a role in the incentive motivation associated with acute alcohol intoxication. This is so because alcohol consumption can be blocked by injecting low doses of a compound that interferes with dopamine's normal activity (i.e., a dopamine antagonist) directly into the nucleus accumbens.[7,8] Furthermore, the consumption of alcohol and simply the anticipation of availability of alcohol results in production of dopamine in the nucleus accumbens, determined by the increased levels of dopamine in the fluid outside neurons. However, lesions of the mesolimbic dopamine system do not completely abolish alcohol-reinforced behavior, indicating that dopamine is an important, but not essential, component of alcohol-reinforcement. Finally, alcohol withdrawal produces decreases in dopamine function in dependent individuals and this decreased dopamine function may contribute to withdrawal symptoms and alcohol relapse.
The neurotransmitter serotonin (also known as 5-hydroxytryptamine or 5-HT) has been a target of interest for potential pharmacotherapy for alcoholism for a long time because of the well-established link between serotonin depletion, impulsivity and alcohol-drinking behavior in rats and humans. According to pharmacological compounds that target the serotonin system by inhibiting neuronal reuptake of serotonin, thereby prolonging its actions, or by blocking specific serotonin receptor subtypes have been shown to suppress alcohol-reinforced behavior in rats. During alcohol withdrawal, serotonin release in the nucleus accumbens of rats is suppressed and this reduction is partially reversed by self-administration of alcohol during withdrawal.
GABA is the major inhibitory neurotransmitter in the brain. It acts through two receptor subtypes called GABAA and GABAB. Alcohol acts to increase GABA activity in the brain and it does so through two general mechanisms. It can for example, act on the GABA-releasing (i.e., presynaptic) neuron, causing an increase in GABA release or it can act on the signal-receiving (i.e., postsynaptic) neuron facilitating the activity of the GABAA receptor. The consumption of alcohol is suppressed by compounds that interfere with the actions of the GABAA receptor (i.e., GABAA receptor antagonists) as well as compounds that stimulate the GABAB receptor (i.e., GABAB agonists) in the nucleus accumbens, ventral pallidum, bed nucleus of the stria terminalis and amygdala.
Among these regions, the central nucleus of the amygdala is an important brain region involved in the regulation of emotional states. This region is particularly sensitive to suppression of alcohol drinking by compounds acting on the GABA systems (i.e., GABAergic compounds). It has been found that acute and chronic alcohol exposure indeed results in increases in GABA transmission in this region.[17,18] In addition, compounds that target a specific component of the GABAA receptor complex (i.e., the 㬑-subunit) help reduce consumption of alcohol when injected directly into the ventral pallidum, a brain region which receives signals from neurons located in the extended amygdala.[19,20]
The GABA systems in the brain are altered in situations of chronic alcohol exposure. As an example, in some regions of the brain, the expression of genes that encode components of the GABAA receptor is affected due to alcohol. This has been proven by the changes observed in the subunit composition of the receptor in those regions, the most consistent of which are decreases in 㬑- and increases in 㬔-subunits. The function of GABAA receptors also is regulated by molecules known as neuroactive steroids that are produced both in the brain and in other organs (i.e., in the periphery). There is a marked increase in the levels of many neuroactive steroids following exposure to alcohol. Furthermore, stated that the increase in the activity of neuroactive steroids in the brain is not dependent on their production by peripheral organs. These findings therefore indicate that neuroactive steroids are potential key modulators of the altered GABA function which occurs during development of AD by acting directly at GABAA receptors.
Glutamate is the major excitatory neurotransmitter in the brain and it exerts its effects through several receptor subtypes, including one called the N-methyl-D-aspartate (NMDA) receptor. Glutamate systems have been known for a long time to be involved in the acute reinforcing actions of alcohol and the effect of alcohol on an organism can be mimicked with the help of NMDA receptor antagonists. Unlike the case with GABA, alcohol inhibits glutamate activity in the brain. This can be stated from the fact that acute alcohol exposure causes a drop in the extra cellular glutamate levels in a region of the brain called striatum which contains the nucleus accumbens and other structures. Glutamate mediated signal transmission is suppressed in the central nucleus of the amygdala following acute administration and it is an effect which is enhanced following chronic alcohol exposure. The glutamate transmission is most likely affected due to alterations in the functions of both NMDA receptors and another receptor subtype known as metabotropic glutamate subtype 5 receptors. The fact that NMDA receptors are involved in alcoholism is something to take note of as they also play a role in neuroplasticity, a process characterized by neural reorganization that likely contributes to hyper excitability and craving during alcohol withdrawal. Compounds targeting the glutamate systems have also begun to be used for treating AD. As an example, the agent acamprosate modulates glutamate transmission by acting on NMDA and/or metabotropic glutamate receptors. Therefore, by reducing excessive glutamate activity, acamprosate blocks excessive alcohol consumption.
This process appears to depend on the involvement of genes such as Per2, which is typically involved in maintaining the normal daily rhythm (i.e. the circadian clock) of an organism. Acamprosate's capability to reduce alcohol consumption has been seen across different species and the drug has been approved for treatment of alcoholism in humans. This is primarily due to its perceived ability to bring about a reduction in alcohol cravings in abstinent alcoholics.
Genetics of the reward pathways
Alcohol addiction and dependence of late has been shown to be affected by the influence of genes. The presence of such genes does not confirm whether a person will turn into an alcohol addict, but there is a high correlation amongst carriers of such genes and alcohol addiction.
Candidate genes suggested in the development of alcohol addiction are involved in the dopaminergic, serotoninergic, GABA and glutamate pathways.
In the dopaminergic pathway, one such gene is a dopamine receptor D2 (DRD2) which codes for a receptor of dopamine.
Dopamine is an important neurotransmitter involved in reward mechanism in the brain and thereby influences the development and relapse of AD. The dopamine and serotonin pathways are shown as under [ Figure 2 ].
Diagram depicting the dopamine (blue) and serotonin pathways (red) in the brain along with the respective functions of each
It is classified as a catecholamine (a class of molecules that serve as neurotransmitters and hormones). It is a monoamine (a compound containing nitrogen formed from ammonia by replacement of one or more of the hydrogen atoms by hydrocarbon radicals). Dopamine is a precursor (forerunner) of adrenaline and a closely related molecule, noradrenalin.
The DRD2 gene on chromosome 11 (q22-q23) has been found to be associated with increased alcohol consumption through mechanisms involving incentive salience attributions and craving in alcoholic patients. The DRD2 is a G protein-coupled receptor located on postsynaptic dopaminergic neurons that is centrally involved in reward-mediating mesocorticolimbic pathways. The DRD2 gene encodes 2 molecularly distinct isoforms with distinct functions. Signaling through dopamine D2 receptors governs physiologic functions related to locomotion, hormone production and drug abuse.
This DRD2 gene shows polymorphisms of 3 kinds namely: ins/del Taq1B Taq1A. The ins/del allele and Taq1A allele have been implicated with higher risks of AD. With regards to the Taq1A allele, AD patients with the DRD2 A (1) allele, are characterized by greater severity of their disorder across a range of problem drinking indices, when compared with patients without this allele. The Taq1A polymorphism has also been implicated in conduct disorder, behavioral phenotype of impulsivity and problematic alcohol/drug use amongst adolescents. Furthermore, this particular allelic variant has been implicated with increased mortality over a 10 year period in AD individuals. The A1 allele of the DRD2 was significantly associated with paternal history of alcoholism (χ 2 (1) = 4.66 P = 0.031) and male, first-degree, collateral history of alcoholism (χ 2 (1) = 4.40 P = 0.036). Age at the onset of alcohol-related problems as main discriminator between type I and type II AD does not seem to be associated by the Taq1A DRD2 polymorphism. However, the A1 allele of the DRD2 may be a marker of male familial alcoholism, which has been associated with type II AD.
Despite its positive correlation, some studies have produced contradictory results. A study conducted by to assess the association of Taq1A polymorphism and AD in south Indian population yielded negative results.[40,41] also did not find any association with Taq1A polymorphism and AD amongst Mexican-Americans. Amongst other studies which have found a negative correlation between Taq1A polymorphism and alcoholism are ones carried out by.[42,43,44] Study conducted by found conflicting results regarding Taq1A allele frequency amongst assessed and non-assessed controls and assessed and non-assessed alcoholics in a population study comprising of Han Chinese, Caucasians and Europeans. The Taq1A allele frequency of non-assessed controls was more than that of non-assessed alcoholics. However, the allele frequency of assessed alcoholics was found to be 3 times that of assessed controls. The study by found conflicting results for male and female subjects, with female subjects showing AD only on the basis of alcohol disorder. In their study of alcohol-dependence in Polish population reported negative association between Taq1A allele and AD.
The second allele, ins/del has produced much more contradictory results. For example, a study conducted by on Spanish Caucasian AD patients did not find any association with the gene and treatment outcome of AD patients. Even did not find any association with the − 141c ins/del allele and AD Caucasian men. According to them, evidence cannot be provided that in AD Caucasian men a genetic predisposition for alcoholism along with functional variants of the DRD2 and DRD3 genes are associated with differences in dopamine receptor sensitivity. However, a study by[40,41] in a Mexican-American population had found a significant correlation between ins/del polymorphism and AD patients. The genotype frequency for the DRD2 ins/del allele was significantly different between alcoholic and control subjects (P = 0.007). Furthermore, a study conducted by came up with interesting results. According to them, although there were no significant differences in allele frequency between the entire group or subgroups of alcoholics and healthy controls, the − 141c del variant of DRD2 might be a protective factor against development of withdrawal symptoms. However, it might also be a risk factor in a highly burdened subgroup of alcoholics with a paternal and grand paternal history of alcoholism and it might contribute to the substantially higher likelihood of suicide in alcoholics.
Single-nucleotide polymorphism Taq1B is closer to the regulatory and structural coding regions (5’ region) of the DRD2 and thus supposed to play an important role in gene function. It has been rarely investigated for its association with AD. Two studies by[40,41] carried out in Mexican-American population reported conflicting results with regard to the association of this polymorphism with AD. In the study conducted by no allelic or genotypic association of Taq1B polymorphism with AD in North Indians was found, concurring with the findings of which also reported negative association of Taq1B with AD in Mexican-Americans. However, in a subsequent study, the same group reported an association of Taq1B polymorphism with early age of onset for alcohol drinking in Mexican-Americans.
Apart from the dopamine pathways, the addiction to alcohol has also been suggested through the serotonin pathways. Serotonin is another neurotransmitter that is affected by many of the drugs of abuse, including cocaine, amphetamines, LSD and alcohol. Serotonin is produced by neurons in the raphe nuclei. Raphe nuclei neurons extend processes to and dump serotonin onto almost the entire brain, as well as the spinal cord. Serotonin plays a role in many brain processes, including regulation of body temperature, sleep, mood, appetite and pain. Problems with the serotonin pathway can cause obsessive-compulsive disorder, anxiety disorders and depression. Serotonin also modulates the behavioral response to unfairness. Most of the drugs used to treat depression today work by increasing serotonin levels in the brain. The image below, shows, the regions of the brain where serotonin reaches [ Figure 3 ].
Diagram depicting the various regions of the brain under the influence of serotonin
Chemically, serotonin is a monoamine neurotransmitter, known as 5-HT. It is a derivative of tryptophan and is extensively found in the gastrointestinal tract, platelets and the CNS. Some of the functions of serotonin in the CNS include the regulation of mood, appetite, sleep, as well as muscle contraction. Serotonin also has some cognitive functions, including in memory and learning. Most of the brain serotonin is not degraded after use but is collected by serotonergic neurons by serotonin transporters on their cell surfaces. Studies have revealed nearly 10% of the total variance in anxiety-related personality depends on variations in the description of where, when and how many serotonin transporters the neurons should deploy and the effect of this variation was found to interact with the environment in depression.[51,52] Serotonin is released into the space between neurons and diffuses over a relatively wide gap (㸠 μm) to activate 5-HT receptors located on the dendrites, cell bodies and presynaptic terminals of adjacent neurons. Serotonergic action is terminated primarily via uptake of 5-HT from the synapse. This is accomplished through the specific monoamine transporter for 5-HT, serotonin transporter (SERT), on the presynaptic neuron.
Recently mutations in the SERT gene, commonly known as 5’- hydroxtryptamine transporter linked polymorphic region (5’-HTTLPR), has been implicated in cases of alcoholism. This gene is found on chromosome 17 at 17q11.1-q12. The 5’- HTT gene has primarily two mutations. One mutation is known as the “long” allele and the other mutation is known as the “short” allele. The difference between the two alleles is that the “short” version of the allele has a 44 bp deletion in the 5’ regulatory region of the gene. This 44 bp deletion occurs 1 kb upstream from the transcription initiation site of the gene. This is depicted through the following diagram [ Figure 4 ].
Diagram depicting the difference between the 5’-hydroxtryptamine transporter (5-HTT) long allele and 5-HTT short allele
A study by aimed at looking at the differences in the allele frequency amongst non-alcoholic controls and alcohol-dependent patients in the Yunnan Han population. The study found significant differences in the allele frequency in alcohol-dependent patient and non-alcoholic controls. At (P < 0.05), the proportion of L/L and L/S genotype was significantly smaller in case group than that was in the control group (odds ratio [OR] =0.581, P = 0.026). According to the study, 5’-HTTLPR polymorphism may be associated with AD patients and the genotype L/L or L/S may be a genetic factor that is responsible for decreasing susceptibility of AD in Yunnan Han population.
Another study by aimed to look at the availability of the SERT in patients with AD. In the study, 11 healthy controls and 28 alcoholic patients were recruited. SERT availability was measured in vivo with single photon emission computed tomography and (123) I-labeled 2-((2-((dimethyl-amino) methyl) phenyl) thio)-5-iodophenylamine in the midbrain, thalamus and striatum. In addition to this, each subject was genotyped for the 5’-HTTLPR polymorphism. The study found that when compared with healthy controls, patients with pure AD had a significantly lower availability of SERT in the midbrain. The carriers of one L (long) allele showed a significantly higher availability of SERT in the striatum compared with non-L carriers. The study concludes by stating that pure alcoholics may have lower SERT availability in the midbrain and that the 5’-HTTLPR polymorphism may influence SERT availability in patients with anxiety, depression and AD.
Likewise, in a study on Estonian Children and Adolescents, found a positive correlation between substance abuse amongst the adolescents and the 5’-HTTLPR polymorphism. The study involved 583 children from the Estonian Children Personality Behavior and Health Study who were enrolled at the age of 9 and recalled subsequently at the ages of 15 and 18. According to the study, 5’-HTTLPR had age-dependent effects on alcohol, tobacco and drug use: substance use did not differ by genotype at age 9, but at age 15, the participants with the short (s)/s genotype had higher tobacco use and at age 18, they were more active alcohol, drug and tobacco users.
The findings of the team led by produce similar findings. In their study, 360 treatment-seeking African American male patients with single and co morbid DSM-IV lifetime diagnoses of alcohol, cocaine and heroin dependence and 187 African American male controls were genotyped for the triallelic 5’-HTTLPR functional polymorphism in the 5-HT transporter gene (SLC6A4). The study found that low 5’-HTTLPR activity (P = 0.011, OR = 2.5 [1.3-4.6]) due to the presence of the short allele, were more common in men with alcohol drug dependence compared with controls.
However, the study by produced rather contradictory results. In their study, college students (N = 360 192 women) self-reported on drinking motives and negative life events for up to 4 years through an Internet survey. Study participants provided saliva for genotyping the triallelic (LA vs. LG or S) variants of 5-HTTLPR. The study found that among men, individuals with two risk alleles (LG or S), compared with individuals with the LA/LA allele displayed lower drinking-to-cope motives. Among women, individuals with one risk allele (either LG or S), compared with individuals with the LA/LA allele, displayed stronger drinking-to-enhance motives. The association between yearly changes in negative life events and drinking-to-cope motives varied across 5-HTTLPR genotype and gender and was strongest in the positive direction for women with the LA/LA variant. The study concludes by stating that their findings are not consistent with prior speculation that stronger positive associations between life stress and alcohol use among individuals with the LG or S allele are the result of increased use of alcohol as a method for coping with stress. The study goes on to add that the more research is needed in understanding the gender differences in relating 5’-HTTLPR polymorphism with substance abuse.
Likewise, in the study carried out by which aimed at understanding the role of 5’-HTTLPR polymorphism with risky alcohol use in adolescence, there was no correlation with drinking to cope motives and the 5’-HTTLPR polymorphism. The study however found a positive correlation with drinking to cope motives and the Taq1A polymorphism of the DRD2 gene.
The results of the aforementioned study was therefore in complete contrast to the results published by which found a positive correlation of the short (S) allele with binge-drinking behavior, drinking more alcohol per occasion, as well as drinking to get drunk more often.
The SERT gene or SERT, also known as SLC6A4 has another polymorphism in intron 2. This polymorphism has therefore appropriately been named as serotonin intron 2 (STin2). It is a variable number of tandem repeats (VNTR) with three distinct alleles. These alleles are of 9 base pair repeats, 10 base pair repeats as well as 12 base pair repeats. The 9 base pair repeat is extremely rare and in statistical studies, often clubbed with the 10 base pair repeat.
Recently, a study by found an association between STin2 polymorphism and treatment outcome in AD patients. According to study, the SLC6A4 STin2 12/12 carriers, showed poor 6-month time point treatment outcome (32.8% in the good outcome group vs. 64.0% in the poor outcome group). On the other hand, patients having the 10/10 genotype had a better treatment outcome. The study concludes by stating that the functional polymorphism of the SLC6A4 gene may have an influence on treatment outcome in AD patients.
However, a subsequent study by found no role of STin2 VNTR polymorphism in AD. In the study, 165 AD patients, 113 heroin dependent patients and 420 healthy controls from a homogeneous Spanish Caucasian population were genotyped using standard methods. The study found that genotypic frequencies of STin2 VNTR polymorphism did not differ significantly across the three groups. The study concludes by stating that their data does not support a role of serotonergic polymorphisms in AD.
GABA or GABA is the third neurotransmitter whose functioning is critical in understanding the genetics of alcohol addiction. GABA as a neurotransmitter has been long known to be affected by alcohol consumption. Recently, two sub types of the GABAA receptor have come into the spotlight for showing what can possibly be a genetic predisposition to alcohol addiction. These two subtypes are namely GABA A receptor 㬑 (GABRA1) and GABA A receptor 㬖 (GABRA6). The gene encoding GABRA1 is located on chromosome 5 at 5q34-35 while the gene encoding GABRA6 is located on the same chromosome at 5q34. According to a study by, a significant correlation was found with the GABRA1 genotype and Collaborative Study of the Genetics of Alcoholism (COGA) AD, history of blackouts, age at first drunkenness as well as the level of response to alcohol. The study concludes by stating that the efforts to characterize genetic contributions to AD may benefit by examining alcohol-related behaviors in addition to clinical AD.
Furthermore, a study on Korean population by found a positive association between alcoholism and the GABRA1 and GABRA6 receptors. According to the researchers, genetic polymorphisms of the GABAA 㬑 and GABAA 㬖 receptor gene may be associated with the development of alcoholism and that the GG genotype of the GABAA 㬑 receptor gene play a vital role in the development of the early onset and the severe type of alcoholism.
Another study on Taiwanese Han population found similar results. In the study conducted by it was found that GABRA6 and GABRA1 genes account for alcohol susceptibility in Han and exert their genetic influences in a somewhat dominant and synergistic fashion.
However, not all studies have produced favorable results. In a study conducted by, which looked at the data collected from a large number of multiplex, alcoholic families under the COGA, no association was found between the GABRA1 and GABRA6 markers and AD. Similarly, another study conducted by found no association between the genes encoding GABRA1 and GABRA6 with alcoholism.
The fourth pathway which interests us and is of note for alcohol addiction is the pathway of glutamate. There have been some studies conducted into the involvement of this pathway in the process of alcohol addiction. According to one study published by physical dependence, which refers to the pharmacological tolerance induced by chronic alcohol intake, results in AWS and is neurobiologically supported by the imbalance between GABA and glutamate-NMDA neurotransmission.
In addition, one of the latest studies on this pathway found an association between a polymorphism in the promoter of a glutamate receptor subunit gene and alcoholism. The study was conducted by and the study found that short alleles were significantly less frequent among AD subjects. The study concludes by stating that it was the 1 st time that such an association was found with the stated polymorphism and AD.
SOCIAL ANXIETY DISORDER
Anatomical and Neuroimaging Findings in Social Anxiety Disorder
As with PD and PTSD, amygdala activation has been implicated in symptoms of SAD. Social-cue tasks, such as the viewing of harsh faces, were associated with hyperreactivity in the amygdala and other limbic areas in patients who had SAD. Similarly, in response to viewing negative (but not neutral or positive) affective faces, patients who have SAD exhibited bilateral amygdala activation, which positively correlated with symptom severity and which reversed upon successful treatment. In anticipation of public speaking, subcortical, limbic, and lateral paralimbic activity is increased in patients who have SAD, suggesting elevations in automatic emotional processing. Decreased activity in the ACC and PFC in these subjects suggests a decreased ability for cognitive processing (reviewed in 23 ).
In contrast to the social-cue studies, activity in the left hippocampus and right amygdala was decreased during script-guided mental imagery tasks that provoke social anxiety. This decrease may reflect active blunting of the emotional and autonomic response to improve overall functioning during social situations that provoke anxiety. 106 Furthermore, anxiety-provoking imagery (compared with neutral imagery) was associated with increased activation in the left postcentral gyrus and putamen and in the right inferior frontal and middle temporal gyri. Relative decreased activity was observed in the right middle temporal gyrus, left precuneus, and posterior cingulate gyrus. After 8 weeks of treatment with nefazodone, both remitted and partially improved social anxiety was associated with decreased regional CBF (rCBF) in the lingual gyrus, left superior temporal gyrus, and right vlFC and with increased rCBF in the left middle occipital gyrus and inferior parietal cortex. In subjects who achieved remission following nefazodone treatment, posttreatment testing revealed decreased rCBF in the ventral and dorsal ACC, left vlPFC, dorsolateral PFC, and brainstem and increased rCBF in the middle cingulate cortex, left hippocampus, parahippocampal gyrus, subcallosal orbital, and superior frontal gyri. 106
The combined results of imaging analysis in subjects who have SAD suggest dysfunction of a cortico-striato-thalamic network: hyperactivity in the right PFC, striatal dysfunction, and increased hippocampal and amygdala activity with left lateralization. It has been suggested that hyperactivity in the frontolimbic system, including the ACC, which processes negative emotional information and anticipation of aversive stimuli, could result in misinterpretation of social cues (reviewed in 23,107 ).
Neurotransmitter and Neuroendocrine Signaling in Social Anxiety Disorder
Amino acid neurotransmitters
Increased excitatory glutamatergic activity has been reported in patients who have SAD. Compared with matched control subjects, patients who had SAD had a 13.2% higher glutamate/creatine ratio in the ACC as measured by MRS. The glutamate/creatine ratio correlated with symptom severity, suggesting a causal role between excitatory signaling in the ACC and psychopathology (reviewed in 37 ).
The Neurobiology of Anxiety Disorders In addition to benzodiazepines, SSRIs, SNRIs, and monoamine oxidase inhibitors are effective in the treatment of SAD. That SSRI treatment is successful in treating SAD symptoms and reversing some brain abnormalities (eg, elevated amygdala activity) has been cited as evidence for a serotonergic role in the etiology of SAD. 107 Data supporting the hypothesis of disrupted monoaminergic signaling in patients who have SAD include decreased 5HT1A receptor binding in the amygdala, ACC, insula, and dorsal raphe nucleus (DRN). Moreover, trait and state anxiety is elevated in patients who have SAD who have one or two copies of the short SERT allele, and this patient population exhibits amygdala hyperactivity in anxiety-provocation paradigms. Neuroimaging analyses also have revealed decreased density of the dopamine transporter and decreased binding capacity for the D2 receptor (reviewed in 23 ). A role for DA in SAD is supported by the finding that patients who have Parkinson’s disease have high rates of comorbid SAD (reviewed in 107 ). This co-morbidity, however, could result from insecurity regarding display of the physical symptoms of this movement disorder rather than a common etiology of DA malfunction.
A recent study assessed whether a DA agonist (pramipexole, 0.5 mg) or antagonist (sulpiride, 400 mg) influenced response to anxiogenic challenge such as verbal tasks and autobiographical scripts in patients who had SAD. The anxiogenic effect of the behavioral challenges was significantly increased in patients who had untreated SAD following administration of either drug. After successful treatment with SSRIs, however, administration of pramipexole seemed to dampen the behavioral provocation-induced anxiety, whereas sulpiride administration continued to enhance the anxiogenic effects of these tasks. These authors suggested that instability in the dopaminergic response to social stress contributes to anxiety severity and is normalized only partly by successful treatment, perhaps via SSRI-induced desensitization of postsynaptic D3 receptors. 108
As key effectors of social behavior, the neuropeptides oxytocin and vasopressin are of particular interest in SAD and autistic spectrum disorders. Recently direct oxytocin administration to the amygdala in laboratory animals was shown to decrease activation in this region and to dampen amygdala𠄻rainstem communications, which are known to play a role in the autonomic and behavioral components of fear. Furthermore, preliminary data have shown that genetic variants in the central vasopressin and oxytocin receptors (AVP1A and OXTR, respectively) influence amygdalar activity. These data support the hypothesis of amygdala hyperactivity in SAD. Future research in this area may elucidate neural underpinning of human social behavior and the genetic risk for disorders including SAD and autism. 18
Corticotropin-releasing factor and the hypothalamic-pituitary-adrenal axis
Some evidence indicates sensitization of the HPA axis in patients who have SAD. Psychosocial stress produces a greater increase in plasma cortisol, but not ACTH, in patients who have SAD than in control patients despite similar baseline cortisol concentrations. 109 Compared with healthy control subjects or patients who have PTSD, subjects who have SAD tend toward an elevated cortisol response in the Trier Social Stress Test (TSST). The degree of cortisol elevation was correlated with increased avoidance behavior in the approach𠄺voidance task and the predicted stress-induced increased social avoidance above and beyond effects of blood pressure and subjective anxiety. 110 Negative findings also have been reported, however (eg, 111,112 ). For example, an earlier study found that adolescent girls who had social phobia and control subjects exhibited an equal elevation in salivary cortisol following the TSST. To the authors’ knowledge, there are no endocrine-challenge studies (Dex-Suppression, CRF-Stimulation, or Dex/CRF) in patients who have SAD.
Genetic Contribution to Social Anxiety Disorder
The Neurobiology of Anxiety Disorders Unfortunately, there are very few studies specifically examining the genetic underpinnings of SAD. Available data suggest that SAD has a high degree of familial aggregation. In a recent meta-analysis in which SAD was grouped with specific phobia and agoraphobia, an association between phobia in probands and their first-degree relatives was identified. 43
Twin studies in social phobics suggest that additive genetics is responsible for increased incidence of SAD in monozygotic compared with dizigotic twins and suggest no role for common environmental experiences. Adult twin studies of combined phobia diagnoses (including social phobics) suggest that the additive genetics accounts for 20% to 40% of the variance in diagnosis. This result corresponds with a population-based twin study of adolescents diagnosed with social phobia, MDD, and alcoholism, in which genetics accounted for 28% of the risk variance for SAD. Again, the remaining risk was derived from non-shared environmental experiences. Unlike MDD and PTSD, there is little evidence that early-life trauma influences the risk for developing SAD in adulthood. 43
The one genome-wide linkage analysis of SAD implicated a region on chromosome 16 near the gene encoding the norepinephrine transporter. Other genes associated with SAD include (1) a functional variant in ADRB1, the gene encoding the 㬡-adrenergic receptor, and (2) two SNPs and a 3-SNP haplotype in the gene for COMT in female patients who have SAD (reviewed in 107 ). Because SAD is such a complex phenotype, it has been suggested that it may be more fruitful to search for susceptibility genes by examining intermediate phenotypes, quantitative traits, and comorbidity with other illnesses. In fact, SAD heritability includes disorder-specific but also nonspecific genetic factors. SAD is associated with behavioral inhibition in childhood, low extroversion, and high neuroticism. These personality traits are not SAD specific but are hypothesized to contribute to a spectrum of psychopathology inclusive of mood and anxiety disorders. Furthermore, behavioral inhibition, low extroversion, and high neuroticism are each known to be highly heritable and may largely account for the genetic contribution to SAD.
Genes associated with high behavioral inhibition include CRF and SERT. Internalizing neuroticism is associated with the gene encoding glutamic acid decarboxylase, the rate-limiting enzyme in the synthesis of GABA from glutamate (reviewed in 107 ).
Impact of Neurotransmitters on Physical and Mental Behavior
For this assignment, you will identify four major neurotransmitters and:
Analyze the function of each of the four neurotransmitters.
Evaluate the impact of each of the four neurotransmitters on physical and mental behavior.
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The Impact of Neurotransmitters on Physical and Mental Behavior:
Neurotransmitters are chemicals found at the end of the motor neurons which allows for the signals transmission over synapses to other available neurons in the brain. Through this form of transmission, the muscles fibers are stimulated which in turn controls an individual's physical and mental behavior. The neurotransmitters are produced by the pituitary and the adrenal glands (Pacheco, Riquelme & Kalergis, 2010). There are several neurotransmitters however this document will identify four major neurotransmitters and at the same time analyze their functions and the impact they have on the mental and physical behavior of the individual.
Functions of the Neurotransmitters:
According to Boeree (2009), there are various major neurotransmitters such as acetylcholine, norepinephrine, dopamine, and serotonin. These neurotransmitters have the capability of influencing the physical and mental behavior of humans in one way or the other. The acetylcholine .
The impact of neurotransmitters on physical and mental behaviors are determined.
Stress and the Function of the Cardiovascular System
The existence of a positive association between stress and cardiovascular disease has been verified (Rozanski et al., 1999). Stress, whether acute or chronic, has a deleterious effect on the function of the cardiovascular system (Rozanski et al., 1999 Kario et al., 2003 Herd, 1991). The effects of stress on the cardiovascular system are not only stimulatory, but also inhibitory in nature (Engler and Engler, 1995). It can be postulated that stress causes autonomic nervous system activation and indirectly affects the function of the cardiovascular system (Lazarus et al., 1963 Vrijkotte et al., 2000). If these effects occur upon activation of the sympathetic nervous system, then it mainly results in an increase in heart rate, strength of contraction, vasodilation in the arteries of skeletal muscles, a narrowing of the veins, contraction of the arteries in the spleen and kidneys, and decreased sodium excretion by the kidneys (Herd, 1991). Sometimes, stress activates the parasympathetic nervous system (Pagani et al., 1991). Specifically, if it leads to stimulation of the limbic system, it results in a decrease, or even a total stopping of the heart-beat, decreased contractility, reduction in the guidance of impulses by the heart stimulus-transmission network, peripheral vasodilatation, and a decline in blood pressure (Cohen et al., 2000). Finally, stress can modulate vascular endothelial cell function and increase the risk of thrombosis and ischemia, as well as increase platelet aggregation (Rozanski et al., 1999).
The initial effect of stress on heart function is usually on the heart rate (Vrijkotte et al., 2000). Depending upon the direction of the shift in the sympatho-vagal response, the heart beat will either increase or decrease (Hall et al., 2004). The next significant effect of stress on cardiovascular function is blood pressure (Laitinen et al., 1999). Stress can stimulate the autonomic sympathetic nervous system to increase vasoconstriction, which can mediate an increase in blood pressure, an increase in blood lipids, disorders in blood clotting, vascular changes, atherogenesis all, of which, can cause cardiac arrhythmias and subsequent myocardial infarction (Rozanski et al., 1999 Vrijkotte et al., 2000 Sgoifo et al., 1998). These effects from stress are observed clinically with atherosclerosis and leads to an increase in coronary vasoconstriction (Rozanski et al., 1999). Of course, there are individual differences in terms of the level of autonomic-based responses due to stress, which depends on the personal characteristics of a given individual (Rozanski et al., 1999). Thus, training programs for stress management are aimed at reducing the consequences of stress and death resulting from heart disease (Engler and Engler, 1995). In addition, there are gender-dependent differences in the cardiovascular response to stress and, accordingly, it has been estimated that women begin to exhibit heart disease ten years later that men, which has been attributed to the protective effects of the estrogen hormone (Rozanski et al., 1999).
Studies have shown that psychological stress can cause alpha-adrenergic stimulation and, consequently, increase heart rate and oxygen demand (Rozanski et al., 1998, 1999 Jiang et al., 1996). As a result, coronary vasoconstriction is enhanced, which may increase the risk of myocardial infarction (Yeung et al., 1991 Boltwood et al., 1993 Dakak et al., 1995). Several studies have demonstrated that psychological stress decreases the microcirculation in the coronary arteries by an endothelium-dependent mechanism and increases the risk of myocardial infarction (Dakak et al., 1995). On the other hand, mental stress indirectly leads to potential engagement in risky behaviors for the heart, such as smoking, and directly leads to stimulation of the neuroendocrine system as part of the autonomic nervous system (Hornstein, 2004). It has been suggested that severe mental stress can result in sudden death (Pignalberi et al., 2002). Generally, stress-mediated risky behaviors that impact cardiovascular health can be summarized into five categories: an increase in the stimulation of the sympathetic nervous system, initiation and progression of myocardial ischemia, development of cardiac arrhythmias, stimulation of platelet aggregation, and endothelial dysfunction (Wu, 2001).
Option E.4 – Neurotransmitters and Synapses
Action potentials are passed between neurons across the synapse using chemical transmission in the form of neurotransmitters. These are stored at the end of the axon.
When the action potential arrives, the ion channels open to allow Ca2+ to enter, activating the enzymes that act on presynaptic proteins. These proteins cause the release of the neurotransmitters from the vesicles and across the membrane of the nerve ending. Neurotransmitters are constantly recycled.
It then diffuses across the synaptic cleft and interacts with the receptors of the next neuron. Glial cells around the synaptic cleft contain transporters to remove any remaining neurotransmitters.
E.4.1 – State that some presynaptic neurons excite postsynaptic transmission and others inhibit postsynaptic transmission
Each neurotransmitter must bind to its matching receptor, which then stimulates the opening of the ion channels, exciting the neuron. If it reaches the threshold, an action potential will form and be passed along the post-synaptic neuron. When the process occurs this way, it is called an excitatory synapse.
On the other hand, there are also inhibitory synapses. Instead of triggering the release of Ca2+, the neurotransmitters cause the ion channels to open to allow the entry of Cl- ion or the exit of K+. The gradient changes in the opposite direction, making the overall charge of the neuron more negative or hyperpolarised. An action potential cannot be initiated.
An action potential may be formed from a number of impulses reaching the synapse in quick
succession, or from the combined effected of impulses from different axons.
E.4.2 – Explain how decision-making in the CNS can result from the interaction between the activities of excitatory and inhibitory presynaptic neurons at synapses
The brain coordinates and controls our body’s functions, as well as storing memories. It can also initiate activity, and allows us to perform abstract reasoning.
Each area of the brain performs a different function, and they are all connected. Using fMRI, these areas can be identified.
Integration is the process of data being taken into the centres and compiled with the existing data, or memories. This is then used in decision making. Each neuron has many synaptic knobs, forming different types of connections.
Decision making is also dependent on the interaction between excitatory and inhibitory synapses and the different connection pathways between neurons to produce a different result.
Divergent connections are when information from one pathway branches out and is passed to a number of others, forming the basis of a variety of responses.
Convergent connections are when information from multiple pathways focuses onto fewer pathways. This leads to stronger excitation or inhibition, and can trigger a response to multiple stimuli.
Circular or Reverbatory connections are when the information returns to its source to reinforce a message or make it last longer
Parallel or After-Discharge connections are when the post synaptic neuron sends out a number of impulses without any feedback, resulting in a precise, strong response.
E.4.3 – Explain how psychoactive drugs affect the brain and personality by either increasing or decreasing postsynaptic transmission
Psychoactive drugs affect the mind by altering the performance of synapses. Some drugs amplify their processes to increase post-synaptic transmission, such as nicotine and atropine. Some inhibit the process of synaptic transmission to decrease transmission, such as amphetamines and beta blocker drugs.
Synaptic transmission is significant in brain function. The brain in integral for the coordination of body functions, storing information, maintaining our memory bank, imagination, create, plan, calculate, predict and for abstract reasoning, but excluding reflexes.
Psychoactive drugs affect behaviour and possibly personality. Many of these drugs are used in medicine as tranquilisers and painkillers to make the brain neurons resistant to excitation. They are also used in horticulture as insecticides, to inhibit enzymic breakdown of transmitter substances after attachment to the post-synaptic membrane. It disrupts the nervous system to the point of death. Nerve gases can be used as weapons.
These are also used in a social and recreational context, but often have dangerous or tragic consequences.
E.4.4 – List three examples of excitatory and three examples of inhibitory psychoactive drugs
E.4.5 – Explain the effects of THC and cocaine in terms of their action at synapses in the brain
This is also called marijuana, pot, grass or weed and is usually smoked. The chief mind altering chemical in it is THC (delta-9-tetrahydrocannabinol), which is typically present in concentration of 1-4%.
It is a mild hallucinogen, showing similar disinhibiting properties to ethanol. It induces a sense of well-being and a dreamy state of relaxation. Also:
- Encourages fantasies
- User becomes suggestible and vulnerable
- Possible paranoia
Emotions peak after 10-30 minutes, and wear off after 2-3 hours.
Affects ability to absorb and retain information, maturity, leads to inappropriate lifestyle choices, gateway to cocaine. Also increases risk of car crashes, STI’s and unwanted pregnancy.
It is a highly addictive stimulant, and is usually ingested, snorted or injected. Crack cocaine is heated to evaporate the water and inhaled from a heated pipe for faster absorption. it affects neurons containing dopamine, which affects pleasure. It has euphoric effects, interfering the reabsorption of dopamine and prolonging stimulation for extended pleasure response.
It induces euphoria and hyperstimulation, reducing fatigue and increasing mental clarity. It causes intense pleasure beyond the normal range of human experience. Faster absorption leads to more intense sensations.
Use of cocaine is then followed by a crash, where the user become restless, irritable and anxious. Some people will binge, and suffer auditory hallucinations, paranoid psychosis and lose contact with reality
Users can quickly become addicted, and the cravings lead to repetitive and compulsive behaviours. It gives sensations of insects crawling under skin, severe depression, agitated delirium and paranoid psychosis. It has destructive social consequences, causing the user’s family to become alienated, with the user becoming isolated and suspicious. They will spend all their time and money obtaining more.
- Spend time and money obtaining more
- Often resort to crime
- Put aside loved ones
E.4.6 – Discuss the causes of addiction, including genetic predisposition, social factors and dopamine secretion
Addiction – State of taking a mood-altering drug habitually, and being unable to give it up without experience unpleasant side-effects. The user is unable to control or abandon their drug use.
Drug addiction is characterised by a pathological desire for drugs. It occupies their thoughts and they can only think of obtaining more. They will spend time seeking drugs, with use occurring at the expense of other activities such as study, work and social activity. They cannot control the frequency of use or stop altogether, even if they want to.
The initial motivation for taking the drug affects the likelihood of addiction. If it is taken for medical purposes, then it rarely leads to addiction. However, if it is taken for pleasure, then they are more likely to get addicted.
Some people are predisposed to addiction because their brain is changed in complex ways. This specifically happens in the regions including the reward system and areas involved in executive functions and judgement. Their decision-making ability is also affected.
Other personality types are more likely to become addicted, including those who are inclined to risk-taking or hedonistic.
They might also have a metabolic state that makes drugs more effective, such as the absence of an enzyme to dispose of the drug. These conditions may be inherited.
Environmental factors, such as stress, affect people’s response to the drug. Poor diet, high unemployment and limited access to education and training are also contributing factors to susceptibility. Little opportunity for personal fulfilment leads to a sense of hopelessness, so that the drugs become an escape.
Drug abuse can eventually alter the structure and chemical makeup of the brain. Since they affect the reward system, they can produce please, or remove stress and pain. This area is involved in learning, natural rewards, and causes the body to expect more or repeat the action.
Some drugs mimic dopamine, causing them to want to repeat use. However, they will eventually become less sensitive to or more tolerant of it, and they will need higher doses to get the same effect. Eventually, they may become dependent and feel like they can’t function without it. If they try to stop use, they will suffer from withdrawal symptoms.
Drugs interfere with the dopamine metabolism to produce a state of dependence. This often starts with gateway drugs, then later experimentation with more harmful ones, as more is required to produce the same effect. This drug use is habit-forming and users feel that they cannot live without it.
10 types of neurotransmitters and functions
Although nowadays, we know about more than 100 types of neurotransmitters with different functions, in this article we are only going to mention some of the most significant ones: dopamine, adrenaline, noradrenaline, serotonin, acetylcholine, glutamic acid, glycine, GABA (or Gamma-aminobutyric acid), histamine, and endogenous opioid peptide.
One of the most popular neurotransmitters is dopamine, which is involved in brain networks related to motivation and reward-driven behavior. In this sense, many people associate dopamine with pleasure, although it would be better to say that its activity depends on salience or the degree of surprise caused by specific stimuli.
This neurotransmitter is also essential for movement: lesions in dopaminergic pathways, which are produced for example in Parkinson's disease (PD), cause motor-type symptoms such as resting tremors, muscle stiffness, slowness of movement, and difficulty walking or even keeping balance.
Dopamine is a catecholamine, like epinephrine and norepinephrine, which we are going to talk about next. These types of neurotransmitters have the precursor in common from which they are synthesized: tyrosine, a non-essential amino acid (because the body produces it from phenylalanine, an essential amino acid we get from our diet).
2. Epinephrine (or adrenaline)
Epinephrine or adrenaline is considered a neurotransmitter when it works in the nervous system, but it is probably more relevant as a hormone -this is, the effects it has when it is secreted in the bloodstream by adrenal glands.
Epinephrine depends on the fight-or-flight response of our organism, which is activated in front of situations that we perceive as a threat to our physical or psychological integrity. It depends on the sympathetic nervous system, it is closely related to stress, and it implies physiological changes such as the increase of breathing and heart rate, subordination and the contraction of blood vessels.
3. Norepinephrine (or noradrenaline)
Norepinephrine can also be conceptualized as a neurotransmitter or as a hormone depending on whether it works inside or outside of the nervous system. But, what is the difference between epinephrine and norepinephrine? In this case, the function of the neurotransmitter is more relevant than the one of the hormone.
Both adrenaline and noradrenaline are synthesized from dopamine. Tyrosine, the amino acid that is used as the precursor for all the catecholamines, is transformed into DOPA due to the effects of the tyrosine hydroxylase enzyme. When decarboxylated, DOPA becomes dopamine if it oxidizes it becomes noradrenaline, and finally, adrenaline is obtained from the methylation of noradrenaline.
4. Serotonin (5-HT)
Serotonin is also called "5-hydroxytryptamine" (5-HT). In this case, the amino acid used as a precursor is not tyrosine (and in consequence serotonin doesn't belong to the group of catecholamines) but the tryptophan, which can be obtained from food such as eggs, milk, whole grains or chocolate, among others.
Serotonin is in charge of the regulation of other neurotransmitters' activities. Nowadays, it is known that it is involved in several processes such as the decrease of the levels of anxiety and physiological stress, the feeling of increased tiredness and appetite, the improvement of the mood or cell division.
5. Acetylcholine (ACh)
Acetylcholine comes from the glucose we obtain from food. Among the functions of the organism in which this neurotransmitter participates, we can highlight the stimulation (the contraction) of muscle cells in general and the brain, the production of saliva, urination, erection or the decrease of the heart rate frequency.
6. Glutamic acid (Glu)
Glutamic acid is the primary excitatory neurotransmitters of the human brain. It is widespread throughout this organ but, despite the importance of its excitatory effects, the neurons that use it as a neurotransmitter are relatively few they usually use it for other purposes, such as transamination or protein synthesis.
7. Gamma-aminobutyric acid (GABA)
The GABA neurotransmitter or gamma-aminobutyric acid is the most important neurotransmitter for the neuronal inhibition in the central nervous system, and particularly in the brain. The muscle tone depends on the GABA -so the deficits of this neurotransmitter are related to hypertonia and rigidity.
8. Glycine (Gly)
The eighth neurotransmitter that we have included in this list is glycine, which also has inhibitory effects in the central nervous system but, contrary to GABA, its activity is more important in the spine than in the brain. Glycine is also very important for the synthesis of collagen, present in the skin and bones.
When it acts as a neurotransmitter in the nervous system, histamine is in charge of the regulation of tiredness and alertness, as well as the secretion of hormones by the hypothalamic system.
Histamine is especially known by its role in the immunity system responses. Among other body processes, this type of neurotransmitters is associated with inflammation and itching.
10. Endogenous opioid peptide
There are a lot of opioid peptides that the brain produces and that are considered neurotransmitters due to the way they fulfill their functions.
Within this type of neurotransmitters, encephalins, endorphins, and dynorphins stand out. Their functions have to do with the regulation of sensations of pain and hunger, body temperature or reproduction, among other aspects.
What are neurotransmitters?
Neurotransmitters are chemical messengers in the body. Their job is to transmit signals from nerve cells to target cells. These target cells may be in muscles, glands, or other nerves.
The brain needs neurotransmitters to regulate many necessary functions, including:
- heart rate
- sleep cycles
- muscle movement
The nervous system controls the body’s organs, psychological functions, and physical functions. Nerve cells, also known as neurons, and their neurotransmitters play important roles in this system.
Nerve cells fire nerve impulses. They do this by releasing neurotransmitters, which are chemicals that carry signals to other cells.
Neurotransmitters relay their messages by traveling between cells and attaching to specific receptors on target cells.
Each neurotransmitter attaches to a different receptor — for example, dopamine molecules attach to dopamine receptors. When they attach, this triggers action in the target cells.
After neurotransmitters deliver their messages, the body breaks down or recycles them.
Share on Pinterest Many bodily functions need neurotransmitters to help communicate with the brain.
Experts have identified more than 100 neurotransmitters to date.
Neurotransmitters have different types of action:
- Excitatory neurotransmitters encourage a target cell to take action.
- Inhibitory neurotransmitters decrease the chances of the target cell taking action. In some cases, these neurotransmitters have a relaxation-like effect.
- Modulatory neurotransmitters can send messages to many neurons at the same time. They also communicate with other neurotransmitters.
Some neurotransmitters can carry out various functions, depending on the type of receptor that they are connecting to.
The following sections describe some of the best-known neurotransmitters.
Acetylcholine triggers muscle contractions, stimulates some hormones, and controls the heartbeat. It also plays an important role in brain function and memory. It is an excitatory neurotransmitter.
Low levels of acetylcholine are linked with issues with memory and thinking, such as those that affect people with Alzheimer’s disease. Some Alzheimer’s medications help slow the breakdown of acetylcholine in the body, and this can help control some symptoms, such as memory loss.
Having high levels of acetylcholine can cause too much muscle contraction. This can lead to seizures, spasms, and other health issues.
The nutrient choline, which is present in many foods, is a building block of acetylcholine. People must get enough choline from their diets to produce adequate levels of acetylcholine. However, it is not clear whether consuming more choline can help boost levels of this neurotransmitter.
Choline is available as a supplement, and taking high doses can lead to serious side effects, such as liver damage and seizures. Generally, only people with certain health conditions need choline supplements.
Dopamine is important for memory, learning, behavior, and movement coordination. Many people know dopamine as a pleasure or reward neurotransmitter. The brain releases dopamine during pleasurable activities.
Dopamine is also responsible for muscle movement. A dopamine deficiency can cause Parkinson’s disease.
A healthful diet may help balance dopamine levels. The body needs certain amino acids to produce dopamine, and amino acids are found in protein-rich foods.
Meanwhile, eating high amounts of saturated fat can lead to lower dopamine activity, according to research from 2015 . Also, certain studies suggest that a deficiency in vitamin D can lead to low dopamine activity.
While there are no dopamine supplements, exercise may help boost levels naturally. Some research has shown that regular exercise improves dopamine signaling in people who have early stage Parkinson’s disease.
Endorphins inhibit pain signals and create an energized, euphoric feeling. They are also the body’s natural pain relievers.
One of the best-known ways to boost levels of feel-good endorphins is through aerobic exercise. A “runner’s high,” for example, is a release of endorphins. Also, research indicates that laughter releases endorphins.
Endorphins may help fight pain. The National Headache Foundation say that low levels of endorphins may play a role in some headache disorders.
A deficiency in endorphins may also play a role in fibromyalgia. The Arthritis Foundation recommend exercise as a natural treatment for fibromyalgia, due to its ability to boost endorphins.
Also known as adrenaline, epinephrine is involved in the body’s “fight or flight” response. It is both a hormone and a neurotransmitter.
When a person is stressed or scared, their body may release epinephrine. Epinephrine increases heart rate and breathing and gives the muscles a jolt of energy. It also helps the brain make quick decisions in the face of danger.
While epinephrine is useful if a person is threatened, chronic stress can cause the body to release too much of this hormone. Over time, chronic stress can lead to health problems, such as decreased immunity, high blood pressure, diabetes, and heart disease.
People who are dealing with ongoing high levels of stress may wish to try techniques such as meditation, deep breathing, and exercise.
Anyone who thinks that their levels of stress could be dangerously high or that they may have anxiety or depression should speak with a healthcare provider.
Meanwhile, doctors can use epinephrine to treat many life threatening conditions, including:
Epinephrine’s ability to constrict blood vessels can decrease swelling that results from allergic reactions and asthma attacks. In addition, epinephrine helps the heart contract again if it has stopped during cardiac arrest.
Gamma-aminobutyric acid (GABA) is a mood regulator. It has an inhibitory action, which stops neurons from becoming overexcited. This is why low levels of GABA can cause anxiety, irritability, and restlessness.
Benzodiazepines, or “benzos,” are drugs that can treat anxiety. They work by increasing the action of GABA. This has a calming effect that can treat anxiety attacks.
GABA is available in supplement form, but it is unclear whether these supplements help boost GABA levels in the body, according to some research .
Serotonin is an inhibitory neurotransmitter. It helps regulate mood, appetite, blood clotting, sleep, and the body’s circadian rhythm.
Serotonin plays a role in depression and anxiety. Selective serotonin reuptake inhibitors, or SSRIs, can relieve depression by increasing serotonin levels in the brain.
Seasonal affective disorder (SAD) causes symptoms of depression in the fall and winter, when daylight is less abundant. Research indicates that SAD is linked to lower levels of serotonin.
Serotonin-norepinephrine reuptake inhibitors (SNRIs) increase serotonin and norepinephrine, which is another neurotransmitter. People take SNRIs to relieve symptoms of depression, anxiety, chronic pain, and fibromyalgia.
Some evidence indicates that people can increase serotonin naturally through:
A precursor to serotonin, called 5-hydroxytryptophan (5-HTP), is available as a supplement. However, some research has found that 5-HTP is not a safe or effective treatment for depression and can possibly make the condition worse.
Neurotransmitters play a role in nearly every function in the human body.
A balance of neurotransmitters is necessary to prevent certain health conditions, such as depression, anxiety, Alzheimer’s disease, and Parkinson’s disease.
There is no proven way to ensure that neurotransmitters are balanced and working correctly. However, having a healthful lifestyle that includes regular exercise and stress management can help, in some cases.
Before trying a supplement, ask a healthcare provider. Supplements can interact with medications and may be otherwise unsafe, especially for people with certain health conditions.
Health conditions that result from an imbalance of neurotransmitters often require treatment from a professional. See a doctor regularly to discuss physical and mental health concerns.