How does the brain alter/inhibit muscle reflexes?

How does the brain alter/inhibit muscle reflexes?

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I can find lots of information on how stretch-reflexes/reciprocal-inhibition/autogenic-inhibition work but from them all it's unclear how exactly the brain interfaces/controls/disables such automatic muscle reflexes when it needs to?

Can it alter the weighting of inhibition in antagonistic muscles? As well as 'set the length' for a stretch reflex to target? Or does it somehow control both 'with one value'. Where and how exactly does it interject into the feedback loops?

I am trying to understand it more from a programmers pseudocode or equation point of view rather then get lost in meandering biological terms I have seen everywhere that gloss over this point.

how exactly the brain interfaces/controls/disables such automatic muscle reflexes when it needs to?

A: At multiple places within a hierarchical system:

In a simplified way, the Motor cortex is the executor of movement via projections to the brain stem and spinal cord, this is accomplished via excitatory signals to a muscle, the agonist, and inhibitory signals to the antagonist, so in one sense, spinal interneurons would be the answer, since they interface with the motor cortex and alpha motor neurons at the muscle site.

There are also feedback loops all over the motor hierarchy, premotor and supplementary motor cortex regions for instance help plan the movement direction, we don't seem to code a target in the strict sense, but rather a movement direction and then correct via sensory feedback.

The cerebellum projects to premotor, motor cortex and the brainstem, and receives projections from premotor areas, it is involved in stopping and timing movement,the brakes for action if you will.

The circuitry of the Basal Ganglia which loops with premotor and projects to the motor provides the go, no go and graded modulation via inhibition to the motor cortex, which in turn affect less spinal interneurons, so in another sense this circuitry would be responsible.

Can it alter the weighting of inhibition in antagonistic muscles?

Yes, via spinal interneurons (Henshaw cells, Ia inhibitory interneurons and Ib inhibitory interneurons)

As well as 'set the length' for a stretch reflex to target?

Yes, via a the motor,basal ganglia,cerebellum motor hierarchy, although as mentioned, there is no target but rather a direction vector and feedback that tells you when to stop the movement, i.e. you reached your target. ( Higher cognitive areas do seem to have a representation of the target though).

Or does it somehow control both 'with one value'.

Depends on the interneuron, but basically they serve as information relays ( they also convey sensory information )

Where and how exactly does it interject into the feedback loops?

As mentioned there are multiple feedback loops, the brain is not a unit, but a system and as such I would rephrase the question as which subsystems, brain regions, neuronal tracts and neurons create feedback loops in the motor system.

I am trying to understand it more from a programmers pseudocode

I am a software developer myself, so let me try switching hats, this is one scheme:

If all you want is to control agonist/antagonists, tie up 2 or more variables together such that when one goes up, the other goes down, and presumably change 2 effectors ( virtual or real ) and their position relative to each other,

If you want specific control, you would then need to send 2 channels of information and modulate both variables, if you just send one to either one, the other will respond based on the above configuration.

The neural control of micturition

Micturition, or urination, occurs involuntarily in infants and young children until the age of 3 to 5 years, after which it is regulated voluntarily. The neural circuitry that controls this process is complex and highly distributed: it involves pathways at many levels of the brain, the spinal cord and the peripheral nervous system and is mediated by multiple neurotransmitters. Diseases or injuries of the nervous system in adults can cause the re-emergence of involuntary or reflex micturition, leading to urinary incontinence. This is a major health problem, especially in those with neurological impairment. Here we review the neural control of micturition and how disruption of this control leads to abnormal storage and release of urine.

The storage and periodic elimination of urine depend on the coordinated activity of smooth and striated muscles in the two functional units of the lower urinary tract, namely a reservoir (the urinary bladder) and an outlet consisting of the bladder neck, the urethra and the urethral sphincter 1 , 2 . The coordination between these organs is mediated by a complex neural control system that is located in the brain, the spinal cord and the peripheral ganglia.

The lower urinary tract differs from other visceral structures in several ways. First, its dependence on CNS control distinguishes it from structures that maintain a level of function even after the extrinsic neural input has been eliminated. It is also unusual in its pattern of activity and in the organization of its neural control mechanisms. For example, the bladder has only two modes of operation: storage and elimination. Thus, many of the neural circuits that are involved in bladder control have switch-like or phasic patterns of activity, unlike the tonic patterns that are characteristic of the autonomic pathways that regulate cardiovascular organs. In addition, micturition is under voluntary control and depends on learned behaviour that develops during maturation of the nervous system, whereas many other visceral functions are regulated involuntarily.

Owing to the complexity of the neural mechanisms that regulate bladder control, the process is sensitive to various injuries and diseases. This Review summarizes the results of recent studies in animals and humans that have provided new insights into the sensory and motor mechanisms that underlie voluntary and reflex micturition, the changes in neural pathways that occur following disease or injury that alters lower-urinary-tract function, and new therapies for the treatment of neurogenic bladder dysfunction.


T.M. SRINIVASAN , K. VINOD KUMAR , in Biomedical Engineering I , 1982


The study of the human spinal reflex was first introduced by Hoffman (1918) . The reflex described by him was subsequently named the H reflex and is accepted as a spinal reflex. ( Hoffman, 1918 Magladery and Mc Dougal, 1950 ). The H reflex is a sub-threshold monosynaptic discharge and is usually a triphasic response of short duration. Low intensity stimulation of the posterior tibial nerve evokes the classical H reflex in the calf muscle.

The H wave has been used as a measure of monosynaptic reflex activity and hence spinal motoneuron excitablity. With this technique, patients with spasticity and rigidity have been studied and compared with normals in an attempt to understand the mechanisms of altered motor function. ( Teasdall et al, 1952 Angel and Hoffman, 1963 Landau and Clare, 1964 ).

The maximum M response in muscles represent the activity of all motor units in the muscle, while the maximum H reflex recorded with the same position of electrodes represents the total activity of the motor units activated by the LA afferents. The ratio of H/M is an index of motoneuron excitablity, and of what portion of the motoneuron pool can be activated by this reflex. ( Angel and Hoffman, 1963 Landau and Clare, 1964 ).

The spinal motoneuron excitablity in man can be tested by studying the recovery cycle of the H reflex after a conditioning electrical stimulus using the paired shock (H1, H2) technique ( Magladery, 1955 Pillard, 1955 Yap, 1967 ).

This paper describes a dedicated microprocessor (μP) based system for automatic neurological monitoring. The associated instrument ation used includes a stimulator controlled by the μP, EMG/ECG preamplifier, electrodes, and an oscilloscope. The system can be used for obtaining various neurophysiological data with ease in clinical work and also for analysing this required information and processing them to obtain requisite parameters and waves. An extra feature of averaging sensory evoked potentials (typically auditory) is also incorporated in the system.

How does brain structure change when we make a skill memory?

Using magnetic resonance imaging (MRI), researchers can study the many different types of changes that allow us to learn and remember a motor skill. One of these changes involves increasing the connections between the different areas of the brain that are required for a particular skill. In one study, performed in Oxford, healthy adults had MRI scans before and after six weeks of juggling training. These scans could detect white matter, the long fibres that connect different parts of the brain together. The researchers found that after the juggling training there was an increase in the white matter connections between regions of the brain responsible for vision and regions responsible for making movements[3]. The increased connections between visual and movement areas results in faster and easier sharing of information, perhaps allowing for greater hand-eye coordination.

It is not just white matter that can change with training: studies have shown that there are changes in grey matter as well. Grey matter is made up of the brain cell (neuron) bodies, and is where information processing in the brain occurs. Another juggling study showed that after training there were increases in grey matter in parts of the brain that are involved in the processing of visual information about moving objects[4], perhaps allowing the visual information about the moving juggling balls to be processed more accurately.

Learning of new skills also results in changes in the primary motor cortex, the area of the brain responsible for causing actions. Cells in this area make connections with other neurons that travel down the spinal cord to contact the muscles of the body and cause them to contract. Parts of the body that are close to each other, such as the fingers, are controlled by areas that are close to each other in the motor cortex. We can safely and easily study how different parts of the motor cortex connect to muscles in healthy humans using a technique called transcranial magnetic stimulation (TMS). We use TMS to apply small magnetic pulses to the surface of the scalp in different places and record twitches in the muscles of the body.

Research using TMS and other techniques has discovered that ‘representations’ of the muscles of the body in the motor cortex vary between individuals depending on their use. For example, professional players of stringed instruments tend to have larger areas representing their left hand [5,6]. Having a larger representation, and so a greater number of connections from the brain to the muscles of the hand, perhaps allows for finer movement control. Although these changes are probably the result of years of intensive practice, small changes in representation can also occur over much shorter periods. One study asked healthy volunteers to learn a short hand and foot movement task. Results showed that the area of the motor cortex representing the hand muscles spread temporarily towards the area representing the foot[7]. Changing how the brain connects to the muscles is likely to be another way of improving skills, and if these changes are permanent then the skill will be preserved.

Changes in white matter, grey matter and in motor cortex representation all appear to be important for skill learning and memory. The brain of a person who is very good at a particular skill, such as lindy-hop dancing or playing a certain video game, might have stronger white matter connections between the different brain areas needed for each task, more grey matter in some of these regions, and might have larger motor cortex representations of the muscles needed. However, there are probably many other types of structural changes that occur when we learn a new motor skill that are yet to be discovered.


Like the sensory systems, the motor system is also organized in a topographic fashion. Within the spinal cord, alpha motor neurons that innervate muscles in the arms and legs are located in the lateral portion of the ventral horn, whereas alpha motor neurons that innervate muscles in the trunk are located in the medial portion.

Figure 25.6. The ventral horn is organized in a topographic manner, with proximal muscles (like those in the trunk) located more medially than distal muscles (like the arms or legs). Additionally, motor neurons are organized by function with extensor motor neurons located together and flexor neurons located together. ‘Spinal Cord Map’ by Casey Henley is licensed under a Creative Commons Attribution Non-Commercial Share-Alike (CC BY-NC-SA) 4.0 International License.

How rabies can induce frenzied behavior

Scientists may finally understand how the rabies virus can drastically change its host's behavior to help spread the disease, which kills about 59,000 people annually.

A new study published in the journal Scientific Reports shows how a small piece of the rabies virus can bind to and inhibit certain receptors in the brain that play a crucial role in regulating the behavior of mammals. This interferes with communication in the brain and induces frenzied behaviors that favor the transmission of the virus.

Dr. Karsten Hueffer, lead author and a professor of veterinary microbiology at the University of Alaska Fairbanks, said he hopes the findings will help scientists better understand and treat the infectious viral disease.

"Many infectious agents change behavior in their host, but we do not understand how they do this," he said. "Our study provides, for the first time, a detailed molecular mechanism for how an infectious agent induces specific behaviors."

Hueffer said that although vaccinations for rabies were first developed in the mid-19th century, scientists have struggled to explain how the virus can induce aggressive behavior in animals like dogs, which contribute up to 99 percent of all rabies transmissions to humans, according to World Health Organization estimates.

"The rabies virus only has five genes and very little information," he said. "Dogs have more than 20,000 genes with sophisticated immune and central nervous systems. Yet this virus can reprogram a dog's behavior so it loses fear, becomes aggressive and bites, which allows the virus to spread through the dog's saliva."

Hueffer said these behavioral changes are well known and cemented into the American narrative. In the novel "Old Yeller," Travis must put down his beloved dog after it is bitten and infected by a rabid wolf. In "To Kill a Mockingbird," Atticus Finch is called to shoot a rabid dog.

"Yet the behavior is easier to study than the virus itself," said Hueffer. He said studying rabies in the brain is difficult because the rabies virus doesn't physically alter the brain in very telling ways. Usually, there is brain inflammation, but scientists must sample the brain and specifically test for rabies virus to confirm infection.

Prior research in the 1980s and 1990s focused on how the rabies virus binds to and interacts with specific muscle receptors that receive signals from nerves to control muscle contraction. The research revealed that a molecule called a glycoprotein on the surface of the rabies virus can bind to nicotinic acetylcholine receptors in the muscles. The virus then enters and hijacks muscle and nerve cells where it replicates and travels up the nerves to infect the brain and other tissues.

Other research found a string of amino acids within the rabies glycoprotein that is almost identical to an amino acid sequence found in snake venom that inhibits nicotinic acetylcholine receptors.

Hueffer said he and co-author Marvin Schulte realized a connection. Schulte, an expert on nicotine receptors, is a former UAF professor now at the University of the Sciences in Philadelphia.

"Dr. Schulte and I put two and two together," Hueffer said. "We knew that nicotinic acetylcholine receptors, which bind to the virus in muscles, are also found in the brain, and we presumed that virus could also bind to such receptors. If snake venom has a similar structure to parts of the virus, and inhibits these receptors, we thought maybe the virus could also inhibit these receptors in the brain. Furthermore, we thought that this interaction could influence behavior."

Hueffer then teamed with another co-author, Michael Harris, to develop experiments to demonstrate whether the rabies virus glycoprotein alters behavior in animals. Harris, also formerly of UAF, is now a professor at California State University Long Beach.

"The viruses collect in the spaces between brain cells during the early stages of infection," Harris said. "These spaces are where brain cells communicate. We thought that if viruses could bind to receptors in these spaces and change how brain cells normally communicate, the virus could change behavior of the infected animal."

This change of behavior could work to the advantage of the virus, changing the behavior of infected animals to increase the chances that infection will spread to other animals.

In one of the experiments, Hueffer and his colleagues injected a small piece of the rabies virus glycoprotein into the brains of mice.

"When we injected this small piece of the virus glycoprotein into the brain of mice, the mice started running around much more than mice that got a control injection," he said. "Such a behavior can be seen in rabies infected animals as well."

Hueffer said that this is the first experimental evidence showing a molecular mechanism inducing a specific behavioral change in a host that favors a disease's transmission.

While rabies is now rare in the United States and largely preventable through vaccinations, there is no known cure once symptoms occur. This viral disease is still devastating poor, rural regions mostly in Africa and Asia that lack the means to vaccinate dogs or provide treatment if infection is suspected.

Ways to Increase GABA Levels Naturally

Some studies have suggested that it may be possible to boost GABA levels without drugs or supplements. One possible route may be exercise, and yoga may be particularly effective. A small study of yoga practitioners found that yoga increased GABA in the brain by 27 percent.

The thing about yoga is that it is a discipline of the mind as well as the body. Some studies have shown that meditation alone may also boost GABA or at least markers of GABA activity. In a famous experiment from the 1970’s, 70-year-old Yogi Satyamurti was able to induce a hibernation-like state through deep meditation for eight days in a sealed underground pit. Perhaps he was able to produce extra GABA through the process of meditation.

Dietary adjustments might also raise GABA levels. Since it is a byproduct of the fermentation process, fermented foods like yogurt, kimchi and sauerkraut may increase GABA without the need for a supplement.

Your body cannot make GABA without Vitamin B6, so it might also be helpful to increase B6 by eating foods like raw pumpkin or sunflower seeds, pistachio nuts, sweet potatoes, potatoes, spinach, bananas, lean meats and fish.

Some websites steer people toward eating foods that increase glutamate. However, the value of that strategy seems questionable. While it is true that the brain builds GABA from glutamate, the overall goal is to change the balance of GABA and glutamate in favor of GABA, so boosting glutamate could actually be detrimental.

In the end, balance is the true goal. Modern life with its many stressors may tend to throw the glutamate-GABA system off track so that we live in a world of chronic GABA deprivation. It may be beneficial to try to tip the balance the other direction to maintain a healthier lifestyle.

The link between increased statin use and the dementia epidemic

As noted by the organization Be Brain Fit (BBF), there has been a massive increase in the number of Americans taking statin drugs like Crestor and Lipitor in recent years. At the same time, there has been an astronomical increase in the number of people experiencing memory loss, dementia and Alzheimer’s disease, which is now the sixth leading cause of death in the United States. BBF suggests that these two statistics may be no coincidence.

People are generally only told about the link between cholesterol and heart disease, but cholesterol also has incredibly important functions in the body. It is found in particularly high concentrations in the brain, with more than 60 percent of this important organ consisting of fat. The brain uses cholesterol to manufacture neurotransmitters, the chemicals which enable brain cells to communicate with each other. Neurotransmitters are also responsible for regulating mood, as well as facilitating focus and the ability to remember things, learn new things and cope with stress.

When normal neurotransmitter activity is disrupted, psychiatric disorders and nervous system diseases can be triggered.

For this reason, doctors admit that high cholesterol levels help prevent dementia in the elderly but will not admit the inverse: that low cholesterol levels can be linked to an increased risk of Alzheimer’s and other forms of dementia.

The Brain

The authors of the most cited neuroscience publication, The Rat Brain in Stereotaxic Coordinates, have written this introductory textbook for neuroscience students. The text is clear and concise, and offers an excellent introduction to the essential concepts of neuroscience.

  • Based on contemporary neuroscience research rather than old-style medical school neuroanatomy
  • Thorough treatment of motor and sensory systems
  • A detailed chapter on human cerebral cortex
  • The neuroscience of consciousness, memory, emotion, brain injury, and mental illness
  • A comprehensive chapter on brain development
  • A summary of the techniques of brain research
  • A detailed glossary of neuroscience terms
  • Illustrated with over 130 color photographs and diagrams

This book will inspire and inform students of neuroscience. It is designed for beginning students in the health sciences, including psychology, nursing, biology, and medicine.

The authors of the most cited neuroscience publication, The Rat Brain in Stereotaxic Coordinates, have written this introductory textbook for neuroscience students. The text is clear and concise, and offers an excellent introduction to the essential concepts of neuroscience.

  • Based on contemporary neuroscience research rather than old-style medical school neuroanatomy
  • Thorough treatment of motor and sensory systems
  • A detailed chapter on human cerebral cortex
  • The neuroscience of consciousness, memory, emotion, brain injury, and mental illness
  • A comprehensive chapter on brain development
  • A summary of the techniques of brain research
  • A detailed glossary of neuroscience terms
  • Illustrated with over 130 color photographs and diagrams

This book will inspire and inform students of neuroscience. It is designed for beginning students in the health sciences, including psychology, nursing, biology, and medicine.

The Effects of Painkillers on the Brain and Body

Drug abuse of painkillers can cause harmful effects on the brain and body of the person using the substance. Painkillers can refer to a number of both over-the-counter (OTC), prescription and illicit drugs, but more often than not related to narcotic painkillers like Percocet, OxyContin and heroin. It is these narcotic painkillers that carry the highest risk of dependency and addiction.

Whether a painkiller is prescribed by a doctor or acquired on the street, these drugs can cause serious changes to the brain and body of the user. Although some damage can occur with short-term drug use, the most extreme or dangerous changes to the brain and body typically occur with long-term use and abuse of painkillers. Long-term use also increases the possibility of addiction and physical dependency on the drugs. After a while, users need these drugs just to keep away physical withdrawal symptoms and to physically feel normal. Painkillers are the second most abuse substances in the United States, ranking behind only marijuana use.

Painkillers work by blocking the brain’s perception of pain by binding to opiate receptors. This interferes with the signals transmitted by the central nervous system to the brain. Narcotic pain relievers are depressants, meaning they have a depressant effect on the central nervous system and decrease the feeling of pain while increasing a feeling of relaxation. By binding to the opiate receptors, painkillers also cause feelings of euphoria. It is these euphoric feelings that are often associated with painkiller use and the “high” that users get when abusing painkillers.

Narcotic painkillers bind to opiate receptors which are typically bound by special hormones called neurotransmitters. When painkillers are used for a long period of time, the body slows down production of these natural chemicals and makes the body less effective in relieving pain naturally. That is because narcotic painkillers fool the body into thinking it has already produced enough chemicals as there becomes an overabundance of these neurotransmitters in the body. Existing neurotransmitters have nothing to bind with, as the drugs have taken their place on the opiate receptors. Because of this occurrence, the levels of naturally occurring neurotransmitters in the body decreases and the body builds an increased tolerance to the painkillers so more of the substance is needed to produce the same effect. Many of the neurotransmitters that are decreased include natural endorphins that are considered feel-good chemicals in the brain that also help with pain. Therefore, chemical dependency increases and likelihood of addiction increases as the body is unable to produce the natural chemical needed to relieve pain.

Neurotransmitters are necessary to send signals between the nerves to complete the brain and body connections. Although painkillers take the place of neurotransmitters on the opiate receptors, they cannot fill all of the neurotransmitters roles. Painkillers also depress the central nervous system, meaning the brain and the nerves, leading to slower breathing, slurred speech, and slower bodily reactions.

Painkiller physical dependency often comes after prolonged use and abuse of the drug, but consistent daily use of painkillers over a period of several straight days can also cause a physical addiction. Once someone is physically addicted to painkillers, they will experience extreme physical withdrawal symptoms once they stop taking painkillers. These physical symptoms can occur as soon as 4-6 hours after last use. Physical withdrawal symptoms can include: agitation, restlessness, hot and cold sweats, nausea and vomiting, muscle aches, irritability, headaches, sleeplessness, bone and joint pain, emotional instability, depression and basically like the worst flu ever multiplied by one hundred. Often simply this fear of the pain of withdrawal will keep an addict using for years past the point where they’ve recognized a drug problem and a need to stop.

Painkillers cause chemical changes to the brain and also kills brain cells. The most affected areas of the brain are those areas that deal with cognition, learning and memory. Painkiller use and abuse also can affect nerve cells. Additionally, based on the manner in which the drug is used, painkiller abuse can cause long-term heart damage and increase the likelihood of a heart attack. Crushing and snorting the drug can cause damage to the nose and lungs and crushing and injecting the drug increases the risk of infection.

If you or someone you know is suffering from a drug and alcohol addiction and needs treatment please call us for help. Maryland Addiction Recovery Center offers the most comprehensive addiction treatment in the area. If we aren’t the best fit, we will work with you to find a treatment center that fits your needs. Please call us at (888) 491-8447 or email our team at [email protected] For more information on all of our alcohol and addiction treatment services and resources, please visit the web site at

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