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What are reciprocal inhibitory synapses?

What are reciprocal inhibitory synapses?


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Quoting Kandel's Principles of Neural Science, 2013,

Amacrine cells generally receive excitatory signals from bipolar cells at glutamatergic synapses. Some amacrine cells feed back directly to the presynaptic bipolar cell at a reciprocal inhibitory synapse. Some amacrine cells are electrically coupled to others of the same type, forming an electrical network much like that of the horizontal cells.

(Page 593)

I tried searching for what a reciprocal inhibitory synapse is but could not find any relevant information.


It might be better understood if written with a comma as:

reciprocal, inhibitory synapse

though the rules for this comma usage in English might discourage this because writing "inhibitory reciprocal synapse" doesn't sound quite right. I would say the author wrote it correctly even though it is not perfectly clear.

In this context, they are separate adjectives describing the synapse: inhibitory, because it suppresses firing, and reciprocal because Cell A gives input to Cell B, and Cell B also gives input to Cell A (where Cell A is the amacrine cell and Cell B is the bipolar cell).

The word reciprocal in this context is the adjective definition of the word reciprocal:

given, felt, or done in return.

Note that it isn't the synapse itself that is reciprocal or in both directions, but that the cells have a reciprocal relationship.


Excitatory dyad synapse in rabbit retina.

In the inner plexiform layer of the rabbit retina, the synaptic endings of bipolar cells contact a pair of postsynaptic processes at an unusual type of specialized junction, the dyad synapse. One of the members of the postsynaptic dyad may return conventional feedback synapses onto the bipolar endings. Freeze-fracturing demonstrates that, opposite the presynaptic active zone, both postsynaptic membranes contain an aggregate of intramembrane particles that remain associated with the outer leaflet (E face) of the fractured plasmalemma this is a feature typical of excitatory synapses in the central nervous system. Intracellular recordings followed by injection of horseradish peroxidase showed that at the dyad synapse the endings of rod bipolar cells are usually presynaptic to the dendrites of two amacrine cells, one narrow-field and bistratified (AII) and the other wide-field (A17). Only the A17 rod amacrine cell returns feedback synapses onto the bipolar endings. Both amacrine cells respond to illumination with transient-sustained depolarizations, dominated by rods thus, the polarity of their light responses is the same as that of rod bipolar cells. We conclude that the dyad synapses established by rod bipolar cells with the two types of amacrine cells are excitatory.


What you'll learn:

The two components that are part of inhibitory postsynaptic potential are as follows: 1. Types: The subthreshold and suprathreshold excitatory post synaptic potential. These are responsible for reducing the amplitude of the resultant post synaptic potential. The positive potential cancels the negative potential. The balance between the inhibitory postsynaptic potential as well as the excitatory postsynaptic potential plays a vital role in integration of electrical information that is produced by inhibitory and excitatory synapses. 2. Factors: Size of the neuron. Simple summation of synapse potential takes place in smaller neurons while a large number of synapses and ionotropic receptors from the synapse prolong the interaction between large neurons.


Abstract

Postsynaptic scaffold proteins immobilize neurotransmitter receptors in the synaptic membrane opposite to presynaptic vesicle release sites, thus ensuring efficient synaptic transmission. At inhibitory synapses in the spinal cord, the main scaffold protein gephyrin assembles in dense molecule clusters that provide binding sites for glycine receptors (GlyRs). Gephyrin and GlyRs can also interact outside of synapses, where they form receptor-scaffold complexes. Although several models for the formation of postsynaptic scaffold domains in the presence of receptor-scaffold interactions have been advanced, a clear picture of the coupled dynamics of receptors and scaffold proteins at synapses is lacking. To characterize the GlyR and gephyrin dynamics at inhibitory synapses, we performed fluorescence time-lapse imaging after photoconversion to directly visualize the exchange kinetics of recombinant Dendra2-gephyrin in cultured spinal cord neurons. Immuno-immobilization of endogenous GlyRs with specific antibodies abolished their lateral diffusion in the plasma membrane, as judged by the lack of fluorescence recovery after photobleaching. Moreover, the cross-linking of GlyRs significantly reduced the exchange of Dendra2-gephyrin compared with control conditions, suggesting that the kinetics of the synaptic gephyrin pool is strongly dependent on GlyR-gephyrin interactions. We did not observe any change in the total synaptic gephyrin levels after GlyR cross-linking, however, indicating that the number of gephyrin molecules at synapses is not primarily dependent on the exchange of GlyR-gephyrin complexes. We further show that our experimental data can be quantitatively accounted for by a model of receptor-scaffold dynamics that includes a tightly interacting receptor-scaffold domain, as well as more loosely bound receptor and scaffold populations that exchange with extrasynaptic pools. The model can make predictions for single-molecule data such as typical dwell times of synaptic proteins. Taken together, our data demonstrate the reciprocal stabilization of GlyRs and gephyrin at inhibitory synapses and provide a quantitative understanding of their dynamic organization.

Jonas Ranft and Christian G. Specht contributed equally to this work.


Synapse: Definition, Mechanism and Properties (With Diagram)

In this article we will discuss about:- 1. Definition of Synapse 2. Mechanism of Synaptic Transmission 3. Properties.

Definition of Synapse:

Synapse can be defined as functional junction between parts of two different neurons. There is no anatomical continuity between two neurons involved in the formation of synapse.

At level of synapse, impulse gets conducted from one neuron to another due to release of neuro­transmitters, like ACh, noradrenaline, serotonin, etc.

The synapses, which require release of some chemical substance (neurotransmitter) during synaptic transmission, are termed as chemical synapses. In human body, almost all synapses are chemical type. Parts involved in a synapse are given in Fig. 9.5.

Presynaptic region is mostly contributed by axon and postsynaptic region may be contributed by dendrite or soma (cell body) or axon of another neuron.

Accordingly, synapses can be of following types based on different parts of neuron involved information of synapse:

Mechanism of Synaptic Transmission:

b. Depolarization of pre-synaptic region

c. Influx of calcium ions from ECF into presynaptic region

d. Release of neurotransmitter

e. Passage of neurotransmitter through synaptic cleft.

f. Binding of neurotransmitter to receptors on post­synaptic region.

g. Change in electrical activity of postsynaptic region. Depending on transmitter substance released, there can be generation of EPSP or IPSP (EPSP or excitatory postsynaptic potential or IPSP or inhibitory postsynaptic potential). If EPSP is produced, postsynaptic region becomes less negative and if IPSP is produced, postsynaptic region becomes more negative.

h. When EPSP reaches firing level, there will be generation of action potential in postsynaptic region. EPSP is due to influx of sodium ion. If IPSP is produced, postsynaptic region becomes hyperpolarized and hence there will not be development of action potential in postsynaptic region. IPSP will be due to efflux of potassium ions or influx of chloride ions at postsynaptic regions.

Properties of Synapse:

1. One-way conduction (unidirectional conduction):

In chemical synapse, since neurotransmitter is present only in presynaptic region, impulse gets conducted from pre- to postsynaptic region only and not vice versa.

2. Synaptic delay is for neurotransmitter to:

a. Get released from synaptic vesicles when action potential has reached presynaptic region.

b. Pass through synaptic cleft.

c. Act on postsynaptic region to bring about production of action potential in postsynaptic region.

For all the above events to be brought about, sometime is required. This is known as synaptic delay, which is normally about 0.5 msec at every synapse.

When synapses are continuously stimulated, after some time, due to exhaustion of neurotransmitter at presynaptic terminals, impulses fail to get conducted. This results in fatigue occurring at level of synapse. Fatigue is a temporary phenomenon. If some rest is given to neurons, resting facilitates resynthesis of neurotransmitter for further conduction of impulse across synapse.

4. Convergence and divergence:

Impulses from one pre­synaptic nerve fiber may end on postsynaptic region of large number neurons and this is called as divergence. When nerve fibers of different pre­synaptic neurons end on a common postsynaptic neuron, this is known as convergence. In CNS, on an average about 10000 synapses are found on any one neuron.

When a stimulus of subthreshold strength is applied, there will not be development of action potential in postsynaptic region. But if many subthreshold stimuli are applied at pre­synaptic region, effects of these stimuli can get added up and lead to action potential development in postsynaptic region. This is known as summation.

There are two types of summation namely spatial and temporal. In temporal summation, pre­synaptic neuron stimulated will be same, but many stimuli are applied in rapid succession (timing of stimuli will be different, but place of stimulation will be same).

In spatial summation, presynaptic neurons stimulated will be different but stimuli will be applied simultaneously (time of stimulation shall be same, but places of stimulation will be different). This is possible because of the property of convergence.

6. Excitation or inhibition:

The impulse conduction across a synapse may either stimulate or inhibit activity of postsynaptic region. If there is stimulatory influence, then there will be production of action potential in postsynaptic neuron and if it has an inhibitory influence, then there is no action potential generation in postsynaptic region.

Synaptic Inhibitions:

Examples of inhibition are:

i. Postsynaptic inhibition (direct)

ii. Presynaptic inhibition

iii. Renshaw cell inhibition (feedback or recurrent)

iv. Reciprocal inhibition (feed forward)

Postsynaptic Inhibition:

Events in postsynaptic inhibition:

i. Arrival of impulse at presynaptic region

ii. Release of neurotransmitter

iii. Stimulation of internuncial neuron

iv. Action potential production in internuncial neuron

v. Release of neurotransmitter from internuncial neuron

vi. Binding of neurotransmitter to receptors on post­synaptic region

vii. Influx of chloride ions into postsynaptic region

viii. Postsynaptic membrane becoming more negative (development of inhibitory postsynaptic potential or also known as IPSP)

ix. Hyperpolarization of postsynaptic region

x. No action potential production in postsynaptic region.

Glycine substance is a classical example of inhibitory neurotransmitter at postsynaptic region. For example, when biceps muscle is contracting there will be associated relaxation of triceps muscle because of postsynaptic inhibition.

The mechanism of inhibition in all other types namely Renshaw cell (Fig. 9.6), lateral (Fig. 9.7) and reciprocal inhibitions (Fig. 9.8), will be like what has been explained for postsynaptic inhibition but orientation of neuron involved in inhibition will be different.

Presynaptic Inhibition (Fig. 9.9):

In presynaptic inhibition, the events occurring are as follows:

i. The neuron ending on presynaptic terminal liberates neurotransmitter.

ii. Because of this, presynaptic terminal becomes less negative (because of influx of potassium ions)

iii. So the presynaptic terminal fails to remain in resting state.

Now when action potential reaches this pre­synaptic region, depolarization of presynaptic terminal will not be to the extent it normally occurs.

The amplitude of spike potential will be less than normal. When presynaptic neuron is kept in normal resting, during development of action potential, membrane potential will reach plus 35 mV from resting state of minus 70 mV. In which case, net change in potential will be about 105 mV.

When action potential reaches a neuron which has been kept in a partially depolarized state (when membrane potential is made to be less negative), the net change in potential will be less than usual (will be less than 105 mV).

i. This leads to release of less than normal amount of neurotransmitter from presynaptic terminals.

ii. Neurotransmitter on binding to receptors on post­synaptic region brings about development of EPSP.

iii. But the amplitude of EPSP will be less than normal and hence it will not be able to bring postsynaptic region to threshold state of stimulation.

iv. Because of this, there will not be production of action potential in postsynaptic region.

In reciprocal inhibition (Fig. 9.10), impulse from presynaptic terminal, will stimulate motor neuron supplying agonist muscle and through an intern-uncial neuron inhibits motor neuron supplying antagonist muscle.


2. Methods

2.1. Morphological and Physiological Parameters.

The physiological and morphological data of the five α-motoneurons (MNs) of the muscle triceps surea were taken from previous publications on anesthetized cats (the data were provided by I. Segev). The input resistance (RN), membrane time constant (τo), and surface area (Am) were determined according to previous intracellular recordings (Cullheim, Fleshman, Glenn, & Burke, 1987b). Cullheim, Fleshman, Glenn, and Burke (1987a, 1987b) reconstructed the three-dimensional morphological structure of the α-MNs with the aid of a light microscope after a color reaction with injected horseradish peroxidase (HRP). The model simulated one slow (S), two fast fatigue (FF), and two fast fatigue resistance (FR) type α-MNs. The numbers of the synapses and their spatial distribution on the dendrites were taken from earlier studies (Burke & Glenn, 1996 Ornung, Ottersen, Cullheim, & Ulfhake, 1998) based on light microscopy after HRP injection.

2.2. Computer Model.

2.2.1. Simulation and Passive Membrane Properties.

2.2.2. Synaptic Input.

A number of 70 postsynaptic glycinergic REC and REN inhibitory synapses (see Figure 1) were incorporated in the model. The number of the synapses involved in the REC inhibition was based on the observation that an average of 69 Ia-interneurons are in contact with a single MN (Jankowska & Roberts, 1972). Indeed, every contact yields about two to three synaptic buttons (Brown & Fyffe, 1981 Fyffe, 1991), but if the probability of the glycinergic neurotransmitter release is smaller than one (Jack, Redman, & Wong, 1981), for example, 0.5, it will yield about 70 active synapses. A similar number was assumed for the synapses of the REN inhibition.

Schematic presentation of the inhibitory REN and REC inhibition and the Ia excitatory paths. Also, the conductances of these inhibitory inputs are shown. Note that the conductance duration of the REN is longer than that of the REC, whereas the maximal conductance amplitudes are similar.

Schematic presentation of the inhibitory REN and REC inhibition and the Ia excitatory paths. Also, the conductances of these inhibitory inputs are shown. Note that the conductance duration of the REN is longer than that of the REC, whereas the maximal conductance amplitudes are similar.

We fixed the REC inhibitory synapses on the proximal dendrite near the MN soma (Curtis & Eccles, 1959) and assumed an exponential behavior of the density distribution of the REC inhibition as a function of the distance from the soma. A Gauss function mimicked the REN inhibition similar to the EPSP density distribution (Segev et al., 1990 Gradwohl & Grossman, 2008) (see Figure 2A). The activation time of the inhibitory synaptic activation was distributed in a time window of 0 to 1.4 ms (Luscher, Ruenzel, & Henneman, 1979).

(A) Dendritic distribution of the REC proximally and REN distally located inhibitory synapses. Samples of IPSPs in the five MNs evoked by inhibitory REN (B), REC (C), and PREC (D) conductances at the minimal active conductance density ( ⁠⁠ ) of the ED distribution (see the text). The PREC synapses are located similarly to the REN synapses and have a conductance duration of the REC synapses. For clarity, the baseline of the IPSPs was digitally shifted.

(A) Dendritic distribution of the REC proximally and REN distally located inhibitory synapses. Samples of IPSPs in the five MNs evoked by inhibitory REN (B), REC (C), and PREC (D) conductances at the minimal active conductance density ( ⁠⁠ ) of the ED distribution (see the text). The PREC synapses are located similarly to the REN synapses and have a conductance duration of the REC synapses. For clarity, the baseline of the IPSPs was digitally shifted.

2.2.3. The Numerical Model.

2.2.4. Types of Simulation Models.

The simulations were based on a model containing voltage-dependent channels solely on the dendrites, distributed by three different functions. The simulations deal with subthreshold potentials based on the premise that even subthreshold depolarizing IPSPs may activate multiple voltage-dependent conductances (Stuart & Sakmann, 1995 Andreasen & Lambert, 1999 Gonzalez-Burgos & Barrionuevo, 2001), similar to what is observed in EPSP (Magee, 1998 Gradwohl & Grossman, 2008). The model had three types of voltage-dependent channels: a fast inactivating Na + conductance (gNa) (Barrett, Barrett, & Crill, 1980) and both a fast (gKf) and a slow (gKs) potassium conductance (Barrett et al., 1980). Spike repolarization was caused mainly by the gKf, whereas the AHP is influenced by gKs (Schwindt & Crill, 1981). There are undoubtedly other currents on the MN's initial segment, soma, and dendrites, for example, persistent sodium (INap), calcium current producing a plateau potentials (Bui, Cushing, Dewey, Fyffe, & Rose, 2003), and multiple K + channels, like IKCa, shaping firing properties (Viana, Bayliss, & Berger, 1993). However, in our present model, our goal was to analyze the IPSP and its modification due to basic voltage-dependent channels as gNa, gK, and gKs. We consequently did not include the Ca 2+ currents INaP and IKCa (see Luscher & Larkum, 1998). Locating low-voltage-dependent conductances on the dendrites in the presence of a passive soma and axon diminished the potential relative to a full passive neuron. MNs' voltage-dependent channels, in contrast to the ones in the cortical pyramidal neurons (Stuart & Sakmann, 1995), are absent in certain dendrites, while their neighbors may include these channels (Larkum, Rioult, & Luscher, 1996). Even the density distributions of voltage-dependent conductances in the active dendrites are not known. We therefore simulated three types of channel distributions as detailed previously (Gradwohl & Grossman, 2008) at a distance of 0 to 400 μm from the soma: (1) a step function (ST), where the active conductance density was kept uniform over the dendritic tree, (2) an exponential decay (ED), where high-conductance density, located proximal to the soma, decays exponentially away from the soma and (3) an exponential rise (ER), where proximal low-conductance density increases exponentially with distance. Densities of the sodium conductance (gNa) were varied relative to the type of conductance distribution between a minimum and a maximum value in order to attain equal total conductance, G (S, Siemens) for each MN. The densities of the delayed rectifier (gK) and slow (gKs) potassium conductances were one-third relative to gNa (Luscher & Larkum, 1998). For each density model, we ran simulations with two, four, six, and eight active dendrites. The total numbers of the dendrites of MN 36, MN 38, MN 41, MN 42, and MN43 were 10, 13, 12, 8, and 11, respectively. In each case, we executed 10 runs of randomly selected dendrites.


What are reciprocal inhibitory synapses? - Biology

- operation of NS depends on flow of information through network of neurons functionally connected by synapses

B. Functional classification

1. electrical synapses

- gap junctions

2. chemical synapses

- release of neurotransmitter (NT) -- direct opening of ion channels/activation of second messenger systems.

C. Complexity of neuronal network

III. Mechanism of synaptic transmission

B. Events of synaptic transmission

1. NT binds receptors

a. opens channels -- fast synaptic potentials

b. 2 nd messenger system activated -- slow synaptic potentials

2. Termination of NT effects

a. degradation NT

b. removal NT

c. diffusion NT

a. V-snare/t-snare proteins

b. Cycling of presynaptic vesicles

IV. Postsynaptic potentials + synaptic integration

- graded depolarizing response opens Na + , Ca ++ , or Na + /K + channels

- excitation vs. facilitation

-graded hyperpolarizing response opens Cl - or K + channels

- single neuron forms synapses with thousands of other neurons/receives input from thousands of other neurons

- response of postsynaptic neuron depends on additive effect or summation of all EPSPs and IPSPs and their integration at axon hillock -- the grand postsynaptic potential

1. temporal summation

-addition of PSPs occurring very close together in time because of rapid firing of a single presynaptic neuron

- one (or more. ) presynaptic fibers transmit impulses in rapid succession

2. spatial summation

- addition of PSPs originating simultaneously from several different presynaptic neurons

- when postsynaptic neuron is stimulated by large number of terminals at same time

D. Modification of synaptic events

1. postsynaptic inhibition

a. IPSP

b. inhibitory interneurons -- example of reciprocal innervation

2. presynaptic inhibition - involves axoaxonal synapse

3. presynaptic facilitation

4. negative feedback inhibition - involves axon collateral to inhibitory interneuron

- increased basal levels intracellular calcium

V. Organization of neurons in neuronal pools -- types of circuits

- determine integration and transmission of information.

D. Parallel after-discharge

F. Functional zones within neuronal pools

1. discharge zones

2. facilitation zones

VI. Neurotransmitter systems

- excitatory at neuromuscular junction (NMJ)

- ANS - inhibitory/excitatory to visceral effector excitatory at ANS ganglia

a. serotonin

- location

- receptors and mode of action

b. histamine

- location

- receptors and mode of action


Inhibitory synapses influence signals in the brain with high precision

In our brain, information is passed from one cell to the next via trillions of synapses. However, optimal data flow is not just about the transfer of information its targeted inhibition is also a key factor. Scientists from the Max Planck Institute of Neurobiology in Martinsried have now been able to show in mice that even individual inhibitory synapses can have a major influence on signal processing. The study provides an important piece in the puzzle for understanding this fundamental brain function, which is also a factor in a number of illnesses.

Inhibitory nerve cells (green) can use individual synapses to modulate or block signal processing in cells in the cerebral cortex (red).

© MPI for Neurobiology / Müllner

Inhibitory nerve cells (green) can use individual synapses to modulate or block signal processing in cells in the cerebral cortex (red).

The human brain is made up of around 100 billion nerve cells, each of which is connected to other cells by several hundred to thousands of synapses. Apart from our organ and physiological functions, the way we think, act and feel are controlled by the synaptic transmission of information – many quadrillion impulses occur every second. Excitatory synapses that pass the information between cells and inhibitory synapses that limit and change the flow of information are needed for this huge flow of data to run on regulated tracks.

Any disruption to the function of the inhibitory synapses shows how important the suppression of unwanted signals is: there is increased excitation of the brain, such as is seen in epilepsy. Moreover, in order to learn or to remember, the brain needs nerve cells that regulate the activity of other nerve cells. The majority of these inhibitory synapses dock onto the receiver unit of the target cell, the dendrites. Until now, however, there has been no research into exactly what effect these inhibitory synapses actually have and how precisely they act.

Scientists from the Max Planck Institute of Neurobiology have now been able to show in mice that even individual inhibitory synapses have a significant influence on signal processing in the dendrites of other cells. The neurobiologists examined the effect of dendritic inhibition on nerve cells in the hippocampus, the area of the brain in which for example short-term memories are converted into long-term memories. The researchers used a finely-tuned combination of different methods to observe under the microscope how individual inhibitory synapses significantly changed the strength and propagation of a signal in the inhibited nerve cell. The results show that the amplitude of nerve cell signals can be regulated by inhibitory synapses with a precision of a few milliseconds and micrometres.

It was known that inhibitory nerve cells fulfil a very fundamental function in the brain. "But the fact that individual inhibitory synapses play an important role and have such a precise effect really fascinated us", explains Fiona Müllner, lead author of the study which has now been published. Building on their results, the scientists used a model to show how individual inhibitory synapses could control even synaptic plasticity, the basis for learning and memory. "Naturally, we are now interested particularly in what effects such a precise inhibition has on the storage of information in the nervous system", adds Tobias Bonhoeffer who, with his Department at the Max Planck Institute of Neurobiology, is investigating the bases of synaptic plasticity.


Inhibition

in biology, an active nervous process that leads to the suppression or prevention of excitation. A distinction is made between peripheral inhibition, which takes place in the synapses and directly affects the muscular and glandular elements, and central inhibition, which takes place within the central nervous system.

The best-known types of inhibition are based on the interaction between a mediator, secreted and discharged from presynaptic elements (usually nerve endings), and specific molecules of the postsynaptic membrane. Such interaction is accompanied by the postsynaptic membrane&rsquos momentarily higher permeability to K + and Cl &ndash ions this causes a reduction in the membrane&rsquos electrical input impedance and in many cases also generates a hyper-polarizing inhibitory postsynaptic potential. As a result, the membrane&rsquos excitability is diminished&mdashan effect which may last from a few milliseconds in some cases to tens of milliseconds in others thus the membrane is much less likely to be affected by the spreading excitation.

Inhibition always develops as a consequence of excitation of the corresponding inhibitory neurons. The postsynaptic effect may be excitatory or inhibitory, depending on changes in the postsynaptic membrane&rsquos ionic permeability associated with the interaction between the mediators and the receptors. Some mediators can therefore be the means of both excitation and inhibition. For example, acetylcholine inhibits the fibers of the myocardium and excites the skeletal muscles in vertebrates. In the nerve ganglia of mollusks, the synapses of cholinergic neurons produce excitation in some cells and inhibition in others. In the view of several researchers, some mediators are specifically inhibitory&mdashfor example, glycine in the spinal cord and medulla oblongata or gamma-aminobutyric acid in the brain centers and peripheral synapses of crustaceans. Neurons with specific inhibitory functions have been discovered, such as the Renshaw cells in the spinal cord, Purkinje&rsquos cells in the cerebellum, and the basket cells in the hippocampus, which is part of the limbic system. The synapses formed by these neurons have ultrastructural properties that make it possible to distinguish them from excitatory synapses. In some types of neurons, the dendrites and the areas adjacent to them are the locus of the inhibitory synapses in this case, inhibition is found to be highly effective by virtue of proximity to the triggering zone in which excitation is initiated. There are exceptions to this rule&mdashfor example, the inhibitory synapses of stellate neurons on Purkinje&rsquos cells in the cerebellum are located on remote sections of the dendrites.

The functional significance of postsynaptic inhibition is varied. Afferent (direct) inhibition serves to weaken the excitation of functionally antagonistic elements, thereby promoting a coordinated, spatially directed flow of excitation in chains of neurons. In the spinal cord in particular, this type of inhibition is the basis of reciprocal inhibition of the motoneurons that innervate antagonistic muscles. Collateral inhibition, which is effected through the reciprocal collaterals, or branches, of the axons of efferent neurons and specialized intercalary inhibitory neurons, stabilizes the proper level of excitation of a given structural-functional bloc of neurons and limits the spread of excitation to neighboring populations of neurons.

Fewer studies have been made of presynaptic inhibition&mdasha term applied to the suppression of excitation in the nerve endings, or at the point of entry of the postsynaptic cellular element. This type of inhibition is of especially long duration, lasting some hundreds of milliseconds, and it coincides with the period of depolarization of incoming afferents. It is generally assumed that the basis of presynaptic inhibition is depolarization, and that the morphological substrate of presynaptic inhibition consists of axon-to-axon synapses, the origin of whose presynaptic elements is unknown. Convincing arguments have been presented for regarding gamma-aminobutyric acid as a mediator of presynaptic inhibition, at least in the neuromuscular synapses of crustaceans and in the spinal cord of vertebrates. Sechenov&rsquos inhibition, as demonstrated in the frog, is apparently a function of presynaptic inhibition. Another type of inhibition is the secondary type, also known as pessimum in the theory of parabiosis, this term is applied to the blocking of excessive excitation, as first described by N. E. Vvedenskii. It is difficult to elicit such inhibition under experimental physiological conditions, but the phenomenon can be demonstrated in abnormal (specifically, convulsive) states.

In his work on the conditioned reflex, I. P. Pavlov identified two types of inhibition: external inhibition is the inhibition of any ongoing activity by an orienting reflex in response to an extraneous stimulus, while internal inhibition refers to the extinction of conditioned reflexes, the differentiation of conditioned reflexes, or the formation of delayed and trace-conditioned reflexes. Another type of inhibition identified by Pavlov is protective inhibition, which prevents the overstimulation or overexhaustion of the nerve centers. Disruption of the relationship between inhibition and excitation results in various nervous and mental disorders.


The Effects of Drugs

Different types of drugs can affect the chemical transmission and change the effects of neurotransmitters. This can include medications used to alleviate the symptoms of certain mental health conditions, such as SSRIs, benzodiazepines, and anti-psychotics. Neurotransmission can also be affected by illicit drugs such as cocaine, marijuana, and heroin.

Medication

    Selective Serotonin Re-uptake Inhibitors (SSRIs) are a type of antidepressant used to relieve symptoms of conditions such as depression, anxiety, posttraumatic stress disorder, panic disorder, obsessive compulsive disorder, and phobias.

Illicit Drugs

Depending on the type, illicit drugs can either slow down or speed up the central nervous system and autonomic functions. Marijuana contains the psychoactive chemical tetrahydrocannabinol (THC) which interacts with, and binds to cannabinoid receptors. This produces a relaxing effect and can also increase levels of dopamine.

Heroin binds to the opioid receptors and triggers the release of extremely high levels of dopamine. The more that heroin is used, the more likely a tolerance will develop from it, meaning that the brain will not function the way it did before starting the drug.

This can cause levels of dopamine to drop when the drug is stopped, which can ultimately lead to this drug being addictive so the user can feel the ‘high’ from the dopamine again.

Cocaine is a stimulant drug as it speeds up the central nervous system, increasing heart rate, blood pressure, alertness, and energy. Cocaine essentially gives the brain a surge of dopamine with quick effects. The effects of cocaine do not typically last very long and can make a person irritable or depressed afterwards, leading to a craving of more.

Cocaine can be highly addictive due to the way it affects the dopamine levels and reward system of the brain. Ecstasy is a psychoactive drug, which works as a stimulant as well as a hallucinogenic. Ecstasy works by binding to serotonin receptors and stimulating them, as well as influencing norepinephrine and dopamine.

Ecstasy can bring about feelings of pleasure and warmth, overall decreasing anxiety in the moment. However, regular use and aftereffects can increase anxiety, irritability, sleep difficulties, and depressed feelings.

About the Author

Olivia Guy-Evans obtained her undergraduate degree in Educational Psychology at Edge Hill University in 2015. She then received her master’s degree in Psychology of Education from the University of Bristol in 2019. Olivia has been working as a support worker for adults with learning disabilities in Bristol for the last four years.

How to reference this article:

How to reference this article:

Guy-Evans, O. (2021, Feb 21). Neurotransmitters: types, function and examples. Simply Psychology. https://www.simplypsychology.org/neurotransmitter.html

APA Style References

Boto, T., & Tomchik, S. M. (2019). The excitatory, the inhibitory, and the modulatory: mapping chemical neurotransmission in the brain. Neuron, 101(5), 763-765.

Martin, E. I., Ressler, K. J., Binder, E., & Nemeroff, C. B. (2009). The neurobiology of anxiety disorders: brain imaging, genetics, and psychoneuroendocrinology. The Psychiatric Clinics of North America, 32(3), 549–575. https://doi.org/10.1016/j.psc.2009.05.004.

Haam, J., & Yakel, J. L. (2017). Cholinergic modulation of the hippocampal region and memory function. Journal of Neurochemistry, 142, 111-121. Tabet, N. (2006). Acetylcholinesterase inhibitors for Alzheimer’s disease: anti-inflammatories in acetylcholine clothing!. Age and Ageing, 35(4), 336-338..


Watch the video: Proprioceptive Neuromuscular Facilitation PNF and Reciprocal Inhibition RI (May 2022).


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