Synaptic receptors

Numerous processes modulate neurotransmitter synthesis, presynaptic excitabihty, neurotransmitter release, post-synaptic receptors, and post-synaptic excitabihty. 

ChEs control the duration of ACh-mediated action on post-synaptic receptors in cholinergic synapses, and have non-hydrolytic roles in nervous systems development and plasticity. 

N. A. Sharif (1985). Multiple synaptic receptors for neuroactive amino acid transmitters—new... 

Recall from our discussion of cocaine and amphetamines that the body responds to the long-term abuse of these stimulants by creating more depressant receptor sites. Likewise, the body recognizes the excessive inhibitory actions produced by alcohol and tries to recover by increasing the number of synaptic receptor sites that lead to nerve excitation. A tolerance for alcohol therefore develops. To receive the same inhibitory effect, the drinker is forced to drink more, which induces the body to create even more excitable synaptic receptor sites. Eventually, an excess of these excitatory receptor sites leads to perpetual body tremors, which can be subdued either by more drinking or, with greater difficulty, by a long-term cessation of alcohol consumption. 

Fig. 2. Representative hallucinogenic drugs which hear structural similarities to some of the monoamine transmitters. It has been hypothesized that these similarities may cause the hallucinogens 10 mimic natural transmitters at synaptic receptors in the brain. Note presence of benzene-ring structure in these substances, a structure that is present in four out of the live monoamines previously shown. Also note presence of indole ring in psilocybin and lyseigic acid diethylamide, a structure that is also present in the monoamines serotonin and histamine...

Binding to receptor Acetylcholine released from the synaptic vesicles diffuses across the synaptic space and binds to either post-synaptic receptors on the target cell or to presynaptic receptors in the membrane of the neuron that released the acetylcholine. 

Neurotransmitters can be classified as excitatory or inhibitory, depending on the nature of the action they elicit. Stimulation of excitatory neurons causes a movement of ions that results in a depolarization of the postsynaptic membrane. These excitatory postsynaptic potentials (EPSP) are generated by the following (1) Stimulation of an excitatory neuron causes the release of neurotransmitter molecules, such as norepinephrine or acetylcholine, which bind to receptors on the postsynaptic cell membrane. This causes a transient increase in the permeability of sodium (Na+) ions. (2) The influx of Na+ causes a weak depolarization or excitatory postsynaptic potential (EPSP). (3) If the number of excitatory fibers stimulated increases, more excitatory neurotransmitter is released, finally causing the EPSP depolarization of the postsynaptic cell to pass a threshold, and an all-or-none action potential is generated. [Note The generation of a nerve impulse typically reflects the activation of synaptic receptors by thousands of excitatory neurotransmitter molecules released from many nerve fibers.] (See Figure 8.2 for an example of an excitatory pathway.)... 

When fluoxetine or other effective but less specific serotonin uptake inhibitors are given, a rapid decrease in serotonin turnover occurs and the rate of firing of single neural units in the serotonin rich raphe area of the brain is reduced. This decrease in serotonin turnover and release may be a compensatory mechanism in response to an enhanced action of serotonin on the synaptic receptors. 

Martin, P., Tissier, M. H., Adrien, J., and Puech, A. J. 1991. Antidepressant-like effects of buspirone mediated by the 5-HT1A post-synaptic receptors in the learned helplessness paradigm. Life Sci., 48(26), 2505-2511. 

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