Synaptic transmission is a key process whereby presynaptic neurotransmitter release drives electrical and biochemical signals via opening of postsynaptic channels.
7 Steps of Synaptic Transmission
Step 1: An action potential arrives at the axon terminal
Step 2: Membrane depolarization from action potential causes influx of calcium ions
Step 3: Docking of synaptic vesicles at the membrane
Step 4: Release of neurotransmitters into the synapse
Step 5: Receptor Activation
Step 6: Postsynaptic potentials generated in postsynaptic cell summate
Step 7: Neurotransmitter Inactivation
Synaptic transmission is a highly complex and regulated process. Not surprisingly, numerous neurological diseases are thought to result from alterations in one or several steps involved in synaptic transmission. In particular, alterations in dopaminergic transmission are widely believed to contribute to schizophrenia, whereas abnormalities in biogenic amine transmission might contribute to affective disorders. Furthermore, learning and memory are generally considered to be due to activity-dependent modifications of synaptic efficacy along the networks involved in the processing of information.
Fatigue of Synaptic Transmission
When excitatory synapses are repetitively stimulated at a rapid rate, the number of discharges by the postsynaptic neuron is at first very great, but the firing rate becomes progressively less in succeeding milliseconds or seconds. This is called fatigue of synaptic transmission.
Effect of Acidosis or Alkalosis on Synaptic Transmission
Most neurons are highly responsive to changes in pH of the surrounding interstitial fluids. Normally, alkalosis greatly increases neuronal excitability. For instance, a rise in arterial blood pH from the 7.4 norm to 7.8 to 8.0 often causes cerebral epileptic seizures because of increased excitability of some or all of the cerebral neurons.
Conversely, acidosis greatly depresses neuronal activity; a fall in pH from 7.4 to below 7.0 usually causes a comatose state. For instance, in very severe diabetic or uremic acidosis, coma virtually always develops.
Effect of Hypoxia on Synaptic Transmission.
Neuronal excitability is also highly dependent on an adequate supply of oxygen. Cessation of oxygen for only a few seconds can cause complete in-excitability of some neurons. This is observed when the brain’s blood flow is temporarily interrupted because within 3 to 7 seconds, the person becomes unconscious.
Effect of Drugs on Synaptic Transmission
Many drugs are known to increase the excitability of neurons, and others are known to decrease excitability. For instance, caffeine, theophylline, and theobromine, which are found in coffee, tea, and cocoa, respectively, all increase neuronal excitability, presumably by reducing the threshold for excitation of neurons.
Strychnine is one of the best known of all agents that increase excitability of neurons. However, it does not do this by reducing the threshold for excitation of the neurons; instead, it inhibits the action of some normally inhibitory transmitter substances, especially the inhibitory effect of glycine in the spinal cord. Therefore, the effects of the excitatory transmitters become overwhelming, and the neurons become so excited that they go into rapidly repetitive discharge, resulting in severe tonic muscle spasms.
Most anesthetics increase the neuronal membrane threshold for excitation and thereby decrease synaptic transmission at many points in the nervous system. Because many of the anesthetics are especially lipid soluble, it has been reasoned that some of them might change the physical characteristics of the neuronal membranes, making them less responsive to excitatory agents.
Synaptic Delay
During transmission of a neuronal signal from a presynaptic neuron to a postsynaptic neuron, a certain amount of time is consumed in the process of (1) discharge of the transmitter substance by the presynaptic terminal, (2) diffusion of the transmitter to the postsynaptic neuronal membrane, (3) action of the transmitter on the membrane receptor, (4) action of the receptor to increase the membrane permeability, and (5) inward diffusion of sodium to raise the excitatory postsynaptic potential to a high enough level to elicit an action potential. The minimal period of time required for all these events to take place, even when large numbers of excitatory synapses are stimulated simultaneously, is about 0.5 millisecond. This is called the synaptic delay.
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