Some Special Characteristics of Synaptic Transmission
Fatigue of Synaptic Transmission. When excitatorysynapses 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 progres-sively less in succeeding milliseconds or seconds. This is called fatigue of synaptic transmission.
Fatigue is an exceedingly important characteristic of synaptic function because when areas of the nervous system become overexcited, fatigue causes them to lose this excess excitability after awhile. For example, fatigue is probably the most important means by which the excess excitability of the brain during an epileptic seizure is finally subdued so that the seizure ceases. Thus, the development of fatigue is a protective mech-anism against excess neuronal activity..
The mechanism of fatigue is mainly exhaustion or partial exhaustion of the stores of transmitter sub-stance in the presynaptic terminals. The excitatory ter-minals on many neurons can store enough excitatory transmitter to cause only about 10,000 action poten-tials, and the transmitter can be exhausted in only a few seconds to a few minutes of rapid stimulation. Part of the fatigue process probably results from two other factors as well: (1) progressive inactivation of many of the postsynaptic membrane receptors and (2) slow development of abnormal concentrations of ions inside the postsynaptic neuronal cell.
Effect of Acidosis or Alkalosis on Synaptic Transmission. Mostneurons are highly responsive to changes in pH of the surrounding interstitial fluids. Normally, alkalosisgreatly increases neuronal excitability. For instance, arise 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. This can be demonstrated especially well by asking a person who is predisposed to epileptic seizures to overbreathe. The overbreathing blows off carbon dioxide and therefore elevates the pH of the blood momentarily, but even this short time can often precip-itate an epileptic attack.
Conversely, acidosis greatly depresses neuronal activ-ity; a fall in pH from 7.4 to below 7.0 usually causes acomatose state. For instance, in very severe diabetic or uremic acidosis, coma virtually always develops.
Effect of Hypoxia on Synaptic Transmission. Neuronalexcitability is also highly dependent on an adequate supply of oxygen. Cessation of oxygen for only a few seconds can cause complete inexcitability 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 areknown to increase the excitability of neurons, and others are known to decrease excitability. For instance, caffeine, theophylline, and theobromine, which arefound 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 nor-mally inhibitory transmitter substances, especially theinhibitory effect of glycine in the spinal cord. Therefore, the effects of the excitatory transmitters become over-whelming, 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 signalfrom 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 presy-naptic 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 excita-tory 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. Neurophysiologists can measure the minimal delay time between an input volley of impulsesinto a pool of neurons and the consequent output volley. From the measure of delay time, one can then estimate the number of series neurons in the circuit.
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