have the neuron as their primary site of action. CNS neurons are capable of transmitting information to and
receiving information from other neurons and peripheral end organs, such as muscle cells, glandular cells, and
specialized receptors, for example, those involved with proprioception, temperature sensing, and so on.
The depolarization associated with an action potential results in the calcium-facilitated release of a specific
chemical substance at the synapse between two neurons. This chemical substance or neurotransmitter is released, diffuses across the synaptic cleft, and interacts with the membrane of the second neuron to initiate a local change in the ionic composition and a local altered potential difference in the second neuron. This
potential difference change is known as a postsynaptic potential, and the direction of the potential change may
be either depolarizing or hyperpolarizing.A depolarizing postsynaptic potential is called an excitatory postsynaptic potential (EPSP). If the magnitude of depolarization produced by EPSPs in the second neuron is great enough, an action potential produced in the second neuron will be transmitted in an all-or-none fashion through the neuron and its processes. If, on the other hand, a hyperpolarizing potential (known as an inhibitory postsynaptic potential,or IPSP) is produced, it will inhibit the formation of depolarizing action potentials.
Most cells normally receive a large excitatory input with a more or less constant generation of action potentials.The net result of generated IPSPs will be to decrease the number of nerve impulses per unit of time.
By these mechanisms, neurotransmitters producing either an EPSP (excitatory neurotransmitter) or an IPSP
(inhibitory transmitter) directly influence the number of action potentials generated by the neurons with which
they interact.Morphologically, many synapses in the CNS appear
to be quite similar to those for the peripheral autonomic nervous system. Electron microscopic studies
have verified the similarities and have shown the presence of several types of storage vesicles in the areas of
synapses. Neurons may synthesize, store, and release one or more transmitters. Many more synapses exist in
the CNS than in the periphery, and many more neurotransmitters appear to be involved.
The several ways in which pharmacological agents can either increase or decrease neurotransmission are
illustrated in . The agent can increase the amount of transmitter at the synapse and thereby produce an exaggerated effect. This can be accomplished by (1) increasing the rate of transmitter synthesis, (2) increasing the rate of transmitter release, or (3) prolonging the time the transmitter is in the synapse. This last
mechanism can be accomplished either by inhibiting enzymatic breakdown or by inhibiting the reuptake of a
previously released transmitter.
In contrast, an agent can produce a diminished response by (1) decreasing synthesis of transmitter, (2) increasing transmitter metabolism, (3) promoting an increased neuronal uptake, or (4) blocking access of the
transmitter to its receptor.The first three processes tend to diminish the amount of transmitter in the synaptic
cleft. Some agents (including several useful drugs) possess most of these capabilities at norepinephrine,
dopamine, serotonin, histamine, and acetylcholine (ACh) synapses. Several important drugs interfere with
other CNS transmitter systems, particularly some of the amino acid transmitters, in some of the above mentioned ways to produce their effects.
In the mammalian CNS powerful inhibitory systems function continually to slow the number of action potentials generated. The effects of stimulating an excitatory pathway can appear to be exaggerated if normal inhibitory influences to that region are diminished.
Correspondingly, an inhibitory pathway will appear exaggerated if part of the excitatory influence to that system has been removed.
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Unknown - Monday, 10 January 2011
