Neurophysiological Properties of Neuroleptic Agents in Animals

  • I. Jurna
Part of the Handbook of Experimental Pharmacology book series (HEP, volume 55 / 1)


When one tries to give an account of the action of neuroleptic agents on neurons in the central nervous system, it seems reasonable to start from the principle that drugs such as reserpine or CPZ impair impulse transmission at synapses where monoamines act as transmitter substances. Reserpine depletes NA from sympathetically innervated tissues (for literature see Carlsson et al., 1957b; Carlsson, 1966), and diminishes or abolishes the effect of electrical or chemical stimulation of adrenergic nerves due to lack of the transmitter (Bertler et al., 1956; Bertler et al., 1958; Muscholl and Vogt, 1957, 1958, Trendelenburg and Gravenstein, 1958). There is better time correlation between the depression of adrenergic impulse transmission and a reduced tissue uptake of NA than between the disturbed nerve function and the reduced NA levels in the tissues (Andén et al., 19641). Similarly, reserpine decreases the content of NA, DA, and 5HT in the brain and spinal cord (Shore and Brodie, 1957; Shore et al., 1957; Carlsson, 1959,1965; Andén et al., 1967b) and inhibits the accumulation of NA in the brain when the amine is administered into the lateral ventricles (Glowinski and Axelrod, 1965, 1966). It is now generally accepted that changes in central nervous functions produced by reserpine are due to lack of the monoamines as transmitters (Carlsson, 1964), i.e., reserpine acts presynaptically in inhibiting monoaminergic impulse transmission. However, there is considerable disagreement when an attempt is made to correlate central effects in terms of changes in animal behavior with the impairment of the function of a particular monoaminergic transmitter.


Substantia Nigra Adenylate Cyclase Caudate Nucleus Ergot Alkaloid Neuroleptic Drug 
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