Abstract
The mechanism of depression of the activating system by chlorpromazine was investigated on potentials recorded in the reticular formation and evoked by stimulation of the sciatic nerve.
The latency, duration and recovery cycles of two types of evoked potentials, "slow" and "fast," recorded in the medial reticular formation, have been described and differentiated on the basis of their latency and recovery cycle.
Chlorpromazine enhanced the amplitude of single evoked "fast" and "slow" potentials and markedly slowed the rate of recovery of both the "fast" and "slow" potentials. The "absolute" refractory period for the "fast" potential was not measurably increased, whereas the "absolute" refractory period for the "slow" potential was markedly increased.
Pentobarbital decreased the amplitude of single evoked potentials. It increased the "absolute" refractory period and slowed the rate of recovery of the "fast" potential. The effects of pentobarbital were thus differentiated from the effects of chlorpromazine.
It is suggested that chlorpromazine may act selectively by depressing the frequency response of neurones responsible for the "slow" potential recorded in the medial reticular formation.
Footnotes
- Received May 19, 1958.
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