Erowid References Database
Marczynski TJ, Burns LL.
“Reward Contingent Positive Variation (RCPV) and Post-Reinforcement EEG Synchronization (PRS) in the Cat: Physiological Aspects, the Effect of Morphine and LSD-25, and a New Interpretation of Cholinergic Mechanisms”.
The literature on reward contingent positive variation (RCPV) and post-reinforcement EEG synchronization (PRS) in the cat is reviewed with reference to physiological aspects and reward induced inhibition of the ascending reticular activating system (ARAS). The pharmacological aspects of PRS and RCPV are discussed. In cats trained to perform in the dark and not displaying PRSRCPV, LSD-25 (15-30 mcg/kg i.m.) restored these responses, which were normally only seen in the light. This did not occur with chlorpromazine, morphine, barbiturates and other tranquilizers. Morphine (0.1-0.4 mg/kg i.m.) caused dramatic enhancement of the PRS and RCPV responses. Higher doses had a biphasic action. The possible mechanism of this morphine effect is discussed with reference to the effects of central catecholamine depletors, (e.g. reserpine, tetrabenazine), haloperidol, phenoxybenzamine, propranolol, atropine, mepyramine, LSD-25. The suppression of PRS and the simultaneous increase in background electrocorticogram synchronization by antimuscarine drugs is described as well as the restoration of PRS -RCPV by physotigmine-salicylate (0.06-0.08 mg/kg i.v.) after blockage by atropine or scopolamine hydrobromide. A new interpretation of the cholinergic mechanism in PRS and human alpha activity is proposed. ACh is primarily an excitatory transmitter at the hypothalamic and cortical levels; GABA plays role of hyperpolarizing transmitter in the recurrent inhibitory athways. It is not necessary to assume 2 functionally opposed cholinergic systems to explain the action of antimuscarinic drugs on PRS and human a-activity. Also, a spontaneous slackening of tonus of the cholinergic component of ARAS and/or blockade of its facilitatory influences on input to the thalamic relay nuclei and cortex, do not explain the suppression of the PRS and human a-activity. The irregular PRS and ECoG slow wave activity characteristic of antimuscarinics and spontaneous slow wave sleep, reflect the irregular 'idling' of the recurrent inhibitory phasing, due to insufficient synaptic pressure on thalamic relay neurons.
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