Blockade of intracranial self-stimulation by antipsychotic drugs: failure to correlate with central alpha-noradrenergic blockade

The involvement of central alpha-noradrenergic receptors in intracranial self-stimulation (ICSS) was studied. Dose-response curves were established for the blockade of ICSS by the antipsychotic drugs chlorpromazine, thioridazine, clozapine, and pimozide and the alpha-antagonist phenoxybenzamine. Ant...

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Bibliographic Details
Published in:Psychopharmacology 1977-01, Vol.53 (3), p.283-288
Main Authors: Zarevics, P, Weidley, E, Setler, P
Format: Article
Language:English
Subjects:
Animals
Antipsychotic Agents - pharmacology
Chlorpromazine - pharmacology
Clozapine - pharmacology
Depression, Chemical
Electric Stimulation
Male
Muscle Contraction - drug effects
Phenoxybenzamine - pharmacology
Pimozide - pharmacology
Rats
Receptors, Adrenergic - drug effects
Receptors, Adrenergic, alpha - drug effects
Reflex - drug effects
Self Stimulation - drug effects
Thioridazine - pharmacology
Time Factors
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Summary:The involvement of central alpha-noradrenergic receptors in intracranial self-stimulation (ICSS) was studied. Dose-response curves were established for the blockade of ICSS by the antipsychotic drugs chlorpromazine, thioridazine, clozapine, and pimozide and the alpha-antagonist phenoxybenzamine. Antagonism of the facilitation, produced by the central alpha-agonist clonidine, of flexor withdrawal reflexes in the reserpinized spinal rat was used to assess the central alpha-blocking potency of the same drugs, and dose-response curves were established. No correlation was found between central alpha-blockade, as reflected by the ED50 for blockade of clonidine-facilated spinal reflexes, and the ED50 for blockade of ICSS. Pimozide blocked ICSS at doses virtually devoid of central alpha-blocking activity, while phenoxybenzamine was a potent alpha-antagonist and a weak blocker of ICSS. The lack of correlation between central alpha-blockade and decreased ICSS suggests that alpha-receptors are not critically involved in self-stimulation behavior.
ISSN:0033-3158
1432-2072
DOI:10.1007/BF00492365