Premium
Antiepileptic Agents Affect Hypothalamic β‐Endorphin Concentrations
Author(s) -
Martini Alberto,
Sacerdote Paola,
Mantegazza Paolo,
Panerai Alberto E.
Publication year - 1984
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1984.tb12811.x
Subject(s) - chemistry , ethosuximide , pharmacology , anticonvulsant , medicine , endocrinology , epilepsy , psychiatry
β‐Endorphin, Met‐enkephalin, substance P, and somatostatin concentrations were evaluated in the hypothalami of rats treated either acutely or chronically (15 days) with sodium valproate, diphenylhydantoin, phenobarbital, or ethosuximide. All of these drugs, with the exception of ethosuximide, induced significant decreases in β‐endorphin concentrations after acute treatment, while only sodium valproate induced a decrease after chronic treatment. The acute and chronic effects of sodium valproate were also produced by aminooxyacetic acid, an inhibitor of γ‐aminobutyric acid (GABA) transaminase, while another GABA transaminase inhibitor, ethanolamine‐ O ‐sulphate, and THIP, a GABA receptor agonist, were effective after acute administration. Metenkephalin, substance P, and somatostatin concentrations were never affected by the drugs used. The present results, indicating that antiepileptic agents specifically decrease β‐endorphin concentrations, seem to correlate well with the capacity of these agents to blunt the epileptic activity of the peptides tested. Moreover, our data suggest that GABA may be involved in the anticonvulsant‐induced reduction of β‐endorphin concentrations.