Document Detail

Inhibition by apomorphine of the potassium-evoked release of [3H]-gamma-aminobutyric acid from the rat substantia nigra in vitro.
MedLine Citation:
PMID:  7317688     Owner:  NLM     Status:  MEDLINE    
1 The spontaneous and potassium-evoked release of tritium from the rat substantia nigra prelabelled with [(3)H]-gamma-aminobutyric acid [(3)H]-GABA were assessed in vitro under conditions of superfusion.2 Kainic acid lesions performed in the right caudate nucleus resulted in a 70% reduction in the ability of the homolateral nigral cells to take up and retain [(3)H]-GABA when compared with the unlesioned side. The potassium-evoked release of [(3)H]-GABA remained proportional to the radioactivity retained in the tissue suggesting that the nigral GABA neurones that survived kainic acid treatment were still functional.3 The spontaneous outflow of [(3)H]-GABA was significantly increased by exposure to different concentrations of exogenous GABA (10 to 1000 muM) when amino-oxyacetic acid was present in the incubation medium.4 Apomorphine in concentrations ranging from 1 to 30 muM inhibited the calcium-dependent release of [(3)H]-GABA induced by 1 min exposure to 30 mM K(+). These concentrations of apomorphine did not affect the spontaneous outflow of radioactivity. In vivo administration of haloperidol 0.2 mg/kg antagonized the in vitro inhibition by apomorphine of the K(+)-evoked release of [(3)H]-GABA.5 The results obtained with apomorphine and haloperidol suggest the presence of presynaptic dopamine-like inhibitory receptors in gabaergic nerve terminals.6 Dopamine in concentrations ranging up to 300 muM did not modify either the spontaneous or the K(+)-evoked release of [(3)H]-GABA from the substantia nigra. These concentrations of dopamine effectively displaced [(3)H]-dopamine recently taken up into the substantia nigra.7 Our results do not support the view that dendritic release of dopamine from the substantia nigra might be involved in the physiological modulation of the spontaneous or the stimulation-evoked release of GABA.
S Arbilla; L A Kamal; S Z Langer
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Publication Detail:
Type:  In Vitro; Journal Article    
Journal Detail:
Title:  British journal of pharmacology     Volume:  74     ISSN:  0007-1188     ISO Abbreviation:  Br. J. Pharmacol.     Publication Date:  1981 Oct 
Date Detail:
Created Date:  1982-03-13     Completed Date:  1982-03-13     Revised Date:  2009-11-18    
Medline Journal Info:
Nlm Unique ID:  7502536     Medline TA:  Br J Pharmacol     Country:  ENGLAND    
Other Details:
Languages:  eng     Pagination:  389-97     Citation Subset:  IM    
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MeSH Terms
Apomorphine / pharmacology*
Dopamine / pharmacology
Haloperidol / pharmacology
Kainic Acid / pharmacology
Potassium / pharmacology*
Receptors, Dopamine / physiology
Substantia Nigra / drug effects,  secretion*
gamma-Aminobutyric Acid / secretion*
Reg. No./Substance:
0/Receptors, Dopamine; 10028-17-8/Tritium; 487-79-6/Kainic Acid; 52-86-8/Haloperidol; 56-12-2/gamma-Aminobutyric Acid; 58-00-4/Apomorphine; 7440-09-7/Potassium

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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