The presence of autoreceptors for gamma-aminobutyric acid (GABA) in the CNS was reinvestigated using rat cortex synaptosomes prelabeled with [3H]GABA and exposed to GABA by superfusion in the presence of a new GABA uptake inhibitor, N-(4,4-diphenyl-3-butenyl)-nipecotic acid (SK&F 89976A). This compound itself did not increase the basal or the depolarization-evoked release of [3H]GABA. GABA reduced in a concentration-dependent way the release of [3H]GABA evoked by 15 mM K+. The effect was not antagonized by bicuculline, picrotoxin or by the new GABAA antagonist SR 95531. The GABAA agonist muscimol did not affect [3H]GABA release. This was reduced by (-)baclofen (but not by the (+) isomer) and the concentration-inhibition curve of (-)baclofen was superimposable on to that of GABA. Also the K+-evoked release of endogenous GABA was stereoselectively and concentration dependently inhibited by the (-) enantiomer of baclofen. It is concluded that the release of GABA from rat cortical nerve endings may be inhibited through the activation of autoreceptors which appear to belong to the GABAB type.

Studies on 3H-GABA and endogenous GABA release in rat cerebral cortex suggest the presence of autoreceptors of the GABA B type / Pittaluga, A; Asaro, D; Pellegrini, Graziella; Raiteri, M.. - In: EUROPEAN JOURNAL OF CLINICAL PHARMACOLOGY. - ISSN 0031-6970. - STAMPA. - 144:(1987), pp. 45-52.

Studies on 3H-GABA and endogenous GABA release in rat cerebral cortex suggest the presence of autoreceptors of the GABA B type

PELLEGRINI, Graziella;
1987

Abstract

The presence of autoreceptors for gamma-aminobutyric acid (GABA) in the CNS was reinvestigated using rat cortex synaptosomes prelabeled with [3H]GABA and exposed to GABA by superfusion in the presence of a new GABA uptake inhibitor, N-(4,4-diphenyl-3-butenyl)-nipecotic acid (SK&F 89976A). This compound itself did not increase the basal or the depolarization-evoked release of [3H]GABA. GABA reduced in a concentration-dependent way the release of [3H]GABA evoked by 15 mM K+. The effect was not antagonized by bicuculline, picrotoxin or by the new GABAA antagonist SR 95531. The GABAA agonist muscimol did not affect [3H]GABA release. This was reduced by (-)baclofen (but not by the (+) isomer) and the concentration-inhibition curve of (-)baclofen was superimposable on to that of GABA. Also the K+-evoked release of endogenous GABA was stereoselectively and concentration dependently inhibited by the (-) enantiomer of baclofen. It is concluded that the release of GABA from rat cortical nerve endings may be inhibited through the activation of autoreceptors which appear to belong to the GABAB type.
144
45
52
Studies on 3H-GABA and endogenous GABA release in rat cerebral cortex suggest the presence of autoreceptors of the GABA B type / Pittaluga, A; Asaro, D; Pellegrini, Graziella; Raiteri, M.. - In: EUROPEAN JOURNAL OF CLINICAL PHARMACOLOGY. - ISSN 0031-6970. - STAMPA. - 144:(1987), pp. 45-52.
Pittaluga, A; Asaro, D; Pellegrini, Graziella; Raiteri, M.
File in questo prodotto:
Non ci sono file associati a questo prodotto.
Pubblicazioni consigliate

Caricamento pubblicazioni consigliate

Licenza Creative Commons
I metadati presenti in IRIS UNIMORE sono rilasciati con licenza Creative Commons CC0 1.0 Universal, mentre i file delle pubblicazioni sono rilasciati con licenza Attribuzione 4.0 Internazionale (CC BY 4.0), salvo diversa indicazione.
In caso di violazione di copyright, contattare Supporto Iris

Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11380/585245
Citazioni
  • ???jsp.display-item.citation.pmc??? 8
  • Scopus 89
  • ???jsp.display-item.citation.isi??? 110
social impact