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Brain Res. 1995 Jan 30;670(2):308-12.

Effects of thiopental, halothane and isoflurane on the calcium-dependent and -independent release of GABA from striatal synaptosomes in the rat.

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Institut National de la Santé et de la Recherche Médicale (INSERM U408), Faculté de Médecine Xavier Bichat, Paris, France.


The effects of the anesthetic agents thiopental, halothane and isoflurane on the release of GABA induced by depolarization and/or reversal of the GABA carrier were investigated in a synaptosomal preparation obtained from the rat striatum. Veratridine (1 microM) and KCl (9 mM) elicited a significant, Ca(2+)-dependent release of [3H]GABA. The KCl-evoked release was not significantly modified in the presence of nipecotic acid (10(-5) M), a selective blocker of the neuronal GABA carrier. The [3H]GABA release was significantly decreased by omega-conotoxin (10(-7) M, a blocker of the N voltage-dependent Ca2+ channels, but was affected by neither nifedipine (10(-4) M) nor omega-Aga-IVA (10(-7) M which block the L and P Ca2+ channels, respectively. Thiopental application (10(-5) to 10(-3) M) was followed by a dose-related, significant, decrease in both the veratridine and KCl-induced releases, whether nipecotic acid was present or not. In contrast, halothane and isoflurane (1-3%) failed to alter [3H]GABA release. Altogether, these results suggest that reduction of the depolarization-evoked GABA release might contribute to thiopental anesthesia, but this seems unlikely for volatile anesthetics.

[Indexed for MEDLINE]

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