GABA release from mouse brain slices following acute and chronic pentobarbital administration and during withdrawal

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Abstract

Ca2+-dependent K+-stimulated (3H)-γ-aminobutyric acid (GABA) release from mouse striatal and cerebellar slices following acute and chronic pentobarbital administration and during withdrawal was investigated. Acute administration of pentobarbital caused an increase of Ca2+-dependent K+-stimulated (3H)-GABA release from the striatum, but it did not exert any effect on cerebellum. Spontaneous (3H)-GABA release from the striatum and the cerebellum was not affected by acute pentobarbital treatment. This was further confirmed by the finding that pentobarbital (10-8-10-4M) potentiated Ca2+-dependent K+-stimulated (3H)-GABA release from the striatum, but not from the cerebellum in the in vitro assay. On the other hand, chronic administration of pentobarbital resulted in a decrease of spontaneous (3H)-GABA release and had no effect on Ca2+-dependent K+-stimulated GABA release from the striatum. The spontaneous release of (3H)-GABA from the striatum remained at significantly lower levels after an abrupt withdrawal from pentobarbital. In pentobarbital withdrawal mice, a decrease of (3H)-GABA release also was observed in the cerebellum. These results strongly suggest that the GABA system in the central nervous system plays an important role in barbiturate narcosis and further links the GABA system with the development of barbiturate tolerance and dependence.

Original languageEnglish
Pages (from-to)483-497
Number of pages15
JournalResearch Communications in Substances of Abuse
Volume3
Issue number4
Publication statusPublished - 01-01-1982
Externally publishedYes

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Pentobarbital
gamma-Aminobutyric Acid
Brain
Cerebellum
Aminobutyrates
Corpus Striatum
Stupor
Central Nervous System

All Science Journal Classification (ASJC) codes

  • Medicine (miscellaneous)

Cite this

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title = "GABA release from mouse brain slices following acute and chronic pentobarbital administration and during withdrawal",
abstract = "Ca2+-dependent K+-stimulated (3H)-γ-aminobutyric acid (GABA) release from mouse striatal and cerebellar slices following acute and chronic pentobarbital administration and during withdrawal was investigated. Acute administration of pentobarbital caused an increase of Ca2+-dependent K+-stimulated (3H)-GABA release from the striatum, but it did not exert any effect on cerebellum. Spontaneous (3H)-GABA release from the striatum and the cerebellum was not affected by acute pentobarbital treatment. This was further confirmed by the finding that pentobarbital (10-8-10-4M) potentiated Ca2+-dependent K+-stimulated (3H)-GABA release from the striatum, but not from the cerebellum in the in vitro assay. On the other hand, chronic administration of pentobarbital resulted in a decrease of spontaneous (3H)-GABA release and had no effect on Ca2+-dependent K+-stimulated GABA release from the striatum. The spontaneous release of (3H)-GABA from the striatum remained at significantly lower levels after an abrupt withdrawal from pentobarbital. In pentobarbital withdrawal mice, a decrease of (3H)-GABA release also was observed in the cerebellum. These results strongly suggest that the GABA system in the central nervous system plays an important role in barbiturate narcosis and further links the GABA system with the development of barbiturate tolerance and dependence.",
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T1 - GABA release from mouse brain slices following acute and chronic pentobarbital administration and during withdrawal

AU - Nabeshima, Toshitaka

AU - Ho, I. K.

PY - 1982/1/1

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N2 - Ca2+-dependent K+-stimulated (3H)-γ-aminobutyric acid (GABA) release from mouse striatal and cerebellar slices following acute and chronic pentobarbital administration and during withdrawal was investigated. Acute administration of pentobarbital caused an increase of Ca2+-dependent K+-stimulated (3H)-GABA release from the striatum, but it did not exert any effect on cerebellum. Spontaneous (3H)-GABA release from the striatum and the cerebellum was not affected by acute pentobarbital treatment. This was further confirmed by the finding that pentobarbital (10-8-10-4M) potentiated Ca2+-dependent K+-stimulated (3H)-GABA release from the striatum, but not from the cerebellum in the in vitro assay. On the other hand, chronic administration of pentobarbital resulted in a decrease of spontaneous (3H)-GABA release and had no effect on Ca2+-dependent K+-stimulated GABA release from the striatum. The spontaneous release of (3H)-GABA from the striatum remained at significantly lower levels after an abrupt withdrawal from pentobarbital. In pentobarbital withdrawal mice, a decrease of (3H)-GABA release also was observed in the cerebellum. These results strongly suggest that the GABA system in the central nervous system plays an important role in barbiturate narcosis and further links the GABA system with the development of barbiturate tolerance and dependence.

AB - Ca2+-dependent K+-stimulated (3H)-γ-aminobutyric acid (GABA) release from mouse striatal and cerebellar slices following acute and chronic pentobarbital administration and during withdrawal was investigated. Acute administration of pentobarbital caused an increase of Ca2+-dependent K+-stimulated (3H)-GABA release from the striatum, but it did not exert any effect on cerebellum. Spontaneous (3H)-GABA release from the striatum and the cerebellum was not affected by acute pentobarbital treatment. This was further confirmed by the finding that pentobarbital (10-8-10-4M) potentiated Ca2+-dependent K+-stimulated (3H)-GABA release from the striatum, but not from the cerebellum in the in vitro assay. On the other hand, chronic administration of pentobarbital resulted in a decrease of spontaneous (3H)-GABA release and had no effect on Ca2+-dependent K+-stimulated GABA release from the striatum. The spontaneous release of (3H)-GABA from the striatum remained at significantly lower levels after an abrupt withdrawal from pentobarbital. In pentobarbital withdrawal mice, a decrease of (3H)-GABA release also was observed in the cerebellum. These results strongly suggest that the GABA system in the central nervous system plays an important role in barbiturate narcosis and further links the GABA system with the development of barbiturate tolerance and dependence.

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