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gamma-Hydroxybutyric acid and baclofen decrease extracellular acetylcholine levels in the hippocampus via GABA(B)

F Nava¹, G Carta, M Bortolato

¹Department of Neuroscience "Bernard B. Brodie", University of Cagliari, Cagliari, Italy. felnava@tin.it

European Journal of Pharmacology

|November 17, 2001

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Gamma-hydroxybutyric acid (GHB) and baclofen reduce hippocampal acetylcholine. This effect is mediated by GABA(B) receptors, suggesting their role in GHB

Area of Science:

Neuroscience
Pharmacology
Neurochemistry

Background:

Gamma-hydroxybutyric acid (GHB) is a substance with complex neurochemical effects.
Baclofen is a selective agonist for GABA(B) receptors.
Acetylcholine in the hippocampus plays a crucial role in cognitive functions.

Purpose of the Study:

To investigate the effect of GHB and baclofen on extracellular hippocampal acetylcholine levels.
To determine the involvement of GABA(B) receptors in GHB's action on acetylcholine release.

Main Methods:

Microdialysis in freely moving rats.
Administration of GHB and baclofen at varying doses.
Use of GABA(B) receptor antagonist (SCH 50911) and a putative GHB receptor antagonist (NCS 382).

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Main Results:

GHB dose-dependently reduced extracellular hippocampal acetylcholine.
Baclofen also dose-dependently reduced acetylcholine levels.
The GABA(B) receptor antagonist SCH 50911 blocked the effects of both GHB and baclofen.
The putative GHB receptor antagonist NCS 382 was ineffective.

Conclusions:

GHB-induced reduction in hippocampal acetylcholine release is mediated via GABA(B) receptors.
Hippocampal GABA(B) receptors may be involved in cognitive processes.
These findings support a role for GABA(B) receptors in the amnesic effects of GHB intoxication.