Abstract |
The aim of this work was to study the role of pallidal GABAa and GABAb neurotransmission in the behavioral disorders induced by pressure. The effects of GABAb antagonist 5-aminovalleric acid (5-AVA) or GABAa antagonist gabazine administrations in the globus pallidus (GP) on locomotor and motor hyperactivity (LMA) and myoclonia expressions in the model of the rat submitted to 8 MPa of helium- oxygen breathing mixture were analyzed. The administration of GABAa antagonist gabazine enhances the occurrence of the epileptic seizures, slightly increases LMA but decreases myoclonia. In contrast, the administration of GABAb antagonist 5-AVA decreases both LMA and myoclonia during the compression and the beginning of the holding time at 8 MPa. These data indicate that some behavioral disorders induced by pressure are in relation with GABAergic neurotransmission and establish clearly that GABAa and GABAb receptor mediations have distinct functions in the GP of the rat.
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Authors | O Darbin, J J Risso, M Weiss, J C Rostain |
Journal | Pharmacology, biochemistry, and behavior
(Pharmacol Biochem Behav)
2002 Jan-Feb
Vol. 71
Issue 1-2
Pg. 319-24
ISSN: 0091-3057 [Print] United States |
PMID | 11812539
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Amino Acids, Neutral
- GABA Antagonists
- GABA-A Receptor Antagonists
- GABA-B Receptor Antagonists
- Pyridazines
- Receptors, GABA-A
- Receptors, GABA-B
- 5-aminovaleric acid
- gabazine
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Topics |
- Amino Acids, Neutral
(administration & dosage)
- Animals
- Atmospheric Pressure
- Epilepsy
(chemically induced, drug therapy)
- GABA Antagonists
(administration & dosage)
- GABA-A Receptor Antagonists
- GABA-B Receptor Antagonists
- Globus Pallidus
(drug effects, physiology)
- Hyperkinesis
(chemically induced, drug therapy)
- Male
- Mental Disorders
(chemically induced, drug therapy)
- Myoclonus
(chemically induced, drug therapy)
- Pyridazines
(administration & dosage)
- Rats
- Rats, Sprague-Dawley
- Receptors, GABA-A
(physiology)
- Receptors, GABA-B
(physiology)
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