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Endogenous Release of γ‐Aminobutyric Acid from the Medial Preoptic Area Measured by Microdialysis in the Anaesthetised Rat
Author(s) -
Herbison Allan E.,
Heavens Robert P.,
Dyer Richard G.
Publication year - 1990
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1990.tb04947.x
Subject(s) - microdialysis , chemistry , verapamil , aminobutyric acid , tetrodotoxin , medicine , endocrinology , chloral hydrate , extracellular , pharmacology , calcium , biochemistry , biology , receptor , organic chemistry
The characteristics of γ‐aminobutyric acid (GABA) release as monitored by microdialysis have been investigated in the chloral hydrate anaesthetised rat. The high outflow of GABA following insertion of the microdialysis probe (membrane 2 mm in length, 0.5 mm in diameter) into the medial preoptic area was found to decline to a stable baseline level after 2 h. After this time, perfusion with a medium containing 100 m M potassium ions evoked a 56‐fold increase in GABA outflow. The addition of the calcium channel blocker verapamil (100 n M ) to the perfusion medium induced significant 25 and 50% reductions in basal and potassium‐stimulated GABA outflow, respectively. In the same animals, verapamil caused an 80% decrease in potassium‐stimulated noradrenaline outflow. The glutamic acid decarboxylase inhibitors 3‐mercaptopropionic acid and l‐allylglycine added to the perfusion medium at a concentration of 10 m M reduced basal GABA release by approximately 50% with different lime‐courses of action. Ethanolamine‐ O ‐suIfate, a GABA‐transaminase inhibitor, induced significant increases in basal GABA outflow 90 min after inclusion in the perfusion medium. These results demonstrate that microdialysis is a suitable technique with which to monitor extracellular levels of GABA and provide in vivo data on GABA release and degradation mechanisms.