Acetylcholine output from the ischemic rat cerebral cortex: effects of adenosine agonists.

Abstract

The efflux of acetylcholine (ACh) from the ischemic rat cerebral cortex was examined using the cortical cup technique and an HPLC with electrochemical detection assay. Four vessel occlusion of the cerebral circulation caused a rapid increase in ACh efflux into the cortical superfusates, which was then sustained during the 20 min period of occlusion. Reperfusion was associated with a rapid return of ACh efflux to basal levels. The A1 and A2 selective adenosine receptor agonists, N6-cyclopentyladenosine (10(-8) and 10(-10) M) and CGS 21680 (10(-8)), failed to significantly alter ischemia-evoked release of ACh. Because ACh is known to enhance NMDA receptor mediated neuronal depolarization and intracellular Ca2+ levels, and to potentiate L-glutamate-induced neural degeneration, the present findings suggest that ACh could contribute to ischemic brain injury.

• Authors: J W Phillis, M Smith-Barbour, L M Perkins, M H O'Regan
• Journal: Brain research (Brain Res) Vol. 613 Issue 2 Pg. 337-40 (Jun 11 1993) ISSN: 0006-8993 [Print] Netherlands
• PMID: 8186988 (Publication Type: Journal Article, Research Support, U.S. Gov't, P.H.S.)

Chemical References

• Antihypertensive Agents
• Phenethylamines
• Receptors, Purinergic P1
• Receptors, Purinergic P2
• 2-(4-(2-carboxyethyl)phenethylamino)-5'-N-ethylcarboxamidoadenosine
• N(6)-cyclopentyladenosine
• Adenosine
• Acetylcholine

Topics

• Acetylcholine (metabolism)
• Adenosine (analogs & derivatives, pharmacology)
• Animals
• Antihypertensive Agents (pharmacology)
• Cerebral Cortex (drug effects, metabolism)
• Chromatography, High Pressure Liquid
• Ischemic Attack, Transient (metabolism)
• Male
• Phenethylamines (pharmacology)
• Rats
• Rats, Sprague-Dawley
• Receptors, Purinergic P1 (drug effects, physiology)
• Receptors, Purinergic P2 (drug effects, physiology)
• Time Factors