O'Regan M H, Simpson R E, Perkins L M, Phillis J W
Department of Physiology, School of Medicine, Wayne State University, Detroit, MI 48201.
Neurosci Lett. 1992 Apr 13;138(1):169-72. doi: 10.1016/0304-3940(92)90498-v.
The effects of the selective adenosine A2 receptor agonist 2-p-(2-carboxyethyl)phenethylamino-5'-N-ethylcarboxamido adenosine hydrochloride (CGS 21680) on aspartate and glutamate release from the ischemic rat cerebral cortex were studied with the cortical cup technique. Cerebral ischemia (20 min) was elicited by four vessel occlusion. Pretreatment with CGS 21680 failed to alter basal excitatory amino acid levels, however, CGS 21680 at 10(-6) M significantly enhanced the ischemia-evoked release. Thus, aspartate and glutamate release during ischemia can be stimulated via the activation of A2 receptors, in addition to the suppression of excitatory amino acid release mediated by selective A1 receptor agonists.