Glycine antagonism does not block ischemic spontaneous depolarization in the rat.
This study examined the effect of glycine recognition site antagonism (ACEA 1021) on the incidence of spontaneous depolarizations in the penumbra of a focal ischemic lesion. Rats were administered either vehicle (n = 7), ACEA 1021 (n = 7) or dizocilpine (n = 5) and then underwent 90 min middle cerebral artery occlusion. The cortical direct current (DC) potential was recorded. During ischemia, 7 +/- 3 DC shifts occurred in the vehicle group. ACEA 1021 did not reduce this frequency (7 +/- 2 DC shifts) although dizocilpine did (1 +/- 1 DC shifts; p = 0.02). The previously demonstrated neuroprotective property of ACEA 1021 during focal cerebral ischemia cannot be attributed to reduction of spontaneous depolarization in the ischemic penumbra.
Takaoka
S
S
Department of Anesthesiology and Resuscitation, Yamagata University, Japan.
Bart
R D
RD
Pearlstein
R D
RD
Warner
D S
DS
D000818:Animals; D016291:Dizocilpine Maleate / Q000494:pharmacology*; D018691:Excitatory Amino Acid Antagonists / Q000494:pharmacology*; D002546:Ischemic Attack, Transient / Q000503:physiopathology*; D008297:Male; D008564:Membrane Potentials / Q000187:drug effects; D018696:Neuroprotective Agents / Q000494:pharmacology*; D011810:Quinoxalines / Q000494:pharmacology*; D051381:Rats; D017208:Rats, Wistar; D018009:Receptors, Glycine / Q000037:antagonists & inhibitors*
D018691:Excitatory Amino Acid Antagonists; D018696:Neuroprotective Agents; D011810:Quinoxalines; D018009:Receptors, Glycine; C092062:licostinel; D016291:Dizocilpine Maleate