Nimodipine prevents early loss of hippocampal CA1 parvalbumin immunoreactivity after focal cerebral ischemia in the rat.
The effect of focal cerebral ischemia induced by middle cerebral artery occlusion on hippocampal interneurons containing the calcium-binding protein parvalbumin (PV) was studied in rats. Four hours after the onset of ischemia, a reduced number of PV-immunoreactive (-ir) neurons was observed in the lateral part of the CA1 region, while PV-ir was not altered in the CA2 and CA3 areas. Pretreatment with the L-type Ca2+ channel blocker nimodipine prevented the ischemia-induced loss of PV-ir in the CA1, suggesting a role for L-type voltage sensitive calcium channels in the mechanism of early neuronal alterations in the hippocampus CA1 region after focal cerebral ischemia.
Benyó
Z
Z
Department of Animal Physiology, University of Groningen, The Netherlands.
De Jong
G I
GI
Luiten
P G
PG
D000818:Animals; D001157:Arterial Occlusive Diseases / Q000150:complications*; D006624:Hippocampus / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism; D007150:Immunohistochemistry; D007395:Interneurons / Q000187:drug effects* / Q000378:metabolism; D002546:Ischemic Attack, Transient / Q000188:drug therapy* / Q000209:etiology; D008297:Male; D009553:Nimodipine / Q000494:pharmacology*; D010320:Parvalbumins / Q000032:analysis*; D051381:Rats; D017208:Rats, Wistar; D013997:Time Factors
D010320:Parvalbumins; D009553:Nimodipine