Reversed Alterations ofHippocampal Parvalbumin andProtein KinaseC-y Immunoreactivit After Stroke inSpontaneously Hypertensive Stroke-Prone Rats

Background andPurpose: Aging spontaneously hypertensive stroke-prone rats(SHR-SP) werepreviously showntodevelop neocortical strokes. Because thehippocampal CA1isselectively vulnerable toabnormal brainperfusion, theneuropathological effects ofspontaneous strokes were investigated on specific neurochemical alterations intwomajorcell typesofthehippocampal CA1inSHR-SP. Methods: Theimmunoreactivity forthey-isoform ofprotein kinaseC (inpyramidal cells) and parvalbumin (ininterneurons) was determined inthehippocampal CA1 byapplying monoclonal antibodies. Because chronic treatment withthecalcium antagonist nimodipine prevents thedevelopment ofstrokes inSHR-SP,we comparedSHR-SP(stroke) withage-matched nimodipine-treated rats (nonstroke). Results: After stroke incontrol animals, we observed astrikingly enhanced immunoreactivity forprotein kinase C-y inCA1pyramidal cells compared withnimodipine-treated rats, which can beinterpreted as theresult ofan increased activation ofthesecells. Thepathological increase ofprotein kinase C-y immunoreactivity was accompanied bya reduced parvalbuminergic innervation ofthese pyramidal cells insymptomatic SHR-SP. Conclusions: Because parvalbumin ispresent ina subset ofGABAergic inhibitory interneurons, these datasuggest thatincreased activity ofCAlpyramidal cells afterspontaneous stroke may partially be related toa decreased inhibitory input on these cells. (Stroke. 1993;24:2082-2086.)