REVERSED ALTERATIONS OF HIPPOCAMPAL PARVALBUMIN AND PROTEIN-KINASE C-GAMMA IMMUNOREACTIVITY AFTER STROKE IN SPONTANEOUSLY HYPERTENSIVE STROKE-PRONE RATS

Background and Purpose: Aging spontaneously hypertensive stroke-prone rats (SHR-SP) were previously shown to develop neocortical strokes. Be cause the hippocampal CA1 is selectively vulnerable to abnormal brain perfusion, the neuropathological effects of spontaneous strokes were i nvestigated on specific neurochemical alterations in two major cell ty pes of the hippocampal CA1 in SHR-SP. Methods: The immunoreactivity fo r the gamma-isoform of protein kinase C (in pyramidal cells) and parva lbumin (in interneurons) was determined in the hippocampal CA1 by appl ying monoclonal antibodies. Because chronic treatment with the calcium antagonist nimodipine prevents the development of strokes in SHR-SP, we compared SHR-SP (stroke) with age-matched nimodipine-treated rats ( nonstroke). Results: After stroke in control animals, we observed a st rikingly enhanced immunoreactivity for protein kinase C-gamma in CA1 p yramidal cells compared with nimodipine-treated rats, which can be int erpreted as the result of an increased activation of these cells. The pathological increase of protein kinase C-gamma immunoreactivity was a ccompanied by a reduced parvalbuminergic innervation of these pyramida l cells in symptomatic SHR-SP. Conclusions: Because parvalbumin is pre sent in a subset of GABAergic inhibitory interneurons, these data sugg est that increased activity of CA1 pyramidal cells after spontaneous s troke may partially be related to a decreased inhibitory input on thes e cells.