Loss of somatal neuropeptide y immunoreactivity in the rat hippocampus following transient cerebral ischemia.
Adult male Wistar rats were subjected to 20 min of global cerebral ischemia and allowed to survive for 1, 2, 4, or 21 days. The brains were processed for immunocytochemistry and the hippocampal neuropeptide Y (NPY)-immunoreactive (-i) neurons were counted and compared to control values. In order to map out the subregional distribution of ischemic cell loss in the hippocampus, cells were also counted in hematoxylin-eosin (HE)-stained brain sections processed from additional ischemic rats after 21 days survival. Cell counts demonstrated a significant loss of hippocampal NPY-i somata 1-21 days after ischemia. The ischemic loss of somatal NPY-i was in the CAI stratum oriens, the CA1 stratum radiatum, and the CA3(ab) subfield not correlated to hippocampal cell loss. NPY-i fibers were found in all subfields of the hippocampus 1-21 days after ischemia. It is known that the majority (>50%) of hippocampal somatostatin-i (SS) neurons also costore NPY-i and the SS-i neurons in the CA1 and CA3(ab) regions of the hippocampus are preserved following an ischemic insult. The present results showed a 90% ischemic loss of CA1 and CA3 NPY-i somata. Based on these findings, it is concluded that ischemia selectively damaged NPY-i and not SS-i within some surviving hippocampal neurons that co-localized both peptides prior to the ischemia.
Johansen
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University of Copenhagen, Institute of Neuropathology, PharmaBiotec and Laboratory of Molecular Endocrinology, University Department of Clinical Chemistry, Rigshospitalet, Copenhagen, Denmark.
O'Hare
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MM