作者: C. Ananth , S. Thameem Dheen , P. Gopalakrishnakone , C. Kaur
DOI: 10.1002/HIPO.10060
关键词: Hippocampus 、 Dentate gyrus 、 Nissl body 、 Glutamate receptor 、 Hippocampal formation 、 Chemistry 、 Neurotoxicity 、 Nitric oxide 、 Neuroscience 、 In situ hybridization
摘要: Neuronal degeneration followed by detection of nitric oxide (NO)-producing neurons the hippocampus was investigated at 4 h, 16 24 2 days, 5 and 14 days after administration domoic acid (DA), in present study. Histopathological analysis (Nissl staining) displayed dark-stained degenerating h to DA administration, with most severe 5–14 days. NADPH-d-positive were observed different subfields control rats treated 4–24 h. Complete loss CA1 CA3 also hilus dentate gyrus (DG) DA. In contrast, neuronal synthase (nNOS)-immunoreactive cells absent from hippocampal DA-treated animals but administration. N-methyl-D-aspartate receptor (NMDAR1) immunoreactivity increased double immunofluorescence demonstrated its coexpression induced nNOS expression. No significant change could be non-NMDA (GlutR2) as compared controls, while occasional immunoreactive colocalized Reverse transcription-polymerase chain reaction showed upregulated expression downregulated NMDAR1 Although mRNA rapidly situ hybridization revealed complete region The study has shown that NADPH-d express differentially DA-induced neurotoxicity. It is speculated induction glutamate genes response neurotoxicity have contributed degeneration. Hippocampus 2003;13:260–272. © 2003 Wiley-Liss, Inc.