title: Neuronal nitric oxide synthase contributes to pentylenetetrazole-kindling-induced hippocampal neurogenesis.
abstract: Neuronal nitric oxide synthase (nNOS), the major nitric oxide synthase isoform in the mammalian brain, is implicated in the pathophysiology of several neurological conditions, including epilepsy. Neurogenesis in hippocampal dentate gyrus (DG) persists throughout life in the adult brain. Alterations in this process occur in many neurological diseases, including epilepsy. Few studies, however, have addressed the role of nNOS in hippocampal DG neurogenesis in epileptic brain. The present study, therefore, investigated the role of nNOS in pentylenetetrazole (PTZ)-kindling-induced neurogenesis in hippocampal DG. Our results showed that nNOS expression and enzymatic activity were significantly increased in the hippocampus of PTZ-kindled mice. Meanwhile, these PTZ-kindled mice were characterized by significant enhancement of new born cells proliferation and survival in hippocampal DG, and these survived cells are co-labeled with NeuN and GFAP. Selective inhibition of nNOS by 7-NI, however, suppressed PTZ-kindling-induced hippocampal DG new born cells proliferation and survival, suggesting that nNOS contributes to PTZ-kindling-induced hippocampal neurogenesis.
authors.affiliation: Department of Pharmacology, Medical School of Southeast University, Nanjing, China. Electronic address: xinjianzhu@seu.edu.cn.
authors.forename: Xinjian
authors.initials: X
authors.lastname: Zhu
authors.affiliation: Department of Geriatric Neurology, Nanjing Brain Hospital Affiliated to Nanjing Medical University, Nanjing, China.
authors.forename: Jingde
authors.initials: J
authors.lastname: Dong
authors.affiliation: Department of Pharmacology, Medical School of Southeast University, Nanjing, China.
authors.forename: Kai
authors.initials: K
authors.lastname: Shen
authors.affiliation: Department of Pharmacology, Medical School of Southeast University, Nanjing, China.
authors.forename: Ying
authors.initials: Y
authors.lastname: Bai
authors.affiliation: Department of Physiology, Medical School of Southeast University, Nanjing, China.
authors.forename: Jie
authors.initials: J
authors.lastname: Chao
authors.affiliation: Department of Pharmacology, Medical School of Southeast University, Nanjing, China.
authors.forename: Honghong
authors.initials: H
authors.lastname: Yao
mesh_terms: D000818:Animals; D001973:Bromodeoxyuridine / Q000378:metabolism; D002452:Cell Count; D049109:Cell Proliferation / Q000187:drug effects; D003292:Convulsants / Q000494:pharmacology*; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005786:Gene Expression Regulation / Q000187:drug effects; D006624:Hippocampus / Q000187:drug effects* / Q000502:physiology; D007191:Indazoles / Q000494:pharmacology; D007696:Kindling, Neurologic / Q000187:drug effects*; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D055495:Neurogenesis / Q000187:drug effects / Q000502:physiology*; D009569:Nitric Oxide / Q000378:metabolism; D052248:Nitric Oxide Synthase Type I / Q000235:genetics / Q000378:metabolism*; D010433:Pentylenetetrazole / Q000494:pharmacology*; D012333:RNA, Messenger / Q000378:metabolism; D055748:SOXB1 Transcription Factors / Q000378:metabolism; D012640:Seizures / Q000139:chemically induced; D018709:Statistics, Nonparametric; D013997:Time Factors
chemical_list: D003292:Convulsants; D004791:Enzyme Inhibitors; D007191:Indazoles; D012333:RNA, Messenger; D055748:SOXB1 Transcription Factors; C527784:Sox2 protein, rat; D009569:Nitric Oxide; D052248:Nitric Oxide Synthase Type I; D001973:Bromodeoxyuridine; C080122:7-nitroindazole; D010433:Pentylenetetrazole
keywords: Epilepsy; Kindling; Neurogenesis; nNOS