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The hippocampal neurons of neuronal apoptosis inhibitory protein 1 (NAIP1)-deleted mice display increased vulnerability to kainic acid-induced injury
Author(s) -
Martin Holčı́k,
Charlie S. Thompson,
Zahra Yaraghi,
Charles Lefebvre,
Alex MacKenzie,
Robert G. Korneluk
Publication year - 2000
Publication title -
proceedings of the national academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.011
H-Index - 771
eISSN - 1091-6490
pISSN - 0027-8424
DOI - 10.1073/pnas.040469797
Subject(s) - kainic acid , biology , hippocampal formation , inhibitory postsynaptic potential , apoptosis , hippocampus , neuroscience , in vivo , microbiology and biotechnology , endogeny , central nervous system , biochemistry , glutamate receptor , genetics , receptor
The neuronal apoptosis inhibitory protein (NAIP) is a member of a novel family of inhibitor of apoptosis (IAP) proteins. The IAP genes are highly conserved from baculovirus to metazoans and suppress apoptosis induced by a variety of triggers both in vitro and in vivo. Here we describe the generation and characterization of mice with the targeted deletion of NAIP1. We demonstrate that the NAIP1-deleted mice develop normally. However, the survival of pyramidal neurons in the hippocampus after kainic acid-induced limbic seizures is greatly reduced in the NAIP1 knock-out animals. Thus, although NAIP1 is not necessary for normal development of murine central nervous system, the endogenous NAIP1 is required for neuronal survival in pathological conditions.

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