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Selective sparing of NADPH‐diaphorase–somatostatin–neuropeptide Y neurons in ischemic gerbil striatum
Author(s) -
Uemura Yoshihiko,
Kowall Neil W.,
Beal M. Flint
Publication year - 1990
Publication title -
annals of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.764
H-Index - 296
eISSN - 1531-8249
pISSN - 0364-5134
DOI - 10.1002/ana.410270606
Subject(s) - striatum , gerbil , somatostatin , medicine , endocrinology , neuropeptide , glutamate receptor , nmda receptor , nadph dehydrogenase , neuropeptide y receptor , neuron , chemistry , ischemia , biology , neuroscience , receptor , dopamine , nitric oxide synthase , nitric oxide
In the present study we investigated the relative vulnerability of neuronal subsets in the striatum to ischemia that was induced by bilateral transient ligation of the common carotid arteries in gerbils. After 4 days of survival, brains were evaluated using histochemical methods (NADPH‐diaphorase and silver degeneration procedures) and neurochemical methods with radioimmunoassays for somatostatin‐, neuropeptide Y–, and substance P–like immunoreactivity and measurements of amino acids using high‐pressure liquid chromatography with electrochemical detection. NADPH‐diaphorase–positive neurons were strikingly preserved in the ischemic dorsolateral portion of the striatum, in which there was severe neuronal loss. There was no significant depletion of NADPH‐diaphorase‐positive neurons in the striatum or cerebral cortex. Concentrations of neuropeptide Y–like and somatostatin‐like immunoreactivity were unchanged despite a significant 25% depletion of substance P–like immunoreactivity and gamma‐aminobutyric acid. Ischemic brain damage may be mediated by a neurotoxic effect of glutamate acting at the N ‐methyl‐D‐aspartate (NMDA) receptor. Previous studies of NMDA excitotoxin lesions in rat striatum have shown a sparing of neurons containing NADPH‐diaphorase, somatostatin, and neuropeptide Y. The similar sparing of these neurons following ischemic lesions in gerbil striatum provides further evidence that NMDA receptor activation may play a role in ischemic injury.