Neuroprotective nitric oxide synthase inhibitor reduces intracellular calcium accumulation following transient global ischemia in the gerbil

By observing the ultrastructural intracellular Ca 2+ distribution with Ca 2+-oxalate-pyroantimonate method, we examined whether the protective mechanism of the nitric oxide (NO) synthase inhibitor, N ω -nitro- l-arginine (LNNA), involves change of the intracellular Ca 2+ movement in delayed neuronal...

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Bibliographic Details
Published in:Neuroscience letters 1997-03, Vol.224 (1), p.17-20
Main Authors: Kohno, Keiji, Higuchi, Tohru, Ohta, Shinsuke, Kohno, Kanehisa, Kumon, Yoshiaki, Sakaki, Saburo
Format: Article
Language:English
Subjects:
Animals
Biological and medical sciences
Calcium
Calcium - metabolism
Delayed neuronal death
Endoplasmic reticulum
Endoplasmic Reticulum - metabolism
Enzyme Inhibitors - pharmacology
Gerbillinae
Hippocampus
Injections, Intraventricular
Intracellular Membranes - metabolism
Ischemic Attack, Transient - metabolism
Male
Medical sciences
Mitochondria
Mitochondria - metabolism
Mongolian gerbil
Neuropharmacology
Neuroprotective agent
Neuroprotective Agents - pharmacology
Nitric oxide
Nitric Oxide Synthase - antagonists & inhibitors
Nitric oxide synthase inhibitor
Nitroarginine - pharmacology
Pharmacology. Drug treatments
Reperfusion
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Summary:By observing the ultrastructural intracellular Ca 2+ distribution with Ca 2+-oxalate-pyroantimonate method, we examined whether the protective mechanism of the nitric oxide (NO) synthase inhibitor, N ω -nitro- l-arginine (LNNA), involves change of the intracellular Ca 2+ movement in delayed neuronal death (DND) in gerbil hippocampal CA1 neurons following 5-min forebrain ischemia. In the group intraventricularly administered 5.0 mg/ml LNNA, 15 min after reperfusion the intracellular Ca 2+ deposits and the mitochondrial Ca 2+ uptake index increased to levels similar to those in the control group administered only artificial cerebro-spinal fluid, but by 180 min after reperfusion they had returned to the preischemic level. By 15 min after reperfusion Ca 2+ deposits in the endoplasmic reticulum (ER) had almost disappeared in both groups, but at 180 min of reperfusion, the ER in only the LNNA group showed Ca 2+ deposits. It is suggested that the neuronal toxicity of NO involves the dysfunction of the intracellular Ca 2+ transport system including the mitochondria and ER.
ISSN:0304-3940
1872-7972
DOI:10.1016/S0304-3940(97)13459-0