Abstract：
:By observing the ultrastructural intracellular Ca2+ distribution with Ca(2+)-oxalate-pyroantimonate method, we examined whether the protective mechanism of the nitric oxide (NO) synthase inhibitor, N omega-nitro-L-arginine (LNNA), involves change of the intracellular Ca2+ 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 Ca2+ deposits and the mitochondrial Ca2+ 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 Ca2+ 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 Ca2+ deposits. It is suggested that the neuronal toxicity of NO involves the dysfunction of the intracellular Ca2+ transport system including the mitochondria and ER.
journal_name
Neurosci Lettjournal_title
Neuroscience lettersauthors
Kohno K,Higuchi T,Ohta S,Kohno K,Kumon Y,Sakaki Sdoi
10.1016/s0304-3940(97)13459-0subject
Has Abstractpub_date
1997-03-07 00:00:00pages
17-20issue
1eissn
0304-3940issn
1872-7972pii
S0304-3940(97)13459-0journal_volume
224pub_type
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