Abstract
The effect of L-arginine administration on susceptibility/resistance of NO-producing neurons was investigated in non-ischemic neurodegenerative conditions. ChAT mRNA level was measured by in situ hybridization in the basal forebrain after i.c.v. colchicine administration. Colchicine induced down-regulation of ChAT mRNA level followed by degeneration of cholinergic neurons. L-Arginine treatment increased ChAT mRNA level and prevented/delayed ChAT mRNA decrease by colchicine. These data suggest that L-arginine treatment may protect cholinergic neurons from colchicine-induced degeneration.
MeSH terms
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Animals
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Arginine / pharmacology*
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Choline O-Acetyltransferase / genetics
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Choline O-Acetyltransferase / metabolism*
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Colchicine / antagonists & inhibitors
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Colchicine / poisoning*
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Down-Regulation / drug effects
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In Situ Hybridization
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Male
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Nerve Degeneration / chemically induced
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Nerve Degeneration / pathology
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Neurons / drug effects*
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Neurons / metabolism*
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Neurons / pathology
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Neurotoxins / antagonists & inhibitors
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Neurotoxins / pharmacology*
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Prosencephalon / metabolism
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RNA, Messenger / metabolism
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Rats
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Rats, Sprague-Dawley
Substances
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Neurotoxins
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RNA, Messenger
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Arginine
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Choline O-Acetyltransferase
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Colchicine