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KMID : 0376420010250010043
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Chonbuk University Medical Journal
2001 Volume.25 No. 1 p.43 ~ p.52
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mechanism of methamphetamine ebvoked release of 5-hydroxytryptamine in rat cerebral cortex slices
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Abstract
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Methamphetamine (MAP) is a well known psychostimulant. It has been reported that MAP induces. release of various neurotransmitters from brain regions, and is capable of enhancement of cognitive function. Cerebrocortical serotonergic system i.; involved in memory process. We examined the mechamiism. of MAP-induced [3H]5hydroxytryptamine ([3 H]5-HT) release in rat hippocampal slices. MAP induced the release of [3 H]5-HT in a dose dependent manner (1 - 300 1iM). At 10 jiM concentration of MAP, [3H]5-HT was released over 400% of resting period. In the presence of 1 JIM yohimbine, MAP-induced [3H]5-HT release was potentiated. MAP-induced [3H]5-HT release was not inhibited by 1 JIM tetrodotoxin, indicating the action site of MAP is located on the presynaptic terminal. MAP-induced [3H]NE release was not altered by voltage-sensitive calcium channel blockers (nitrendipine, W -conotoxin GVIA and W-agatoxin IVA). Fluoxetine (1 PM), a selective 5-HT transporter blocker, significantly inhibited MAP-induced [3H]5-HT release. MAP-induced [3H]5-HT release was inhibited by MK--801 (10 jM), but not by D-AP5 or DNQX. Also, MAP failed to stimulate the release of [3H]aspartate even in 100 jiM. MAP-induced release of [3H]NE was reduced by inhibitors of nitric oxide (NO) synthase, 7-nitroindazole (10 9M), L-NAME (30 11M) and L-NMMA (300 9M), and
1,ULentiated by cGMP phosphodiesterase inhibitor, zaprinast (30 JIM). Our results suggest that MAP induces 5-HT release by reversal of transporter which is located in presynapt:ic termina;and that NO is involved in this process.
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