1993
DOI: 10.1007/bf01245234
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Dopamine-glutamate interactions in methamphetaminc-induced neurotoxicity

Abstract: Repeated administration of methamphetamine (m-AMPH) to rats induces dopamine (DA) terminal damage, and coadministration of antagonists of the N-methyl-D-aspartate (NMDA) or dopamine D1 or D2 receptors are protective. Striatal microdialysis of rats given a neurotoxic regimen of 4 x m-AMPH (4 mg/kg, s.c.) treatments revealed a dramatic and prolonged elevation of extracellular DA after the final m-AMPH administration. Neuroprotective regimens of MK-801, SCH 23390, or eticlopride greatly attenuated the overflow of… Show more

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Cited by 92 publications
(53 citation statements)
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“…Thus, it is plausible to suspect that the striatal apoptosis induced by METH may be initiated by the excessive release of glutamate. Two pieces of evidence support this hypothesis, (1) METH induces the striatal overflow of glutamate as measured by in vivo microdialysis [23], and (2) antagonists of the NMDA receptor attenuate METH-induced DA terminal injury in the striatum [20,22,32].…”
Section: Discussionmentioning
confidence: 92%
“…Thus, it is plausible to suspect that the striatal apoptosis induced by METH may be initiated by the excessive release of glutamate. Two pieces of evidence support this hypothesis, (1) METH induces the striatal overflow of glutamate as measured by in vivo microdialysis [23], and (2) antagonists of the NMDA receptor attenuate METH-induced DA terminal injury in the striatum [20,22,32].…”
Section: Discussionmentioning
confidence: 92%
“…The latter action could also be relevant to methamphetamine toxicity, which is inhibited by MK-801 by a mechanism that remains to be fully understood (Marshall et al, 1993). Since it appears that the massive methamphetamine-induced release of cytosolic dopamine plays a causal role in the subsequent degeneration of dopaminergic nerve terminals (Weihmuller et al, 1992;Marshall et al, 1993), it will be of interest to examine the possibility that MK-801 inhibits the dopamine transporter in vivo.…”
Section: Discussionmentioning
confidence: 99%
“…Thus, it is plausible to suspect that the striatal apoptosis induced by METH may be mediated by excessive release of glutamate. METH-induced overflow of glutamate in the striatum has been demonstrated (Nash and Yamamoto, 1992), and METH-induced dopamine terminal injury is prevented by NMDA receptor antagonists (Marshall et al, 1993;Muraki et al, 1992;Sonsalla et al, 1991).…”
Section: Discussionmentioning
confidence: 99%