Abstract：
BACKGROUND:Amphetamine administration induces stimulation-independent dopamine release in the nucleus accumbens (NAcc) through reverse dopamine transport, a critical neurochemical event involved in its psychostimulant action, and furthermore decreases stimulation-dependent vesicular dopamine release. These effects may involve possible indirect glutamatergic mechanisms. METHODS:We investigated the effects of nitrous oxide and xenon, which possess antagonistic action at the N-methyl-D-aspartate (NMDA) receptor, on brain slices ex vivo on amphetamine-induced changes in carrier-mediated and KCl-evoked dopamine release in the NAcc, and in vivo on amphetamine-induced locomotor sensitization. RESULTS:Like the low-affinity NMDA receptor antagonist memantine, but not the prototypical compound MK-801, nitrous oxide and xenon at appropriate concentrations blocked both the increase in carrier-mediated dopamine release and locomotor sensitization produced by amphetamine. CONCLUSIONS:In contrast to what has generally been found using prototypical NMDA receptor antagonists, these data regarding the effect of memantine, nitrous oxide, and xenon support the hypothesis that activation of certain NMDA receptors (possibly those containing the NR1a/NR2D subunit) in the NAcc is involved in the amphetamine-induced increase in carrier-mediated dopamine release and the development of behavioral sensitization to amphetamine. Nitrous oxide, xenon, and memantine may be of therapeutic interest for treating drug dependence.
journal_name
Biol Psychiatryjournal_title
Biological psychiatryauthors
David HN,Ansseau M,Lemaire M,Abraini JHdoi
10.1016/j.biopsych.2005.10.007subject
Has Abstractpub_date
2006-07-01 00:00:00pages
49-57issue
1eissn
0006-3223issn
1873-2402pii
S0006-3223(05)01272-2journal_volume
60pub_type
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journal_title：Biological psychiatry
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doi：
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journal_title：Biological psychiatry
pub_type： 临床试验,杂志文章,多中心研究,随机对照试验
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journal_title：Biological psychiatry
pub_type： 杂志文章,评审
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pub_type： 杂志文章,评审
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pub_type： 临床试验,杂志文章
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pub_type： 杂志文章
doi：10.1016/0006-3223(93)90388-t
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journal_title：Biological psychiatry
pub_type： 临床试验,杂志文章
doi：10.1016/j.biopsych.2004.06.031
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journal_title：Biological psychiatry
pub_type： 临床试验,杂志文章
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pub_type： 临床试验,杂志文章
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journal_title：Biological psychiatry
pub_type： 临床试验,杂志文章
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pub_type： 杂志文章
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更新日期：1990-01-01 00:00:00
abstract：BACKGROUND:Evidence indicates involvement of the endocannabinoid (eCB) system in both the pathophysiology of schizophrenia and working memory (WM) function. Additionally, schizophrenia patients exhibit relatively strong WM deficits. These findings suggest the possibility that the eCB system is also involved in WM defic...
journal_title：Biological psychiatry
pub_type： 杂志文章,随机对照试验
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更新日期：2012-04-15 00:00:00
