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Nitrous oxide and xenon prevent amphetamine-induced carrier-mediated dopamine release in a memantine-like fashion and protect against behavioral sensitization.
Biol Psychiatry. 2006 Jul 01; 60(1):49-57.BP

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.

Authors+Show Affiliations

NNOXe Pharmaceuticals, Québec, Canada.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Comparative Study
Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

16427030

Citation

David, Hélène N., et al. "Nitrous Oxide and Xenon Prevent Amphetamine-induced Carrier-mediated Dopamine Release in a Memantine-like Fashion and Protect Against Behavioral Sensitization." Biological Psychiatry, vol. 60, no. 1, 2006, pp. 49-57.
David HN, Ansseau M, Lemaire M, et al. Nitrous oxide and xenon prevent amphetamine-induced carrier-mediated dopamine release in a memantine-like fashion and protect against behavioral sensitization. Biol Psychiatry. 2006;60(1):49-57.
David, H. N., Ansseau, M., Lemaire, M., & Abraini, J. H. (2006). Nitrous oxide and xenon prevent amphetamine-induced carrier-mediated dopamine release in a memantine-like fashion and protect against behavioral sensitization. Biological Psychiatry, 60(1), 49-57.
David HN, et al. Nitrous Oxide and Xenon Prevent Amphetamine-induced Carrier-mediated Dopamine Release in a Memantine-like Fashion and Protect Against Behavioral Sensitization. Biol Psychiatry. 2006 Jul 1;60(1):49-57. PubMed PMID: 16427030.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Nitrous oxide and xenon prevent amphetamine-induced carrier-mediated dopamine release in a memantine-like fashion and protect against behavioral sensitization. AU - David,Hélène N, AU - Ansseau,Marc, AU - Lemaire,Marc, AU - Abraini,Jacques H, Y1 - 2006/01/19/ PY - 2005/04/27/received PY - 2005/09/27/revised PY - 2005/10/12/accepted PY - 2006/1/24/pubmed PY - 2006/8/12/medline PY - 2006/1/24/entrez SP - 49 EP - 57 JF - Biological psychiatry JO - Biol Psychiatry VL - 60 IS - 1 N2 - 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. SN - 0006-3223 UR - https://www.unboundmedicine.com/medline/citation/16427030/Nitrous_oxide_and_xenon_prevent_amphetamine_induced_carrier_mediated_dopamine_release_in_a_memantine_like_fashion_and_protect_against_behavioral_sensitization_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0006-3223(05)01272-2 DB - PRIME DP - Unbound Medicine ER -