D2R striatopallidal neurons inhibit both locomotor and drug reward processes.

Full Abstract

The specific functions of dopamine D(2) receptor-positive (D(2)R) striatopallidal neurons remain poorly understood. Using a genetic mouse model, we found that ablation of D(2)R neurons in the entire striatum induced hyperlocomotion, whereas ablation in the ventral striatum increased amphetamine conditioned place preference. Thus D(2)R striatopallidal neurons limit both locomotion and, unexpectedly, drug reinforcement.

Author information

Author/s: Durieux, Pierre F (PF); Bearzatto, Bertrand (B); Guiducci, Stefania (S); Buch, Thorsten (T); Waisman, Ari (A); Zoli, Michele (M); Schiffmann, Serge N (SN); de Kerchove d'Exaerde, Alban (A);

Affiliation: Laboratory of Neurophysiology, Université Libre de Bruxelles, Brussels, Belgium.

Journal and publication information

Publication Type: Journal Article; Research Support, Non-U.S. Gov't

Journal: Nature neuroscience (Nat Neurosci), published in United States. (Language: eng)

Reference: 2009-Apr; vol 12 (issue 4) : pp 393-5

Dates: Created 2009/03/26; Completed 2009/04/24;

PMID: 19270687, status: MEDLINE (last retrieval date: 4/24/2009, IMS Date: )

Sourced from the National Library of Medicine. Abstract text and other information may be subject to copyright.

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MeSH headings (categories)

This article was linked to the MESH Headings shown below.

Amphetamine - pharmacology
Animals
Autoradiography
Conditioning, Operant - physiology
Corpus Striatum - cytology
Diphtheria Toxin - pharmacology
Dopamine Uptake Inhibitors - pharmacology
Enkephalins - genetics; metabolism
Gene Expression Regulation - drug effects; genetics
Globus Pallidus - cytology
Glutamate Decarboxylase - genetics; metabolism
Intercellular Signaling Peptides and Proteins - genetics
Locomotion - drug effects; genetics

Locomotion - drug effects; genetics
Mice
Mice, Inbred C57BL
Mice, Transgenic
Nerve Tissue Proteins - metabolism
Neurons - drug effects; physiology
Protein Binding - drug effects
Receptors, Adenosine A2 - genetics
Receptors, Dopamine D2 - deficiency; metabolism
Reinforcement Schedule
Reward
Time Factors
Tyrosine 3-Monooxygenase - genetics; metabolism

Associated Chemicals: Diphtheria Toxin (0) ; Dopamine Uptake Inhibitors (0) ; Enkephalins (0) ; Intercellular Signaling Peptides and Proteins (0) ; Nerve Tissue Proteins (0) ; Receptors, Adenosine A2 (0) ; Receptors, Dopamine D2 (0) ; heparin-binding EGF-like growth factor (149176-25-0) ; Amphetamine (300-62-9) ; Tyrosine 3-Monooxygenase (EC 1.14.16.2) ; Glutamate Decarboxylase (EC 4.1.1.15) ; glutamate decarboxylase 1 (EC 4.1.1.15)

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