期刊
NATURE NEUROSCIENCE
卷 14, 期 1, 页码 22-24出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/nn.2703
关键词
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资金
- US National Institutes of Health [K99 DA024762, T32 GM07266, T32 GM07108, T32 AA009455, F32 DA026273, R21 DA021793, R01 DA023206, U19MH82441]
- National Institute of Mental Health
- National Alliance for Research on Schizophrenia and Depression Distinguished Investigator Award
- Achievement Rewards for College Scientists
- [R21 DA021273]
- NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [T32GM007266, T32GM007108] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF MENTAL HEALTH [U19MH082441] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE ON DRUG ABUSE [K99DA024762, R01DA023206, R01DA017204, R21DA021273, F32DA026273, R21DA021793] Funding Source: NIH RePORTER
Dorsal striatum is important for the development of drug addiction; however, a precise understanding of the roles of striatopallidal (indirect) and striatonigral (direct) pathway neurons in regulating behaviors remains elusive. Using viral-mediated expression of an engineered G protein-coupled receptor (hM(4)D), we found that activation of hM(4)D receptors with clozapine-N-oxide (CNO) potently reduced striatal neuron excitability. When hM(4)D receptors were selectively expressed in either direct or indirect pathway neurons, CNO did not change acute locomotor responses to amphetamine, but did alter behavioral plasticity associated with repeated drug treatment. Specifically, transiently disrupting striatopallidal neuronal activity facilitated behavioral sensitization, whereas decreasing excitability of striatonigral neurons impaired its persistence. These findings suggest that acute drug effects can be parsed from the behavioral adaptations associated with repeated drug exposure and highlight the utility of this approach for deconstructing neuronal pathway contributions to behavior.
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