期刊
NATURE NEUROSCIENCE
卷 13, 期 4, 页码 475-U96出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/nn.2506
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资金
- State of California for Medical Research on Alcohol and Substance Abuse through the University of California at San Francisco [NIDA DA15096-01]
- Massachusetts Institute of Technology Peter J. Eloranta Summer Undergraduate Research Fellowship
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [DP2DK102256] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE ON DRUG ABUSE [R01DA015096] Funding Source: NIH RePORTER
Although methylphenidate (Ritalin) has been used therapeutically for nearly 60 years, the mechanisms by which it acutely modifies behavioral performance are poorly understood. Here we combined intra-lateral amygdala in vivo pharmacology and ex vivo electrophysiology to show that acute administration of methylphenidate, as well as a selective dopamine transporter inhibitor, facilitated learning-induced strengthening of cortico-amygdala synapses through a postsynaptic increase in AMPA receptor-mediated currents, relative to those in saline-treated rats. Furthermore, local administration of methylphenidate in the lateral amygdala enhanced cue-reward learning through dopamine D1 receptor-dependent mechanisms and suppressed task-irrelevant behavior through D2 receptor-dependent mechanisms. These findings reveal critical and distinct roles for dopamine receptor subtypes in mediating methylphenidate-induced enhancements of neural transmission and learning performance.
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