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Methylphenidate facilitates learning-induced amygdala plasticity.

ABSTRACT: 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.

SUBMITTER: Tye KM

PROVIDER: S-EPMC2988577 | biostudies-literature | 2010 Apr

REPOSITORIES: biostudies-literature

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Methylphenidate facilitates learning-induced amygdala plasticity.

Tye Kay M KM Tye Lynne D LD Cone Jackson J JJ Hekkelman Evelien F EF Janak Patricia H PH Bonci Antonello A

Nature neuroscience 20100307 4

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-med ...[more]

PMID: 20208527

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