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Cdk5 Modulates Long-Term Synaptic Plasticity and Motor Learning in Dorsolateral Striatum. | LitMetric

Cdk5 Modulates Long-Term Synaptic Plasticity and Motor Learning in Dorsolateral Striatum.

Sci Rep

Departments of Psychiatry, Neurology and Neurotherapeutics and Harold C. Simmons Comprehensive Cancer Center, The University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.

Published: July 2016

AI Article Synopsis

  • The striatum is vital for cognitive functions like motivation, reward perception, decision-making, and motor learning, with particular emphasis on the dorsolateral striatum.
  • This study explores synaptic plasticity in mouse dorsolateral cortico-striatal circuitry, revealing that long-term potentiation (LTP) is driven by dopamine through D1-dopamine receptors and NMDA receptors, requiring calcium-dependent signaling proteins like CaMKII.
  • Inhibition or loss of the protein kinase Cdk5 hinders dopamine-facilitated LTP, which is linked to increased locomotion and reduced motor learning, indicating its crucial role in striatal plasticity and related behaviors.

Article Abstract

The striatum controls multiple cognitive aspects including motivation, reward perception, decision-making and motor planning. In particular, the dorsolateral striatum contributes to motor learning. Here we define an approach for investigating synaptic plasticity in mouse dorsolateral cortico-striatal circuitry and interrogate the relative contributions of neurotransmitter receptors and intracellular signaling components. Consistent with previous studies, we show that long-term potentiation (LTP) in cortico-striatal circuitry is facilitated by dopamine, and requires activation of D1-dopamine receptors, as well as NMDA receptors (NMDAR) and their calcium-dependent downstream effectors, including CaMKII. Moreover, we assessed the contribution of the protein kinase Cdk5, a key neuronal signaling molecule, in cortico-striatal LTP. Pharmacological Cdk5 inhibition, brain-wide Cdk5 conditional knockout, or viral-mediated dorsolateral striatal-specific loss of Cdk5 all impaired dopamine-facilitated LTP or D1-dopamine receptor-facilitated LTP. Selective loss of Cdk5 in dorsolateral striatum increased locomotor activity and attenuated motor learning. Taken together, we report an approach for studying synaptic plasticity in mouse dorsolateral striatum and critically implicate D1-dopamine receptor, NMDAR, Cdk5, and CaMKII in cortico-striatal plasticity. Furthermore, we associate striatal plasticity deficits with effects upon behaviors mediated by this circuitry. This approach should prove useful for the study of the molecular basis of plasticity in the dorsolateral striatum.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4957238PMC
http://dx.doi.org/10.1038/srep29812DOI Listing

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