Format

Send to

Choose Destination
Cell Rep. 2018 May 22;23(8):2264-2272. doi: 10.1016/j.celrep.2018.04.081.

Dorsolateral Striatum Engagement Interferes with Early Discrimination Learning.

Author information

1
Laboratory of Behavioral and Genomic Neuroscience, National Institute on Alcohol Abuse and Alcoholism, NIH, Bethesda, MD, USA. Electronic address: habergstrom@vassar.edu.
2
Laboratory of Behavioral and Genomic Neuroscience, National Institute on Alcohol Abuse and Alcoholism, NIH, Bethesda, MD, USA.
3
Department of Molecular Physiology and Biophysics, Vanderbilt University, Nashville, TN, USA.
4
Behavioral Neuroscience Research Branch, National Institute on Drug Abuse, NIH, Baltimore, MD, USA.
5
Department of Molecular Physiology and Biophysics, Vanderbilt University, Nashville, TN, USA; Vanderbilt Center for Addiction Research, Nashville, TN, USA.

Abstract

In current models, learning the relationship between environmental stimuli and the outcomes of actions involves both stimulus-driven and goal-directed systems, mediated in part by the DLS and DMS, respectively. However, though these models emphasize the importance of the DLS in governing actions after extensive experience has accumulated, there is growing evidence of DLS engagement from the onset of training. Here, we used in vivo photosilencing to reveal that DLS recruitment interferes with early touchscreen discrimination learning. We also show that the direct output pathway of the DLS is preferentially recruited and causally involved in early learning and find that silencing the normal contribution of the DLS produces plasticity-related alterations in a PL-DMS circuit. These data provide further evidence suggesting that the DLS is recruited in the construction of stimulus-elicited actions that ultimately automate behavior and liberate cognitive resources for other demands, but with a cost to performance at the outset of learning.

KEYWORDS:

Arc; cognition; goal-directed; habit; optogenetics; plasticity; reward; striatum

Supplemental Content

Full text links

Icon for Elsevier Science Icon for PubMed Central
Loading ...
Support Center