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Elife. 2018 Oct 8;7. pii: e34032. doi: 10.7554/eLife.34032.

Motor thalamus supports striatum-driven reinforcement.

Author information

1
The Gladstone Institutes, San Francisco, United States.
2
Neuroscience Graduate Program, University of California, San Francisco, United States.
3
Departments of Physiology and Neurology, University of California, San Francisco, United States.

Abstract

Reinforcement has long been thought to require striatal synaptic plasticity. Indeed, direct striatal manipulations such as self-stimulation of direct-pathway projection neurons (dMSNs) are sufficient to induce reinforcement within minutes. However, it's unclear what role, if any, is played by downstream circuitry. Here, we used dMSN self-stimulation in mice as a model for striatum-driven reinforcement and mapped the underlying circuitry across multiple basal ganglia nuclei and output targets. We found that mimicking the effects of dMSN activation on downstream circuitry, through optogenetic suppression of basal ganglia output nucleus substantia nigra reticulata (SNr) or activation of SNr targets in the brainstem or thalamus, was also sufficient to drive rapid reinforcement. Remarkably, silencing motor thalamus-but not other selected targets of SNr-was the only manipulation that reduced dMSN-driven reinforcement. Together, these results point to an unexpected role for basal ganglia output to motor thalamus in striatum-driven reinforcement.

KEYWORDS:

mouse; neuroscience; optogenetics; reinforcement; striatum

PMID:
30295606
PMCID:
PMC6181560
DOI:
10.7554/eLife.34032
[Indexed for MEDLINE]
Free PMC Article

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