Motor thalamus supports striatum-driven reinforcement

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

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.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Basal Ganglia / physiology
  • Electric Stimulation
  • Female
  • Glutamates / metabolism
  • Male
  • Mice
  • Motor Activity / physiology*
  • Neostriatum / physiology*
  • Optogenetics
  • Receptors, N-Methyl-D-Aspartate / metabolism
  • Reinforcement, Psychology*
  • Serotonergic Neurons / metabolism
  • Synaptic Transmission / physiology
  • Thalamus / physiology*

Substances

  • Glutamates
  • Receptors, N-Methyl-D-Aspartate