4.5 Article

Transient and steady-state selection in the striatal microcircuit

期刊

出版社

FRONTIERS RESEARCH FOUNDATION
DOI: 10.3389/fncom.2013.00192

关键词

response selection; action selection; striatum; Huntington's disease; basal ganglia; excitotoxicity

资金

  1. L'Agence Nationale de Recherche NEUROBOT project
  2. MRC Senior non-Clinical Fellowship
  3. EU
  4. EPSRC Green Brain project [EP/J019534/1]
  5. EPSRC DTA student scholarship
  6. Deutsche Forschungsgemeinschaft (DFG) [BE4045/10-1]
  7. MRC [MR/J008648/1] Funding Source: UKRI

向作者/读者索取更多资源

Although the basal ganglia have been widely studied and implicated in signal processing and action selection, little information is known about the active role the striatal microcircuit plays in action selection in the basal ganglia-thalamo-cortical loops. To address this knowledge gap we use a large scale three dimensional spiking model of the striatum, combined with a rate coded model of the basal ganglia-thalamo-corticalloop, to asses the computational role the striatum plays in action selection. We identify a robust transient phenomena generated by the striatal microcircuit, which temporarily enhances the difference between two competing cortical inputs. We show that this transient is sufficient to modulate decision making in the basal ganglia-thalamo-cortical circuit. We also find that the transient selection originates from a novel adaptation effect in single striatal projection neurons, which is amenable to experimental testing. Finally, we compared transient selection with models implementing classical steady-state selection. We challenged both forms of model to account for recent reports of paradoxically enhanced response selection in Huntington's disease patients. We found that steady-state selection was uniformly impaired under all simulated Huntington's conditions, but transient selection was enhanced given a sufficient Huntington's-like increase in NMDA receptor sensitivity. Thus our models provide an intriguing hypothesis for the mechanisms underlying the paradoxical cognitive improvements in manifest Huntington's patients.

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