Activity propagation in an avian basal ganglia-thalamocortical circuit essential for vocal learning.

Full Abstract

In mammalian basal ganglia-thalamocortical circuits, GABAergic pallidal neurons are thought to "gate" or modulate excitation in thalamus with their strong inhibitory inputs and thus signal to cortex by pausing and permitting thalamic neurons to fire in response to excitatory drive. In contrast, in a homologous circuit specialized for vocal learning in songbirds, evidence suggests that pallidal neurons signal by eliciting postinhibitory rebound spikes in thalamus, which could occur even without any excitatory drive to thalamic neurons. To test whether songbird pallidal neurons can also communicate with thalamus by gating excitatory drive, as well as by postinhibitory rebound, we examined the activity of thalamic relay neurons in response to acute inactivation of the basal ganglia structure Area X; Area X contains the pallidal neurons that project to thalamus. Although inactivation of Area X should eliminate rebound-mediated spiking in thalamus, this manipulation tonically increased the firing rate of thalamic relay neurons, providing evidence that songbird pallidal neurons can gate tonic thalamic excitatory drive. We also found that the increased thalamic activity was fed forward to its target in the avian equivalent of cortex, which includes neurons that project to the vocal premotor area. These data raise the possibility that basal ganglia circuits can signal to cortex through thalamus both by generating postinhibitory rebound and by gating excitatory drive and may switch between these modes depending on the statistics of pallidal firing. Moreover, these findings provide insight into the strikingly different disruptive effects of basal ganglia and cortical lesions on songbird vocal learning.

Author information

Author/s: Kojima, Satoshi (S); Doupe, Allison J (AJ);

Affiliation: Department of Physiology, Keck Center for Integrative Neuroscience, University of California, San Francisco, San Francisco, California 94143-0444, USA. skojima(-atsign-)phy.ucsf.edu

Grants: MH055987 (Agency:NIMH NIH HHS) ; MH550012 (Agency:NIMH NIH HHS) ; P50 MH077970-010004 (Agency:NIMH NIH HHS) ; R01 MH055987-13 (Agency:NIMH NIH HHS)

Journal and publication information

Publication Type: Comparative Study; Journal Article; Research Support, N.I.H., Extramural

Journal: The Journal of neuroscience : the official journal of the Society for Neuroscience (J Neurosci), published in United States. (Language: eng)

Reference: 2009-Apr; vol 29 (issue 15) : pp 4782-93

Dates: Created 2009/04/16; Completed 2009/05/12; Revised 2009/10/16;

PMID: 19369547, status: MEDLINE (last retrieved date: 10/19/2009)

Sourced from the National Library of Medicine. Abstract text and other information may be subject to copyright.

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