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Research article summary (published 21 Feb 2005):
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The HVC microcircuit: the synaptic basis for interactions between song motor and vocal plasticity pathways.

Full Abstract

Synaptic interactions between telencephalic neurons innervating descending motor or basal ganglia pathways are essential in the learning, planning, and execution of complex movements. Synaptic interactions within the songbird telencephalic nucleus HVC are implicated in motor and auditory activity associated with learned vocalizations. HVC contains projection neurons (PNs) (HVC(RA)) that innervate song premotor areas, other PNs (HVC(X)) that innervate a basal ganglia pathway necessary for vocal plasticity, and interneurons (HVC(INT)). During singing, HVC(RA) fire in temporally sparse bursts, possibly because of HVC(INT)-HVC(RA) interactions, and a corollary discharge can be detected in the basal ganglia pathway, likely because of synaptic transmission from HVC(RA) to HVC(X) cells. During song playback, local interactions, including inhibition onto HVC(X) cells, shape highly selective responses that distinguish HVC from its auditory afferents. To better understand the synaptic substrate for the motor and auditory properties of HVC, we made intracellular recordings from pairs of HVC neurons in adult male zebra finch brain slices and used spike-triggered averages to assess synaptic connectivity. A major synaptic interaction between the PNs was a disynaptic inhibition from HVC(RA) to HVC(X), which could link song motor signals in the two outputs of HVC and account for some of the song playback-evoked inhibition in HVC(X) cells. Furthermore, single interneurons made divergent connections onto PNs of both types, and either PN type could form reciprocal connections with interneurons. In these two regards, the synaptic architecture of HVC resembles that described in some pattern-generating networks, underscoring features likely to be important to singing and song learning.

 

Author information

Author/s: Mooney, Richard (R); Prather, Jonathan F (JF);

Affiliation: Department of Neurobiology, Duke University School of Medicine, Durham, North Carolina 27710, USA. mooney(-atsign-)neuro.duke.edu

Grants: DC02524 (Agency:NIDCD NIH HHS) ; F32 DC006152-01 (Agency:NIDCD NIH HHS)

Journal and publication information

Publication Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.

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

Reference: 2005-Feb; vol 25 (issue 8) : pp 1952-64

Dates: Created 2005/02/24; Completed 2005/10/26; Revised 2007/11/14;

PMID: 15728835, status: MEDLINE (last retrieval date: 2/18/2009, IMS Date: )

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

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Associated Chemicals: Quinoxalines (0) ; Receptors, AMPA (0) ; Receptors, GABA-A (0) ; Receptors, N-Methyl-D-Aspartate (0) ; 2,3-dioxo-6-nitro-7-sulfamoylbenzo(f)quinoxaline (118876-58-7) ; Picrotoxin (124-87-8) ; 2-Amino-5-phosphonovalerate (76726-92-6)

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