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Research article summary (published 25 May 2009):

In mice lacking V2a interneurons, gait depends on speed of locomotion.

Full Abstract

Many animals are capable of changing gait with speed of locomotion. The neural basis of gait control and its dependence on speed are not fully understood. Mice normally use a single "trotting" gait while running at all speeds, either over ground or on a treadmill. Transgenic mouse mutants in which the trotting is replaced by hopping also lack a speed-dependent change in gait. Here we describe a transgenic mouse model in which the V2a interneurons have been ablated by targeted expression of diphtheria toxin A chain (DTA) under the control of the Chx10 gene promoter (Chx10::DTA mice). Chx10::DTA mice show normal trotting gait at slow speeds but transition to a galloping gait as speed increases. Although left-right limb coordination is altered in Chx10::DTA mice at fast speed, alternation of forelegs and hindlegs and the relative duration of swing and stance phases for individual limbs is unchanged compared with wild-type mice. The speed-dependent loss of left-right alternation is recapitulated during drug-induced fictive locomotion in spinal cords isolated from neonatal Chx10::DTA mice, and high-speed fictive locomotion evoked by caudal spinal cord stimulation also shows synchronous left-right bursting. These results show that spinal V2a interneurons are required for maintaining left-right alternation at high speeds. Whether animals that generate galloping or hopping gaits, characterized by synchronous movement of left and right forelegs and hindlegs, have lost or modified the function of V2a interneurons is an intriguing question.

 

Author information

Author/s: Crone, Steven A (SA); Zhong, Guisheng (G); Harris-Warrick, Ronald (R); Sharma, Kamal (K);

Affiliation: Department of Neurobiology, University of Chicago, Chicago, Illinois 60637, USA.

Grants: NS17323 (Agency:NINDS NIH HHS)

Journal and publication information

Publication Type: In Vitro; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-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: 2009-May; vol 29 (issue 21) : pp 7098-109

Dates: Created 2009/05/28; Completed 2009/06/23; Revised 2009/08/26;

PMID: 19474336, status: MEDLINE (last retrieval date: 8/27/2009, IMS Date: 27 Aug 2009 00:00:00)

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

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MeSH headings (categories)

This article was linked to the MESH Headings shown below.

Associated Chemicals: Chx10 protein, mouse (0) ; Diphtheria Toxin (0) ; GATA3 Transcription Factor (0) ; Gata3 protein, mouse (0) ; Homeodomain Proteins (0) ; Peptide Fragments (0) ; Transcription Factors (0) ; diphtheria toxin fragment A (0) ; Serotonin (50-67-9) ; N-Methylaspartate (6384-92-5) ; Cholinesterases (EC 3.1.1.8)

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