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Motor circuits deciphered by molecul...

Myers, Christopher Patrick.

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Motor circuits deciphered by molecular genetics.

Record Type:	Electronic resources : Monograph/item
Title/Author:	Motor circuits deciphered by molecular genetics./
Author:	Myers, Christopher Patrick.
Description:	183 p.
Notes:	Source: Dissertation Abstracts International, Volume: 65-03, Section: B, page: 1177.
Contained By:	Dissertation Abstracts International65-03B.
Subject:	Neurosciences. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3127632
ISBN:	9780496748969

Motor circuits deciphered by molecular genetics.
Myers, Christopher Patrick.

Motor circuits deciphered by molecular genetics. - 183 p.

Source: Dissertation Abstracts International, Volume: 65-03, Section: B, page: 1177.

Thesis (Ph.D.)--University of California, San Diego, 2004.

This item must not be sold to any third party vendors.

Traditionally, motor circuits of the vertebrate spinal cord have been studied with electrophysiological, anatomical and imaging techniques, and these approaches have provided vast insights into their general organization. More recently, molecular and genetic approaches have been applied to the study of motor circuits. Here, we investigate the role of two genes, choline acetyltransferase (chat) and estrogen-related receptor 3 (err3), in the development and function of mouse motor circuits. The chat mutant mouse is deficient in the rate-limiting enzyme required for the biosynthesis of the neurotransmitter, acetylcholine (ACh). Thus, spinal motor circuits in these mice develop in the absence of cholinergic transmission. Motor circuits of the chat mutant cord are characterized by a reduction in the level of excitability. The chat mutant cord also demonstrates a premature transition to glutamate-mediated excitation and glycine-mediated inhibition. The locomotor CPG of the chat mutant demonstrates: (1) a prolongation of burst duration and cycle period and (2) altered phasic relationships between bursts of left and right L2 and ipsilateral L2 and L5 roots. Overall, these studies demonstrate a critical role for ACh in the organization and development of mouse motor circuits.

ISBN: 9780496748969Subjects--Topical Terms:

588700
Neurosciences.

Motor circuits deciphered by molecular genetics.
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100 1 $a Myers, Christopher Patrick. $3 3174016
245 1 0 $a Motor circuits deciphered by molecular genetics.
300 $a 183 p.
500 $a Source: Dissertation Abstracts International, Volume: 65-03, Section: B, page: 1177.
500 $a Chairs: Samuel Pfaff; Nicholas Spitzer.
502 $a Thesis (Ph.D.)--University of California, San Diego, 2004.
506 $a This item must not be sold to any third party vendors.
506 $a This item must not be added to any third party search indexes.
520 $a Traditionally, motor circuits of the vertebrate spinal cord have been studied with electrophysiological, anatomical and imaging techniques, and these approaches have provided vast insights into their general organization. More recently, molecular and genetic approaches have been applied to the study of motor circuits. Here, we investigate the role of two genes, choline acetyltransferase (chat) and estrogen-related receptor 3 (err3), in the development and function of mouse motor circuits. The chat mutant mouse is deficient in the rate-limiting enzyme required for the biosynthesis of the neurotransmitter, acetylcholine (ACh). Thus, spinal motor circuits in these mice develop in the absence of cholinergic transmission. Motor circuits of the chat mutant cord are characterized by a reduction in the level of excitability. The chat mutant cord also demonstrates a premature transition to glutamate-mediated excitation and glycine-mediated inhibition. The locomotor CPG of the chat mutant demonstrates: (1) a prolongation of burst duration and cycle period and (2) altered phasic relationships between bursts of left and right L2 and ipsilateral L2 and L5 roots. Overall, these studies demonstrate a critical role for ACh in the organization and development of mouse motor circuits.
520 $a The err3 mutant mouse is deficient in the expression of an orphan nuclear hormone receptor expressed in novel neurons of the ventral cord. In contrast to those of the chat mutant, motor circuits of the err3 mutant are characterized by an increase in their level of excitability. The locomotor CPG of the err3 null mouse demonstrates: (1) abnormal phasic activity between bilateral L2 and ipsilateral L2 and L5 lumbar roots and (2) the synchronization of bursting between ipsilateral L2 (flexor) and L5 (extensor) motor neurons. Abnormal 'burst' and 'suppression' phases alternate across the midline and are synchronized along the ipsilateral cord of the err3 mutant, suggesting a role for ERR3-expressing neurons in the modulation of reciprocal inhibition between bilatterally-located motor circuits and ipsilaterally-located extensor and flexor circuits. Overall, studies of the err3 mutant suggest a derangement in the normal 'clock' mechanism that serves to regulate the timing of left-right and ipsilateral L2--L5 reciprocal inhibition.
590 $a School code: 0033.
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710 2 $a University of California, San Diego. $3 1018093
773 0 $t Dissertation Abstracts International $g 65-03B.
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791 $a Ph.D.
792 $a 2004
793 $a English
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3127632