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The Journal of Neuroscience, April 15, 2009, 29(15):4719-4735; doi:10.1523/JNEUROSCI.5790-08.2009

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Development/Plasticity/Repair
Functionally Reduced Sensorimotor Connections Form with Normal Specificity Despite Abnormal Muscle Spindle Development: The Role of Spindle-Derived Neurotrophin 3

Neil A. Shneider,^1,2,3 * George Z. Mentis,^1 * Joshua Schustak,¹ and Michael J. O'Donovan¹

¹Section on Developmental Neurobiology, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892, and ²Department of Neurology and ³Center for Motor Neuron Biology and Disease, Columbia University, New York, New York 10032

Correspondence should be addressed to Michael J. O'Donovan, Section on Developmental Neurobiology, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892. Email: odonovm{at}ninds.nih.gov

The mechanisms controlling the formation of synaptic connections between muscle spindle afferents and spinal motor neurons are believed to be regulated by factors originating from muscle spindles. Here, we find that the connections form with appropriate specificity in mice with abnormal spindle development caused by the conditional elimination of the neuregulin1 receptor ErbB2 from muscle precursors. However, despite a modest (30%) decrease in the number of afferent terminals on motor neuron somata, the amplitude of afferent-evoked synaptic potentials recorded in motor neurons was reduced by 80%, suggesting that many of the connections that form are functionally silent. The selective elimination of neurotrophin 3 (NT3) from muscle spindles had no effect on the amplitude of afferent-evoked ventral root potentials until the second postnatal week, revealing a late role for spindle-derived NT3 in the functional maintenance of the connections. These findings indicate that spindle-derived factors regulate the strength of the connections but not their initial formation or their specificity.

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Received Dec. 4, 2008; revised March 2, 2009; accepted March 4, 2009.

Correspondence should be addressed to Michael J. O'Donovan, Section on Developmental Neurobiology, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892. Email: odonovm{at}ninds.nih.gov

Related articles in J. Neurosci.:

Spindle-Derived NT3 in Sensorimotor Connections: Principal Role at Later Stages

Svetlana Gorokhova, Stéphane Gaillard, and Eduardo Gascon
J. Neurosci. 2009 29: 10181-10183. [Full Text]  

This article has been cited by other articles:

				S. Gorokhova, S. Gaillard, and E. Gascon Spindle-Derived NT3 in Sensorimotor Connections: Principal Role at Later Stages J. Neurosci., August 19, 2009; 29(33): 10181 - 10183. [Full Text] [PDF]

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