RT Journal Article
SR Electronic
T1 Functionally Reduced Sensorimotor Connections Form with Normal Specificity Despite Abnormal Muscle Spindle Development: The Role of Spindle-Derived Neurotrophin 3
JF The Journal of Neuroscience
JO J. Neurosci.
FD Society for Neuroscience
SP 4719
OP 4735
DO 10.1523/JNEUROSCI.5790-08.2009
VO 29
IS 15
A1 Neil A. Shneider
A1 George Z. Mentis
A1 Joshua Schustak
A1 Michael J. O'Donovan
YR 2009
UL http://www.jneurosci.org/content/29/15/4719.abstract
AB 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.