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1.  Principles of interneuron development learned from Renshaw cells and the motoneuron recurrent inhibitory circuit 
Annals of the New York Academy of Sciences  2013;1279:10.1111/nyas.12084.
Renshaw cells provide a convenient model to study spinal circuit development during the emergence of motor behaviors with the goal of capturing principles of interneuron specification and circuit construction. This work is facilitated by a long history of research that generated essential knowledge about the characteristics that define Renshaw cells and the recurrent inhibitory circuit they form with motoneurons. In this review, we summarize recent data on the specification of Renshaw cells and their connections. A major insight from these studies is that the basic Renshaw cell phenotype is specified before circuit assembly, a result of their early neurogenesis and migration. Connectivity is later added, constrained by their placement in the spinal cord. Finally, different rates of synapse proliferation alter the relative weights of different inputs on postnatal Renshaw cells. Based on this work some general principles on the integration of spinal interneurons in developing motor circuits are derived.
doi:10.1111/nyas.12084
PMCID: PMC3870136  PMID: 23530999
Interneuron; spinal cord; neurogenesis; synaptogenesis; differentiation
2.  Permanent reorganization of Ia afferent synapses on motoneurons after peripheral nerve injuries 
After peripheral nerve injuries to a motor nerve the axons of motoneurons and proprioceptors are disconnected from the periphery and monosynaptic connections from group I afferents and motoneurons become diminished in the spinal cord. Following successful reinnervation in the periphery, motor strength, proprioceptive sensory encoding, and Ia afferent synaptic transmission on motoneurons partially recover. Muscle stretch reflexes, however, never recover and motor behaviors remain uncoordinated. In this review, we summarize recent findings that suggest that lingering motor dysfunction might be in part related to decreased connectivity of Ia afferents centrally. First, sensory afferent synapses retract from lamina IX causing a permanent relocation of the inputs to more distal locations and significant disconnection from motoneurons. Second, peripheral reconnection between proprioceptive afferents and muscle spindles is imperfect. As a result, a proportion of sensory afferents that retain central connections with motoneurons might not reconnect appropriately in the periphery. A hypothetical model is proposed in which the combined effect of peripheral and central reconnection deficits might explain the failure of muscle stretch to initiate or modulate firing of many homonymous motoneurons.
doi:10.1111/j.1749-6632.2010.05459.x
PMCID: PMC2997487  PMID: 20536938
stretch reflex; spinal cord; plasticity; motor control; adult
3.  Mechanisms of excitation of spinal networks by stimulation of the ventral roots 
It has recently been demonstrated that motoneurons in neonatal rodents release an excitatory amino acid, in addition to acetylcholine, from their central terminals onto Renshaw cells. Although the function of this amino acid release is not understood, it may mediate the excitatory actions of motor axon stimulation on spinal motor networks. Stimulation of motor axons in the ventral roots or muscle nerves can activate the locomotor central pattern generator or entrain bursting in the disinhibited cord. Both of these effects persist in the presence of cholinergic antagonists and are abolished or diminished by ionotropic and metabotropic glutamate antagonists.
Calcium imaging in the disinhibited cord shows that a ventral root stimulus evokes ventrolateral activity initially which subsequently propagates to the rest of the cord. This finding suggests that excitatory interneurons excited by motoneuron recurrent collaterals are located in this region. However, motoneurons do not exhibit short latency excitatory potentials in response to ventral root stimulation indicating that the excitatory effects are mediated polysynaptically. The significance of these findings is discussed.
doi:10.1111/j.1749-6632.2010.05535.x
PMCID: PMC3033581  PMID: 20536921
calcium imaging; motoneuron; recurrent excitation; spinal cord
4.  Mechanisms regulating the specificity and strength of muscle afferent inputs in the spinal cord 
We investigated factors controlling the development of connections between muscle spindle afferents, spinal motor neurons and inhibitory Renshaw cells. Several mutants were examined to establish the role of muscle spindles, muscle spindle-derived NT3 and excess NT3 in determining the specificity and strength of these connections. The findings suggest that although spindle-derived factors are not necessary for the initial formation and specificity of the synapses, spindle-derived NT3 seems necessary for strengthening homonymous connections between Ia afferents and motor neurons during the second postnatal week. We also found evidence for functional monosynaptic connections between sensory afferents and neonatal Renshaw cells although the density of these synapses decreases at P15. We conclude that muscle spindle synapses are weakened on Renshaw cells while they are strengthened on motor neurons. Interestingly, the loss of sensory synapses on Renshaw cells was reversed in mice over-expresssing NT3 in the periphery, suggesting that different levels of NT3 are required for functional maintenance and strengthening of spindle afferent inputs on motor neurons and Renshaw cells.
doi:10.1111/j.1749-6632.2010.05538.x
PMCID: PMC3027487  PMID: 20536937
Proprioceptor; muscle spindle; motor neuron; Renshaw; stretch reflex

Results 1-4 (4)