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The Journal of Neuroscience, December 20, 2006, 26(51):13297-13310; doi:10.1523/JNEUROSCI.2945-06.2006
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Development/Plasticity/Repair
Primary Afferent Synapses on Developing and Adult Renshaw Cells
George Z. Mentis,2 Valerie C. Siembab,1 Ricardo Zerda,1 Michael J. O'Donovan,2 andFrancisco J. Alvarez1 1Department of Neurosciences, Cell Biology, and Physiology, Wright State University, Dayton, Ohio 45435, and 2Laboratory of Neural Control, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892
Correspondence should be addressed to Francisco J. Alvarez, Department of Neurosciences, Cell Biology, and Physiology, Wright State University, 3640 Colonel Glenn Highway, Dayton, OH 45435. E-mail: Email: francisco.alvarez{at}wright.edu
The mechanisms that diversify adult interneurons from a few pools of embryonic neurons are unknown. Renshaw cells, Ia inhibitory interneurons (IaINs), and possibly other types of mammalian spinal interneurons have common embryonic origins within the V1 group. However, in contrast to IaINs and other V1-derived interneurons, adult Renshaw cells receive motor axon synapses and lack proprioceptive inputs. Here, we investigated how this specific pattern of connectivity emerges during the development of Renshaw cells. Tract tracing and immunocytochemical markers [parvalbumin and vesicular glutamate transporter 1 (VGLUT1)] showed that most embryonic (embryonic day 18) Renshaw cells lack dorsal root inputs, but more than half received dorsal root synapses by postnatal day 0 (P0) and this input spread to all Renshaw cells by P10–P15. Electrophysiological recordings in neonates indicated that this input is functional and evokes Renshaw cell firing. VGLUT1-IR bouton density on Renshaw cells increased until P15 but thereafter decreased because of limited synapse proliferation coupled with the enlargement of Renshaw cell dendrites. In parallel, Renshaw cell postsynaptic densities apposed to VGLUT1-IR synapses became smaller in adult compared with P15. In contrast, vesicular acetylcholine transporter-IR motor axon synapses contact embryonic Renshaw cells and proliferate postnatally matching Renshaw cell growth. Like other V1 neurons, Renshaw cells are thus competent to receive sensory synapses. However, after P15, these sensory inputs appear deselected through arrested proliferation and synapse weakening. Thus, Renshaw cells shift from integrating sensory and motor inputs in neonates to predominantly motor inputs in adult. Similar synaptic weight shifts on interneurons may be involved in the maturation of motor reflexes and locomotor circuitry.
Key words: spinal cord; development; proprioceptive; interneurons; recurrent inhibition; motoneuron
Received July 11, 2006; revised Nov. 9, 2006; accepted Nov. 14, 2006.
Correspondence should be addressed to Francisco J. Alvarez, Department of Neurosciences, Cell Biology, and Physiology, Wright State University, 3640 Colonel Glenn Highway, Dayton, OH 45435. E-mail: Email: francisco.alvarez{at}wright.edu
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