Elimination of intramedullary axon collaterals of cat spinal ?-motoneurons following peripheral nerve injury

1990 ◽  
Vol 79 (1) ◽  
Author(s):  
L. Havton ◽  
J.-O. Kellerth
Keyword(s):  
Peripheral Nerve ◽  
Nerve Injury ◽  
Peripheral Nerve Injury ◽  
Spinal Motoneurons ◽  
Axon Collaterals

scholarly journals Permanent central synaptic disconnection of proprioceptors after nerve injury and regeneration. I. Loss of VGLUT1/IA synapses on motoneurons

2011 ◽  
Vol 106 (5) ◽  
pp. 2450-2470 ◽  
Author(s):  
Francisco J. Alvarez ◽  
Haley E. Titus-Mitchell ◽  
Katie L. Bullinger ◽  
Michal Kraszpulski ◽  
Paul Nardelli ◽  
...  
Keyword(s):  
Peripheral Nerve ◽  
Nerve Injury ◽  
Cell Body ◽  
Peripheral Nerve Injury ◽  
Motor Coordination ◽  
Electrophysiological Study ◽  
Peripheral Nerve Injuries ◽  
Nerve Injuries ◽  
Ia Afferent ◽  
Axon Collaterals

Motor and sensory proprioceptive axons reinnervate muscles after peripheral nerve transections followed by microsurgical reattachment; nevertheless, motor coordination remains abnormal and stretch reflexes absent. We analyzed the possibility that permanent losses of central IA afferent synapses, as a consequence of peripheral nerve injury, are responsible for this deficit. VGLUT1 was used as a marker of proprioceptive synapses on rat motoneurons. After nerve injuries synapses are stripped from motoneurons, but while other excitatory and inhibitory inputs eventually recover, VGLUT1 synapses are permanently lost on the cell body (75–95% synaptic losses) and on the proximal 100 μm of dendrite (50% loss). Lost VGLUT1 synapses did not recover, even many months after muscle reinnervation. Interestingly, VGLUT1 density in more distal dendrites did not change. To investigate whether losses are due to VGLUT1 downregulation in injured IA afferents or to complete synaptic disassembly and regression of IA ventral projections, we studied the central trajectories and synaptic varicosities of axon collaterals from control and regenerated afferents with IA-like responses to stretch that were intracellularly filled with neurobiotin. VGLUT1 was present in all synaptic varicosities, identified with the synaptic marker SV2, of control and regenerated afferents. However, regenerated afferents lacked axon collaterals and synapses in lamina IX. In conjunction with the companion electrophysiological study [Bullinger KL, Nardelli P, Pinter MJ, Alvarez FJ, Cope TC. J Neurophysiol (August 10, 2011). doi:10.1152/jn.01097.2010], we conclude that peripheral nerve injuries cause a permanent retraction of IA afferent synaptic varicosities from lamina IX and disconnection with motoneurons that is not recovered after peripheral regeneration and reinnervation of muscle by sensory and motor axons.

scholarly journals Redistribution of Kv2.1 ion channels on spinal motoneurons following peripheral nerve injury

2014 ◽  
Vol 1547 ◽  
pp. 1-15 ◽  
Author(s):  
Shannon H. Romer ◽  
Kathleen M. Dominguez ◽  
Marc W. Gelpi ◽  
Adam S. Deardorff ◽  
Robert C. Tracy ◽  
...  
Keyword(s):  
Ion Channels ◽  
Peripheral Nerve ◽  
Nerve Injury ◽  
Peripheral Nerve Injury ◽  
Spinal Motoneurons

SynCAM1 expression correlates with restoration of central synapses on spinal motoneurons after two different models of peripheral nerve injury

2009 ◽  
Vol 517 (5) ◽  
pp. 670-682 ◽  
Author(s):  
Johan Zelano ◽  
Alexander Berg ◽  
Sebastian Thams ◽  
Nils P. Hailer ◽  
Staffan Cullheim
Keyword(s):  
Peripheral Nerve ◽  
Nerve Injury ◽  
Peripheral Nerve Injury ◽  
Spinal Motoneurons ◽  
Central Synapses

scholarly journals Neuronal BDNF Signaling Is Necessary for the Effects of Treadmill Exercise on Synaptic Stripping of Axotomized Motoneurons

2015 ◽  
Vol 2015 ◽  
pp. 1-11 ◽  
Author(s):  
Joey Krakowiak ◽  
Caiyue Liu ◽  
Chandana Papudesu ◽  
P. Jillian Ward ◽  
Jennifer C. Wilhelm ◽  
...  
Keyword(s):  
Peripheral Nerve ◽  
Nerve Injury ◽  
Knockout Mice ◽  
Peripheral Nerve Injury ◽  
Treadmill Exercise ◽  
Glutamate Transporter ◽  
Acid Decarboxylase ◽  
Spinal Motoneurons ◽  
Synaptic Inputs ◽  
Glutamate Transporter 1

The withdrawal of synaptic inputs from the somata and proximal dendrites of spinal motoneurons following peripheral nerve injury could contribute to poor functional recovery. Decreased availability of neurotrophins to afferent terminals on axotomized motoneurons has been implicated as one cause of the withdrawal. No reduction in contacts made by synaptic inputs immunoreactive to the vesicular glutamate transporter 1 and glutamic acid decarboxylase 67 is noted on axotomized motoneurons if modest treadmill exercise, which stimulates the production of neurotrophins by spinal motoneurons, is applied after nerve injury. In conditional, neuron-specific brain-derived neurotrophic factor (BDNF) knockout mice, a reduction in synaptic contacts onto motoneurons was noted in intact animals which was similar in magnitude to that observed after nerve transection in wild-type controls. No further reduction in coverage was found if nerves were cut in knockout mice. Two weeks of moderate daily treadmill exercise following nerve injury in these BDNF knockout mice did not affect synaptic inputs onto motoneurons. Treadmill exercise has a profound effect on synaptic inputs to motoneurons after peripheral nerve injury which requires BDNF production by those postsynaptic cells.

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