ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2007
Enhanced transmission at a spinal synapse triggered in vivo by an injury signal independent of altered synaptic activity.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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14 citing papers in PubMed, 19 citations in OpenAlex.
- Structural Preservation Does Not Ensure Function at Sensory Ia-Motoneuron Synapses following Peripheral Nerve Injury and Repair.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Homeostatic Plasticity of the Mammalian Neuromuscular Junction.Advances in neurobiology · 2022Article
- Article
- Synaptic Plasticity on Motoneurons After Axotomy: A Necessary Change in Paradigm.Frontiers in molecular neuroscience · 2020Review
- Activity-dependent redistribution of Kv2.1 ion channels on rat spinal motoneurons.Physiological reports · 2016Article
- Modulation of motoneuron firing by recurrent inhibition in the adult rat in vivo.Journal of neurophysiology · 2014Article
- Normal distribution of VGLUT1 synapses on spinal motoneuron dendrites and their reorganization after nerve injury.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
- Swimming against the tide: investigations of the C-bouton synapse.Frontiers in neural circuits · 2014Review
- Expression of postsynaptic Ca2+-activated K+ (SK) channels at C-bouton synapses in mammalian lumbar -motoneurons.The Journal of physiology · 2013Article
- Permanent central synaptic disconnection of proprioceptors after nerve injury and regeneration. I. Loss of VGLUT1/IA synapses on motoneurons.Journal of neurophysiology · 2011Article
- Permanent central synaptic disconnection of proprioceptors after nerve injury and regeneration. II. Loss of functional connectivity with motoneurons.Journal of neurophysiology · 2011Article
- Permanent reorganization of Ia afferent synapses on motoneurons after peripheral nerve injuries.Annals of the New York Academy of Sciences · 2010Article
- Influence of vagotomy on monosynaptic transmission at second-order nucleus tractus solitarius synapses.Journal of neurophysiology · 2009Article
- Compensatory changes in cellular excitability, not synaptic scaling, contribute to homeostatic recovery of embryonic network activity.Proceedings of the National Academy of Sciences of the United States of America · 2009Article
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
Peripheral nerve crush initiates a robust increase in transmission strength at spinal synapses made by axotomized group IA primary sensory neurons. To study the injury signal that initiates synaptic enhancement in vivo, we designed experiments to manipulate the enlargement of EPSPs produced in spinal motoneurons (MNs) by IA afferents 3 d after nerve crush in anesthetized adult rats. If nerve crush initiates IA EPSP enlargement as proposed by reducing impulse-evoked transmission in crushed IA afferents, then restoring synaptic activity should eliminate enlargement. Daily electrical stimulation of the nerve proximal to the crush site did, in fact, eliminate enlargement but was, surprisingly, just as effective when the action potentials evoked in crushed afferents were prevented from propagating into the spinal cord. Consistent with its independence from altered synaptic activity, we found that IA EPSP enlargement was also eliminated by colchicine blockade of axon transport in the crushed nerve. Together with the observation that colchicine treatment of intact nerves had no short-term effect on IA EPSPs, we conclude that enhancement of IA-MN transmission is initiated by some yet to be identified positive injury signal generated independent of altered synaptic activity. The results establish a new set of criteria that constrain candidate signaling molecules in vivo to ones that develop quickly at the peripheral injury site, move centrally by axon transport, and initiate enhanced transmission at the central synapses of crushed primary sensory afferents through a mechanism that can be modulated by action potential activity restricted to the axons of crushed afferents.
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