Paralysis elicited by spinal cord injury evokes selective disassembly of neuromuscular synapses with and without terminal sprouting in ankle flexors of the adult rat
Autor: | Srishti Bhagat, Sabiha Jawaid, Anthony S. Burns, Young-Jin Son, Alan Tessler, Hui Zhong, Marion Murray, Hiroyuki Yoshihara, Roland R. Roy |
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Rok vydání: | 2006 |
Předmět: |
Time Factors
animal structures Neuromuscular Junction Presynaptic Terminals Schwann cell Nerve Tissue Proteins Biology Models Biological Neuromuscular junction Rats Sprague-Dawley Postsynaptic potential Physical Conditioning Animal medicine Paralysis Animals Receptors Cholinergic Spinal cord injury Spinal Cord Injuries Acetylcholine receptor Analysis of Variance Membrane Glycoproteins General Neuroscience S100 Proteins Anatomy musculoskeletal system Spinal cord medicine.disease Immunohistochemistry Nerve Regeneration Rats medicine.anatomical_structure nervous system Synapse disassembly Female Schwann Cells Ankle medicine.symptom Neuroscience |
Zdroj: | The Journal of Comparative Neurology. 500:116-133 |
ISSN: | 1096-9861 0021-9967 |
DOI: | 10.1002/cne.21143 |
Popis: | Neuromuscular junctions (NMJs) innervated by motor neurons below spinal cord injury (SCI) have been reported to remain intact despite the interruption of supraspinal pathways and the resultant loss of activity. Here we report notably heterogeneous NMJ responses to SCI that include overt synapse disassembly. Complete transection of the thoracic spinal cord of adult rats evoked massive sprouting of nerve terminals in a subset of NMJs in ankle flexors, extensor digitorum longus, and tibialis anterior. Many of these synapses were extensively disassembled 2 weeks after spinal transection but by 2 months had reestablished synaptic organization despite continuous sprouting of their nerve terminals. In contrast, uniform and persistent loss of acetylcholine receptors (AChRs) was evident in another subset of NMJs in the same flexors, which apparently lacked terminal sprouting and largely maintained terminal arbors. Other synapses in the flexors, and almost all the synapses in the ankle extensors, medial gastrocnemius, and soleus, remained intact, with little pre- or postsynaptic alteration. Additional deafferentation of the transected animals did not alter the incidence or regional distribution of either type of the unstable synapses, whereas cycling exercise diminished their incidence. The muscle- and synapse-specific responses of NMJs therefore reflected differential sensitivity of the NMJs to inactivity rather than to differences in residual activity. These observations demonstrate the existence of multiple subpopulations of NMJs that differ distinctly in pre- and postsynaptic vulnerability to the loss of activity and highlight the anatomical instability of NMJs caudal to SCI, which may influence motor deficit and recovery after SCI. |
Databáze: | OpenAIRE |
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