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Functional reorganization of sensory pathways in the rat spinal dorsal horn following peripheral nerve injury
Author(s) -
Okamoto M.,
Baba H.,
Goldstein P. A.,
Higashi H.,
Shimoji K.,
Yoshimura M.
Publication year - 2001
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1111/j.1469-7793.2001.0241g.x
Subject(s) - sciatic nerve , spinal cord , neuroscience , stimulation , sensory system , nociception , chemistry , anatomy , excitatory postsynaptic potential , afferent , medicine , inhibitory postsynaptic potential , biology , biochemistry , receptor
1 Functional reorganization of sensory pathways in the rat spinal dorsal horn following sciatic nerve transection was examined using spinal cord slices with an attached dorsal root. Slices were obtained from animals whose sciatic nerve had been transected 2‐4 weeks previously and compared to sham‐operated controls. 2 Whole‐cell recordings from substantia gelatinosa neurones in sham‐operated rats, to which nociceptive information was preferentially transmitted, revealed that dorsal root stimulation sufficient to activate Aδ afferent fibres evoked a mono‐ and/or polysynaptic EPSC in 111 of 131 (≈85 %) neurones. This is in contrast to the response following Aβ fibre stimulation, where monosynaptic EPSCs were observed in 2 of 131 (≈2 %) neurones and polysynaptic EPSCs were observed in 18 of 131 (≈14 %) neurones. 3 In sciatic nerve‐transected rats, however, a polysynaptic EPSC following stimulation of Aβ afferents was elicited in 30 of 37 (81 %) neurones and a monosynaptic EPSC evoked by Aβ afferent stimulation was detected in a subset of neurones (4 of 37, ≈11 %). 4 These observations suggest that, following sciatic nerve transection, large myelinated Aβ afferent fibres establish synaptic contact with interneurones and transmit innocuous information to substantia gelatinosa. This functional reorganization of the sensory circuitry may constitute an underlying mechanism, at least in part, for sensory abnormalities following peripheral nerve injuries.