Abstract

Kerr's hypothesis (J. Comp. Neurol., 159 (1975) 335–356) that chronic lesion of the lateral spinothalamic tract (LSTT) might cause the ventral STT (VSTT) to take over the nociceptive function of the LSTT was tested electrophysiologically in 4 cats. Recordings were made from 15 antidromically identified deep STT cells in L7 6 months after lesion of the LSTT at L1, confirming that these cells do not project rostrally in the LSTT. The receptive fields of 12 deep STT cells were studied and found to be characteristic of these cells in normal animals; they had not developed the nociceptive characteristics of lamina LSTT cells. Immunohistochemistry showed that substance P-containing afferents were still contained within the dorsal laminae of the L7 grey matter. These results disprove Kerr's hypothesis and suggest that plasticity in other ascending systems must be responsible for the return of pain after lesion of the LSTT.

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