Abstract
A standard suprathreshold mechanical stimulus applied to the hindpaw of decerebrate-spinal rats produces a discharge in hamstring flexor α-motoneurones which is stable for hours, provided no tissue injury is produced. Tissue injury results, however, in a decrease of threshold and an increase in the responsiveness of the reflex. This reflex hypersensitivity can be mimicked by brief (20 s) low frequency (1 Hz) conditioning stimuli to muscle or cutaneous nerves, if C-fibres are recruited. The prolonged post-conditioning facilitation of the flexion reflex by C-afferent volleys is now shown to be independent of changes in the excitability of the test afferent terminals in the dorsal horn and of the motoneurones. The hypersensitivity is therefore due to changes in the interneurones that link cutaneous nociceptive afferents with flexor motoneurones.
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