Injury-induced plasticity of the flexor reflex in chronic decerebrate rats.
The hindlimb-flexor-withdrawal reflex elicited by stimulation of the skin of the hindpaw has been examined in chronic decerebrate rats. This flexor reflex manifests as a typical phasic avoidance response when measured either behaviourally in the decerebrate rat or electrophysiologically in the decerebrate-spinal preparation. Once the threshold of the cutaneous flexor-reflex afferents in the skin have been exceeded a brief burst of activity with only a short afterdischarge occurs in the flexor motoneurones. The response to sustained stimuli adapts rapidly. In the absence of any treatment to the hindlimb the threshold, duration and responsiveness of the reflex remains stable when tested repeatedly. Thermal or chemical stimuli of sufficient intensity to produce tissue injury and prolonged local inflammation in a hindpaw of the chronic decerebrate rat result in marked and long-lasting (several weeks) alterations in the ipsilateral withdrawal reflex. The mechanical threshold necessary to elicit the reflex by stimulation of the hindpaw falls so that light touch or brush can now elicit a response instead of the firm pressure or pinch required pre-injury. Suprathreshold stimuli to the inflamed skin generate a sustained oscillating pattern of flexion in contrast to the brief flicking movement found in control animals. Electromyographic recordings from the hamstring flexor muscles ipsilateral to the inflamed hindpaw show decreased mechanothresholds, increased spontaneous activity, prolonged afterdischarges to brief stimuli and a slowly adapting tonic response to sustained stimulation. Populations of single cutaneous mechanoreceptive C-primary afferents recorded both from untreated decerebrate rats and from rats with an inflamed hindpaw are indistinguishable in terms of their response properties. There is no difference in threshold, spontaneous activity or afterdischarge between the two populations. The possible mechanisms responsible for the conversion of the high threshold phasic flexor reflex into a low threshold tonic reflex are discussed as are the possible implications for sensory disorders that accompany chronic injury in man.
D000818:Animals; D000870:Anterior Horn Cells / Q000502:physiology; D002056:Burns / Q000503:physiopathology*; D002057:Burns, Chemical / Q000503:physiopathology; D003655:Decerebrate State / Q000503:physiopathology*; D004576:Electromyography; D006614:Hindlimb / Q000293:injuries*; D009473:Neuronal Plasticity; D009475:Neurons, Afferent / Q000502:physiology; D051381:Rats; D012021:Reflex, Abnormal; D012867:Skin / Q000294:innervation; D013116:Spinal Cord / Q000503:physiopathology*