Stumbling Corrective Reaction During Fictive Locomotion in the Cat

1 Spinal Cord Research Centre and Department of Physiology, University of Manitoba, Winnipeg, Manitoba, Canada; 2 Department of Physiology, Biophysics and Neuroscience, Centro de Investigacion y de Estudios Avanzados, Mexico City, Mexico; and 3 The Salk Institute, San Diego, California Submitted 18 February 2005; accepted in final form 21 May 2005 An obstacle contacting the dorsal surface of a cat’s hind foot during the swing phase of locomotion evokes a reflex (the stumbling corrective reaction) that lifts the foot and extends the ankle to avoid falling. We show that the same sequence of ipsilateral hindlimb motoneuron activity can be evoked in decerebrate cats during fictive locomotion. As recorded in the peripheral nerves, twice threshold intensity stimulation of the cutaneous superficial peroneal (SP) nerve during the flexion phase produced a very brief excitation of ankle flexors (e.g., tibialis anterior and peroneus longus) that was followed by an inhibition for the duration of the stimulus train (10–25 shocks, 200 Hz). Extensor digitorum longus was always, and hip flexor (sartorius) activity was sometimes, inhibited during SP stimulation. At the same time, knee flexor and the normally quiescent ankle extensor motoneurons were recruited (mean latencies 4 and 16 ms) with SP stimulation during fictive stumbling correction. After the stimulus train, ankle extensor activity fell silent, and there was an excitation of hip, knee, and ankle flexors. The ongoing flexion phase was often prolonged. Hip extensors were also recruited in some fictive stumbling trials. Only the SP nerve was effective in evoking stumbling correction. Delivered during extension, SP stimulus trains increased ongoing extensor motoneuron activity as well as increasing ipsilateral hip, knee, and ankle hindlimb flexor activity in the subsequent step cycle. The fictive stumbling corrective reflex seems functionally similar to that evoked in intact, awake animals and involves a fixed pattern of short-latency reflexes as well as actions evoked through the lumbar circuitry responsible for the generation of rhythmic alternating locomotion. Address for reprint requests and other correspondence: D. A. McCrea, Spinal Cord Research Ctr., Univ. of Manitoba, 730 William Ave., Winnipeg, Manitoba R3E3J7, Canada (E-mail: dave{at}scrc.umanitoba.ca )