DISYNAPTIC GROUP-I EXCITATION OF SYNERGIST ANKLE EXTENSOR MOTONEURONSDURING FICTIVE LOCOMOTION IN THE CAT

1. Intracellular recording from medial gastrocnemius (MG) motoneurones was used to examine postsynaptic potentials produced by electrical st imulation of the plantaris nerve at group I strength at rest and durin g fictive locomotion. Fictive locomotion was evoked by stimulation of the midbrain locomotor region (MLR) in decerebrate cats or in decerebr ate, acute low-spinal cats by perineal stimulation following intraveno us administration of clonidine and naloxone. 2. In both MLR and spinal fictive locomotor preparations, stimulation of plantaris nerve group I afferents at rest evoked short-latency (< 2 ms) IPSPs in MG motoneur ones. During the extensor phase of MLR-evoked locomotion, the same sti mulation produced short-latency (1.6-1.8 ms) EPSPs. Such latencies sug gest mediation by one interneurone interposed between plantaris nerve group I afferents and MG motoneurones. Nonmonosynaptic, short-latency excitation was not seen at rest nor during the flexion phase of the st ep cycle. 3. Group I EPSPs during the extensor phase of MLR-evoked loc omotion were evoked by stimulation at intensities ranging from 1.4-2 t imes threshold (T). The effectiveness of stimulation intensities < 1.5 T suggests that activation of group II afferents is not required to e voke disynaptic excitation. Selective activation of group Ia afferents by stretches of the Achilles tendon also produced disynaptic EPSPs du ring extension. 4. During fictive locomotion in spinal animals pretrea ted with clonidine, short-latency group I IPSPs were not seen but grou p I IPSPs recorded at rest disappeared or were greatly attenuated. The failure of depolarizing current to reveal group I IPSPs suggests that fictive locomotion involves an inhibition of the inhibitory interneur ones that operate at rest. In both clonidine-treated spinal and MLR pr eparations, trains of stimuli at group I strength evoked longer-latenc y and slowly rising potentials that were more prominent during the fle xor phase of fictive locomotion. 5. These results show a reduction in short-latency group I inhibition of synergists in both MLR and clonidi ne-treated spinal preparations during fictive locomotion. In addition, activation of group I afferents evokes short-latency excitation of sy nergists during extension in the MLR preparation. Such excitatory refl exes activated by ankle extensor group Ia and Ib afferents may form an excitatory feedback system, reinforcing on-going extensor activity du ring the stance phase of the step cycle.