Neuronal basis of afferent-evoked enhancement of locomotor activity.

Activation of ankle extensor group Ia muscle spindle or Ib tendon organ afferents during locomotion can prolong and enhance hindlimb extensor motoneuron activity. A growing body of evidence suggests that these group I evoked reflexes not only compensate for a changing environment but also help shape extensor activity during normal, unperturbed locomotion. In this paper we review four mechanisms that underlie the group I evoked enhancement of ipsilateral extensor activity during locomotion. The first three are pre-motoneuronal mechanisms that are part of group I reflex pathway reorganization during locomotion. They are (1) a suppression of group I evoked nonreciprocal inhibition, (2) a release from inhibition of excitatory interneurons in disynaptic pathways from group I afferents to extensor motoneurons, and (3) longer latency excitation evoked through extensor portions of the locomotor circuitry. The fourth factor contributing to group I evoked increases in motoneuron activity during locomotion is the increase in motoneuron excitability produced by postsynaptic changes in motoneuron membrane conductances. Most results to be discussed were obtained during locomotion in decerebrate cats in which fictive locomotion was evoked by stimulation of the midbrain following neuromuscular blockade.