Department of Physiology, University of Manitoba, 730 William Avenue, Winnipeg, Manitoba, Canada R3E 3J7
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.
