Group I extensor afferents evoke disynaptic EPSPs in cat hindlimb extensor motorneurones during fictive locomotion.

Abstract

1. Intracellular recording from extensor motoneurones in paralysed decerebrate cats was used to examine the distribution of short‐latency non‐monosynaptic excitation by group I afferents during fictive locomotion produced by stimulation of the mesencephalic locomotor region (MLR). 2. During the extension but not the flexion phase of fictive locomotion, stimulation of ankle extensor nerves at 1.2‐2.0 times threshold evoked excitatory postsynaptic potentials (EPSPs) in motoneurones innervating hip, knee and ankle extensors. Disynaptic EPSPs were also evoked by selective activation of group Ia muscle spindle afferents by muscle stretch. 3. The central latencies of these group I‐evoked EPSPs (mean, 1.55 ms) suggest their mediation by a disynaptic pathway with a single interneurone interposed between extensor group I afferents and extensor motoneurones. Disynaptic EPSPs were also evoked during periods of spontaneous locomotion following the cessation of MLR stimulation. 4. Hip extensor motoneurones received disynaptic EPSPs during extension following stimulation of both homonymous and ankle extensor nerves. Stimulation of hip extensor nerves did not evoke disynaptic EPSPs in ankle extensor motoneurones. 5. The appearance of disynaptic EPSPs during extension appears to result from cyclic disinhibition of an unidentified population of excitatory spinal interneurones and not postsynaptic voltage‐dependent conductances in motoneurones or phasic presynaptic inhibition of group I afferents during flexion. 6. The reorganization of group I reflexes during fictive locomotion includes the appearance of disynaptic excitation of hip, knee and ankle extensor motoneurones. This excitatory reflex is one of the mechanisms by which group I afferents can enhance extensor activity and increase force production during stance.

Locomotor training improves reciprocal and nonreciprocal inhibitory control of soleus motoneurons in human spinal cord injury

“…6C), suggesting that synergistic group I afferents may contribute to the soleus H-reflex depression during the swing phase, supported by previous findings reported for untrained SCI subjects (Knikou 2012). Last, cyclic disinhibition of group Ib excitatory spinal interneurons was weak compared with that observed in animals (Angel et al 1996), since locomotor training did not induce an extra facilitation of soleus motoneuron responses by group Ib afferents during the stance phase (Fig. 6, B and E).…”

Muscle activation during unilateral stepping occurs in the nonstepping limb of humans with clinically complete spinal cord injury

“…Afferents from both sources could act through reflex pathways directly onto motor neurons or onto locomotor neural networks in the spinal cord 9,[19][20][21][22][23][24][25][26][27] (for review, see Duysens et al 6 ). There is no way to tell from the current data as to which afferents or which pathways were responsible.…”

Genetically Defined Inhibitory Neurons in the Mouse Spinal Cord Dorsal Horn: A Possible Source of Rhythmic Inhibition of Motoneurons during Fictive Locomotion

“…During locomotion in the cat, stimulation of low-threshold muscle afferents produces shortlatency excitation rather than inhibition of motoneurons (Conway et al, 1987;Gossard et al, 1994;McCrea et al, 1995;Angel et al, 1996). This is thought to result from locomotor network-related disinhibition of group I excitatory interneurons (Angel et al, 1996), possibly concurrent with tonic postsynaptic inhibition of group I nonreciprocal inhibitory interneurons (Angel et al, 2005).…”