Direct evidence for decreased presynaptic inhibition evoked by PBSt group I muscle afferents after chronic SCI and recovery with step‐training in rats

Abstract

Presynaptic inhibition is modulated by supraspinal centres and primary afferents in order to filter sensory information, adjust spinal reflex excitability, and ensure smooth movement. r After spinal cord injury (SCI), the supraspinal control of primary afferent depolarization (PAD) interneurons is disengaged, suggesting an increased role for sensory afferents. While increased H-reflex excitability in spastic individuals indicates a possible decrease in presynaptic inhibition, it remains unclear whether a decrease in sensory-evoked PAD contributes to this effect. r We investigated whether the PAD evoked by hindlimb afferents contributes to the change in presynaptic inhibition of the H-reflex in a decerebrated rat preparation. We found that chronic SCI decreases presynaptic inhibition of the plantar H-reflex through a reduction in PAD evoked by posterior biceps-semitendinosus (PBSt) muscle group I afferents. r We further found that step-training restored presynaptic inhibition of the plantar H-reflex evoked by PBSt, suggesting the presence of activity-dependent plasticity of PAD pathways activated by flexor muscle group I afferents.

The corticospinal tract primarily modulates sensory inputs in the mouse lumbar cord

“…Primary afferents have indeed a high chloride content and respond to GABA by a depolarization that has been shown to reduce the amplitude of incoming action potentials and thus inhibit synaptic transmission ( Prescott and De Koninck, 2003 ; Doyon et al, 2011 ). PAD has been involved in the adjustment of reflex excitability ( Rudomin and Schmidt, 1999 ), and its absence results in a pathological context associated with spasticity ( Caron et al, 2020 ). Proprioceptive feedback is required for skilled locomotion ( Akay et al, 2014 ), and presynaptic inhibition of sensory feedback is essential for performing smooth forelimb skilled movements in mice ( Akay et al, 2014 ; Fink et al, 2014 ).…”

Electrophysiological signatures reveal spinal learning mechanisms for a lasting sensorimotor adaptation

“…Ptf1α ON inhibitory spinal recurrent microcircuits gating multimodal afferents are likely essential for various types of motor learning and recovery after spinal cord injury (Casabona et al, 1990; Goode and Van Hoven, 1982; Koceja et al, 2004; Nielsen et al, 1993, Caron et al, 2020; Lavrov et al, 2008; Manella et al, 2013). Ptf1α ON interneurons encompass a heterogeneous group of inhibitory neurons with distinct molecular markers, spatial positioning, and connectivity (Betley et al, 2009; Escalante and Klein, 2020; Zhang et al, 2017).…”

Targeting Sensory and Motor Integration for Recovery of Movement After CNS Injury

“…Following injury, supraspinal control of the spinal network is largely attenuated. Sensory inputs, therefore, have an outsized influence on the spinal cord below the injury (Caron et al, 2020). As a result, afferent sensory fibers become more active.…”