Post-activation depression produces extensor H-reflex suppression following flexor afferent conditioning

Suppression of the extensor H-reflex by flexor afferent conditioning is thought to be produced by a long-lasting inhibition of extensor Ia-afferent terminals via primary afferent depolarization (PAD) activated by GABAA receptors. Considering the recent finding that PAD does not produce presynaptic inhibition of Ia-afferent terminals, we examined if H-reflex suppression is instead mediated by post-activation depression of the test extensor Ia-afferents triggered by PAD-evoked spikes and/or by a long-lasting inhibition of the extensor motoneurons. A brief conditioning vibration of the flexor tendon suppressed both the extensor soleus H-reflex and the tonic discharge of soleus motor units for 300 ms, indicating that part of the H-reflex suppression was mediated by a long-lasting inhibition of the extensor motoneurons. When activating the flexor afferents electrically to produce conditioning, the soleus H-reflex was also suppressed for 300 ms, but only when a short-latency reflex was evoked in the soleus muscle by the conditioning input itself. In mice, a similar short-latency reflex was evoked when optogenetic or afferent activation of GABAergic (GAD2+) neurons produced PAD large enough to evoke orthodromic spikes in the test Ia-afferents, causing post-activation depression of subsequent monosynaptic excitatory-post-synaptic potentials. The time course of this post-activation depression and related H-reflex suppression (lasting 2 s) was like rate-dependent depression that is also due to post-activation depression. We conclude that extensor H-reflex inhibition by brief flexor afferent conditioning is produced by both post-activation depression of extensor Ia-afferents and long-lasting inhibition of extensor motoneurons, rather than from PAD directly inhibiting Ia afferent terminals.