{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,30]],"date-time":"2026-09-30T17:30:57Z","timestamp":1790789457666,"version":"4.1.0"},"reference-count":104,"publisher":"Wiley","issue":"10","license":[{"start":{"date-parts":[[2023,4,9]],"date-time":"2023-04-09T00:00:00Z","timestamp":1680998400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["physoc.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["The Journal of Physiology"],"published-print":{"date-parts":[[2023,5]]},"abstract":"<jats:sec>\n                    <jats:title>Abstract<\/jats:title>\n                    <jats:p>\n                      Suppression of the extensor H\u2010reflex by flexor afferent conditioning is thought to be produced by a long\u2010lasting inhibition of extensor Ia afferent terminals via GABA\n                      <jats:sub>A<\/jats:sub>\n                      receptor\u2010activated primary afferent depolarization (PAD). Given the recent finding that PAD does not produce presynaptic inhibition of Ia afferent terminals, we examined in 28 participants if H\u2010reflex suppression is instead mediated by post\u2010activation depression of the extensor Ia afferents triggered by PAD\u2010evoked spikes and\/or by a long\u2010lasting inhibition of the extensor motoneurons. A brief conditioning vibration of the flexor tendon suppressed both the extensor soleus H\u2010reflex and the tonic discharge of soleus motor units out to 150\u00a0ms following the vibration, suggesting that part of the H\u2010reflex suppression during this period was mediated by postsynaptic inhibition of the extensor motoneurons. When activating the flexor afferents electrically to produce conditioning, the soleus H\u2010reflex was also suppressed but only when a short\u2010latency reflex was evoked in the soleus muscle by the conditioning input itself. In mice, a similar short\u2010latency reflex was evoked when optogenetic or afferent activation of GABAergic (GAD2\n                      <jats:sup>+<\/jats:sup>\n                      ) neurons produced a large enough PAD to evoke orthodromic spikes in the test Ia afferents, causing post\u2010activation depression of subsequent monosynaptic EPSPs. The long duration of this post\u2010activation depression and related H\u2010reflex suppression (seconds) was similar to rate\u2010dependent depression that is also due to post\u2010activation depression. We conclude that extensor H\u2010reflex inhibition by brief flexor afferent conditioning is produced by both post\u2010activation depression of extensor Ia afferents and long\u2010lasting inhibition of extensor motoneurons, rather than from PAD inhibiting Ia afferent terminals.\n                      <jats:boxed-text content-type=\"graphic\" position=\"anchor\">\n                        <jats:graphic xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" mimetype=\"image\/png\" position=\"anchor\" specific-use=\"enlarged-web-image\" xlink:href=\"graphic\/tjp15504-gra-0001-m.png\">\n                          <jats:alt-text>image<\/jats:alt-text>\n                        <\/jats:graphic>\n                      <\/jats:boxed-text>\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Key points<\/jats:title>\n                    <jats:p>\n                      <jats:list list-type=\"bullet\">\n                        <jats:list-item>\n                          <jats:p>\n                            Suppression of extensor H\u2010reflexes by flexor afferent conditioning was thought to be mediated by GABA\n                            <jats:sub>A<\/jats:sub>\n                            receptor\u2010mediated primary afferent depolarization (PAD) shunting action potentials in the Ia afferent terminal.\n                          <\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>In line with recent findings that PAD has a facilitatory role in Ia afferent conduction, we show here that when large enough, PAD can evoke orthodromic spikes that travel to the Ia afferent terminal to evoke EPSPs in the motoneuron.<\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>These PAD\u2010evoked spikes also produce post\u2010activation depression of Ia afferent terminals and may mediate the short\u2010 and long\u2010lasting suppression of extensor H\u2010reflexes in response to flexor afferent conditioning.<\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>Our findings highlight that we must re\u2010examine how changes in the activation of GABAergic interneurons and PAD following nervous system injury or disease affects the regulation of Ia afferent transmission to spinal neurons and ultimately motor dysfunction in these disorders.<\/jats:p>\n                        <\/jats:list-item>\n                      <\/jats:list>\n                    <\/jats:p>\n                  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