{"id":761,"date":"2026-04-13T02:17:54","date_gmt":"2026-04-13T02:17:54","guid":{"rendered":"http:\/\/www.rischool.org\/?p=761"},"modified":"2026-04-13T02:17:54","modified_gmt":"2026-04-13T02:17:54","slug":"note-that-the-termination-of-the-hyperpolarizing-current-anode-break-triggered-an-ap-with-an-increased-amplitude-in-many-axons-when-recorded-in-the-noninjured-spinal-cord-in-47-of-64-axons","status":"publish","type":"post","link":"http:\/\/www.rischool.org\/?p=761","title":{"rendered":"\ufeffNote that the termination of the hyperpolarizing current (anode break) triggered an AP with an increased amplitude in many axons when recorded in the noninjured spinal cord (in 47 of 64 axons recorded,Fig"},"content":{"rendered":"

\ufeffNote that the termination of the hyperpolarizing current (anode break) triggered an AP with an increased amplitude in many axons when recorded in the noninjured spinal cord (in 47 of 64 axons recorded,Fig. USA101: 81688173, 2004b). This result was substantiated by ultrastructural changes seen with electron microscopy, in which an increased number of large-caliber, demyelinated RST axons were found contralateral to the chronic HX. Therefore, an increased rheobase, pathological changes in the distribution of Nav1.6 sodium channels, and the demyelination of contralateral RST axons are likely responsible for their decreased conduction chronically after HX and thus may provide novel targets for strategies to improve function following incomplete spinal cord injury. Keywords:in vivo intra-axonal recording, rheobase, demyelination using in vivo intracellularrecordings from motoneurons in adult rats, we recently recorded synaptic responses from motoneurons after (R)-Nedisertib<\/a> unilateral hemisection (HX) (R)-Nedisertib of the spinal cord at T10, when one side of the cord is lesioned and the other half remains intact (Arvanian et al. 2009). We found that synaptic responses recorded from individual motoneurons in the L5 ventral horn and evoked by electrical stimulation of white matter axons at T7, contralateral to HX, began to decline 1 wk (R)-Nedisertib post-spinal cord injury (SCI). This diminished transmission plateaued at 2 wk post-HX and remained reduced for at least 14 wk postlesion. The decline of synaptic responses was associated with a decrease in the amplitude of the volley responses recorded extracellularly from the L5 ventral horn (Arvanian et al. 2009;Hunanyan et al. 2010), ACAD9<\/a> suggesting that the decay in synaptic transmission during the chronic stage of HX could be determined by conduction deficits in fibers contralateral to HX. Consistent with the decline of responses that we recorded from the intact side below chronic HX and evoked by electric stimulation above,Hubscher and Johnson (2002) reported that in cases of chronic (4 wk) lateral HX at T8, neuronal responses on both sides of the medullary reticular formation to pinching of the hind paw on the side opposite the lesion (intact side) were weak or completely absent, depending on the lesion extent. However, extracellular recording cannot distinguish whether conduction deficits are the result of changes in the axonal resting membrane potential, membrane resistance, or the excitability of individual axons. Therefore the mechanisms that underlie conduction deficits at the level of the solitary axon after unilateral chronic HX were not examined. Intra-axonal recordings, however, have been shown to be a more direct technique for the assessment of an individual axon’s electrical properties (Baker et al. 1987;Blight and Someya 1985;Dpassionate et al. 1995;Honmou et al. 1996;Kocsis and Waxman 1982;Kriz and Padjen 2003). Importantly, intra-axonal recording allows the measurement of rheobase current, which correlates directly with the excitability of the axon. In the present study, to characterize the electrical properties of individual axons contralateral to the HX and to measure the propagation of action potentials (APs) through axons moving across the injury level, we recorded in vivo intra-axonally from lumbar rubrospinal\/reticulospinal tract (RST\/RtST) axons at 26 wk after HX. The RST\/RtST axons are known to be heavily myelinated and to be important for rodent locomotion (Ballermann and Fouad 2006;Brown 1974;Kanagal and Muir 2008; Waldron and Gwyn 1969;Webb and Muir 2003). We found improved rheobase (i.e., larger depolarization pulse through the intra-axonal recording electrode required to result in APs), as well as pathological changes in propagation of APs through individual uncut axons across from chronic HX. Our ultrastructural analysis of the RST axons across from HX exposed an increased quantity of demyelinated axons within the uninjured part of the spinal cord in chronic hurt rats. Demyelination of axons has been attributed to the loss of axonal function and development of neurological deficits in SCI and other types of neurotrauma, including multiple sclerosis and stroke (Blight and Decrescito 1986;McDonald et al. 2000;Nashmi and Fehlings 2001). In the (R)-Nedisertib models of multiple sclerosis and contusion injury, demyelination of axons has been associated with diffuse distribution of Nav1.6 sodium channels along the axons (Craner et al. 2004b). With this study we have demonstrated related changes in the distribution pattern of Nav1.6 channels in lateral white matter axons, opposite the injury, after chronic HX. In the uninjured spinal cord, Nav1.6 channels were clustered along the axons, specifically mostly in the nodes of Ranvier (as identified by flanking.<\/p>\n","protected":false},"excerpt":{"rendered":"

\ufeffNote that the termination of the hyperpolarizing current (anode break) triggered an AP with an increased amplitude in many axons…<\/p>\n","protected":false},"author":1,"featured_media":0,"comment_status":"closed","ping_status":"open","sticky":false,"template":"","format":"standard","meta":{"footnotes":""},"categories":[47],"tags":[],"class_list":["post-761","post","type-post","status-publish","format-standard","hentry","category-l-type-calcium-channels"],"_links":{"self":[{"href":"http:\/\/www.rischool.org\/index.php?rest_route=\/wp\/v2\/posts\/761","targetHints":{"allow":["GET"]}}],"collection":[{"href":"http:\/\/www.rischool.org\/index.php?rest_route=\/wp\/v2\/posts"}],"about":[{"href":"http:\/\/www.rischool.org\/index.php?rest_route=\/wp\/v2\/types\/post"}],"author":[{"embeddable":true,"href":"http:\/\/www.rischool.org\/index.php?rest_route=\/wp\/v2\/users\/1"}],"replies":[{"embeddable":true,"href":"http:\/\/www.rischool.org\/index.php?rest_route=%2Fwp%2Fv2%2Fcomments&post=761"}],"version-history":[{"count":1,"href":"http:\/\/www.rischool.org\/index.php?rest_route=\/wp\/v2\/posts\/761\/revisions"}],"predecessor-version":[{"id":762,"href":"http:\/\/www.rischool.org\/index.php?rest_route=\/wp\/v2\/posts\/761\/revisions\/762"}],"wp:attachment":[{"href":"http:\/\/www.rischool.org\/index.php?rest_route=%2Fwp%2Fv2%2Fmedia&parent=761"}],"wp:term":[{"taxonomy":"category","embeddable":true,"href":"http:\/\/www.rischool.org\/index.php?rest_route=%2Fwp%2Fv2%2Fcategories&post=761"},{"taxonomy":"post_tag","embeddable":true,"href":"http:\/\/www.rischool.org\/index.php?rest_route=%2Fwp%2Fv2%2Ftags&post=761"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}