<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Brown BL</submitter><funding>NINDS NIH HHS</funding><funding>NIH</funding><pagination>114631</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC10922963</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>373</volume><pubmed_abstract>Long ascending propriospinal neurons (LAPNs) are a subset of spinal interneurons that provide direct connectivity between distant spinal segments. Here, we focus specifically on an anatomically defined population of "inter-enlargement" LAPNs with cell bodies at L2/3 and terminals at C5/6. Previous studies showed that silencing LAPNs in awake and freely moving animals disrupted interlimb coordination of the hindlimbs, forelimbs, and heterolateral limb pairs. Surprisingly, despite a proportion of LAPNs being anatomically intact post- spinal cord injury (SCI), silencing them improved locomotor function but only influenced coordination of the hindlimb pair. Given the functional significance of LAPNs pre- and post-SCI, we characterized their anatomy and SCI-induced anatomical plasticity. This detailed anatomical characterization revealed three morphologically distinct subsets of LAPNs that differ in soma size, neurite complexity and/or neurite orientation. Following a mild thoracic contusive SCI there was a marked shift in neurite orientation in two of the LAPN subsets to a more dorsoventral orientation, and collateral densities decreased in the cervical enlargement but increased just caudal to the injury epicenter. These post-SCI anatomical changes potentially reflect maladaptive plasticity and an effort to establish new functional inputs from sensory afferents that sprout post-SCI to achieve circuitry homeostasis.</pubmed_abstract><journal>Experimental neurology</journal><pubmed_title>Long ascending propriospinal neurons are heterogenous and subject to spinal cord injury induced anatomic plasticity.</pubmed_title><pmcid>PMC10922963</pmcid><funding_grant_id>R01 NS112304</funding_grant_id><funding_grant_id>F31 NS116935</funding_grant_id><pubmed_authors>Anil N</pubmed_authors><pubmed_authors>States G</pubmed_authors><pubmed_authors>Brown BL</pubmed_authors><pubmed_authors>Whittemore SR</pubmed_authors><pubmed_authors>Magnuson DSK</pubmed_authors></additional><is_claimable>false</is_claimable><name>Long ascending propriospinal neurons are heterogenous and subject to spinal cord injury induced anatomic plasticity.</name><description>Long ascending propriospinal neurons (LAPNs) are a subset of spinal interneurons that provide direct connectivity between distant spinal segments. Here, we focus specifically on an anatomically defined population of "inter-enlargement" LAPNs with cell bodies at L2/3 and terminals at C5/6. Previous studies showed that silencing LAPNs in awake and freely moving animals disrupted interlimb coordination of the hindlimbs, forelimbs, and heterolateral limb pairs. Surprisingly, despite a proportion of LAPNs being anatomically intact post- spinal cord injury (SCI), silencing them improved locomotor function but only influenced coordination of the hindlimb pair. Given the functional significance of LAPNs pre- and post-SCI, we characterized their anatomy and SCI-induced anatomical plasticity. This detailed anatomical characterization revealed three morphologically distinct subsets of LAPNs that differ in soma size, neurite complexity and/or neurite orientation. Following a mild thoracic contusive SCI there was a marked shift in neurite orientation in two of the LAPN subsets to a more dorsoventral orientation, and collateral densities decreased in the cervical enlargement but increased just caudal to the injury epicenter. These post-SCI anatomical changes potentially reflect maladaptive plasticity and an effort to establish new functional inputs from sensory afferents that sprout post-SCI to achieve circuitry homeostasis.</description><dates><release>2024-01-01T00:00:00Z</release><publication>2024 Mar</publication><modification>2025-04-04T19:26:23.662Z</modification><creation>2025-04-04T19:26:23.662Z</creation></dates><accession>S-EPMC10922963</accession><cross_references><pubmed>38070723</pubmed><doi>10.1016/j.expneurol.2023.114631</doi></cross_references></HashMap>