ArticleDevelopmental neuroscience2026
Effects of Complete Spinal Cord Transection in Neonatal and Juvenile Rats on Parvalbumin-Positive Inputs and Perineuronal Net Formation on Chx10-Positive V2a Interneurons.
Article in Developmental neuroscience, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
introductionNeonatal rats, but not juvenile rats, show spontaneous hindlimb locomotor recovery after complete thoracic spinal cord transection (SCT). Significant increases in parvalbumin-positive proprioceptive nerve terminals are observed on motoneurons in both neonatal and juvenile rats with SCT compared with intact rats.
methodsIn the present study, we focused on Chx10-positive V2a interneurons, which partially comprise the central pattern generator, and examined parvalbumin-positive nerve terminals on Chx10 neurons and the perineuronal net formation around these neurons using Wisteria floribunda agglutinin (WFA) as a marker 2 weeks after SCT on postnatal day 5 (neonatal) or day 20 (juvenile).
resultsRats with CST during the neonatal period had a significantly greater number of parvalbumin-positive terminals on Chx10 neurons compared to age-matched intact rats, whereas no significant difference was detected between rats with SCT during the juvenile period and age-matched intact rats. Chx10 neurons for which ≥50% of the circumference was surrounded by WFA were identified as WFA-positive. The proportion of WFA-positive neurons among Chx10-positive neurons did not differ significantly between neonatal SCT and age-matched intact rats, but was significantly higher in juvenile SCT and age-matched intact rats.
conclusionThese findings suggest that SCT promotes the formation of proprioceptive afferent terminals on Chx10-positive neurons. The significant increase in terminals following SCT in neonatal rats might facilitate spontaneous motor recovery, whereas enhanced perineuronal net formation around Chx10 neurons following juvenile SCT might restrict synaptic formation and impair motor recovery.
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