Neuroreport
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In traumatic axonal injury, Ca2+ influx across a focally damaged axolemma precipitates local mitochondrial failure, degradation of the subaxolemmal spectrin network and compaction of neurofilaments, which collectively contribute to axonal failure. In previous studies, cyclosporin A pretreatment preserved mitochondrial integrity and attenuated axonal failure following trauma. ⋯ CsA pretreatment dramatically reduced Ca2+-induced cytoskeletal damage following injury; CsA-treated rats, compared with vehicle-treated rats, displayed a 70% decrease in immunoreactive/damaged profiles. We suggest that CsA-mediated preservation of mitochondrial integrity enables the restoration of ionic and metabolic homeostasis thereby short-circuiting Ca2+-induced proteolysis in injured axons.
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The postnatal reorganization of rat proprioreceptive muscle afferent spinal terminal fields was explored by labelling transganglionically afferents from extensor digitorum communis with cholera toxin B sub-unit at different ages. Immunocytochemistry revealed labelled afferents in all segments examined (C4-T2) as well as retrogradely labelled motoneurones (C5-T1). ⋯ Between P7 and adult, a significant decrease in bouton density was found in the area dorsomedial to the labelled motoneurones that contained labelled dendrites and antagonist motoneurones. This anatomical reorganization may explain both the increasing stretch reflex threshold and its concomitant decrease in magnitude with age, and the reduction in excitatory connections to antagonist motoneurones, previously described in developmental neurophysiological studies.