AMPK-Nrf2 Signaling Pathway in Phrenic Motoneurons following Cervical Spinal Cord Injury.

High spinal cord injuries (SCI) induce the deafferentation of phrenic motoneurons, leading to permanent diaphragm paralysis. This involves secondary injury associated with pathologic and inflammatory processes at the site of injury, and at the level of phrenic motoneurons. In the present study, we evaluated the antioxidant response in phrenic motoneurons involving the AMPK-Nrf2 signaling pathway following C2 spinal cord lateral hemi-section in rats.

Leptin-dependent neurotoxicity via induction of apoptosis in adult rat neurogenic cells.

Adipocyte-derived hormone leptin has been recently implicated in the control of neuronal plasticity. To explore whether modulation of adult neurogenesis may contribute to leptin control of neuronal plasticity, we used the neurosphere assay of neural stem cells derived from the adult rat subventricular zone (SVZ). Endogenous expression of specific leptin receptor (ObRb) transcripts, as revealed by RT-PCR, is associated with activation of both ERK and STAT-3 pathways via phosphorylation of the critical ERK/STAT-3 amino acid residues upon addition of leptin to neurospheres.

Axotomized bulbospinal neurons express c-Jun after cervical spinal cord injury.

In several central nervous system neuronal populations, axotomy triggers the upregulation of regeneration-associated genes such as c-Jun, which determines neurons ability to regenerate axon in a growth-permissive environment. We analyzed the expression of c-Jun in rat ventral medullary neurons after cervical hemisection in order to investigate their intrinsic regenerative potential. Maximal expression of c-Jun was observed 7 days after injury mainly in axotomized medullary neurons located in the gigantocellularis nucleus, the raphe nucleus and, although less intensively, in the rostral ventral respiratory group.