As a neurochemical mediator of stress resilience, NPY has been shown to oppose excitatory effects of the pro-stress neuropeptide corticotropin-releasing factor (CRF). Previous studies have described the anatomical organization of NPY and CRF in the central nucleus of the amygdala, which sends CRF projections to the locus coeruleus (LC), activating LC norepinephrine release. However, the cellular substrates for interactions between NPY and CRF in the LC remain unknown.
View Article and Find Full Text PDFTherapeutic interventions after spinal cord injury (SCI) routinely are designed to address multiple aspects of the primary and/or secondary damage that occurs. Exercise has a demonstrated efficacy for post-SCI complications such as cardiovascular dysfunction, neuropathic pain, and chronic inflammation, yet there is little understanding of the mechanisms by which improvements might result from this non-invasive approach. Here we review several of our observations of molecular and cellular changes within the injured spinal cord following acute or delayed exercise regimens that illustrate the potential for positive effects on neuroprotection and rehabilitation.
View Article and Find Full Text PDFInsufficient regeneration of central nervous system (CNS) axons contributes to persisting neurological dysfunction after spinal cord injury (SCI). Peripheral nerve grafts (PNGs) support regeneration by thousands of injured intraspinal axons and help them bypass some of the extracellular barriers that form after SCI. However this number represents but a small portion of the total number of axons that are injured.
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