Abstract

Spinal cord injury alters a number of endogenous biological signals known to be involved in the modulation of neurotrophic and neuroprotective events. Nerve growth factor (NGF) is a neurotrophic factor expressed in neuronal and non-neuronal tissues including spinal cord, and increases after spinal cord injury. Recent findings revealed that leptin, an adipocyte-derived cytokine (adipokine), enhance neuronal survival and exert neuroprotective action, and played an important role in nociceptive behavior induced by nerve injury. Whether NGF affects the expression of leptin in injured spinal cord has not been investigated. The present study was designed to evaluate: (i) whether intranasal NGF administration reached the spinal cord of the rat, (ii) if NGF affects the expression of leptin in the spinal cord and adipose tissue, and (iii) whether intranasal NGF affects the behavioral and spinal cord neuronal deficits induced by spinal cord injury. The result showed that intranasal NGF enhances the expression of (i) NGF and NGF-receptors (TrkA and p75NTR) in injured spinal cord exerting behavioral and neuroprotective action, and (ii) leptin in injured spinal cord and in subcutaneous (white) and interscapular (brown) adipose tissue. Altogether, the present data demonstrate the efficacy of intranasal administration of NGF, and suggest a link between the neurotrophin NGF and the adipokine leptin that may be therapeutically explored in injured spinal cord. Adipobiology 2012; 4: 67-75.

Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.