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Thread: Hains, et al. (2001): Subdural engraftment of serotonergic neurons following spinal hemisection restores spinal serotonin, downregulates serotonin transporter, and increases BDNF tissue content in rat

  1. #1

    Hains, et al. (2001): Subdural engraftment of serotonergic neurons following spinal hemisection restores spinal serotonin, downregulates serotonin transporter, and increases BDNF tissue content in rat

    • Hains BC, Fullwood SD, Eaton MJ and Hulsebosch CE (2001). Subdural engraftment of serotonergic neurons following spinal hemisection restores spinal serotonin, downregulates serotonin transporter, and increases BDNF tissue content in rat. Brain Res. 913 (1): 35-46. Summary: Spinal hemisection injury at T13 results in development of permanent mechanical allodynia and thermal hyperalgesia due to interruption and subsequent loss of descending inhibitory modulators such as serotonin (5-HT) and its transporter (5-HT(T)). We hypothesize that lumbar transplantation of non-mitotic cells that tonically secrete 5-HT and brain-derived neurotrophic factor (BDNF) will restore alterations in 5- HT and 5-HT(T) systems within the spinal dorsal horn. We used an immortalized rat neuronal cell line derived from E13 raphe (RN46A-B14) which is shown to secrete 5-HT and BDNF in vitro and in vivo. Three groups (n=35) of 30 day old male Sprague-Dawley rats were spinally hemisected at T13 and 28 days later received either lumbar RN46A-V1 control empty-vector (n=15) or RN46A-B14 (n=15) intrathecal grafts, or no transplant. Twenty-eight days following transplantation, animals were perfused and tissue examined for changes in 5-HT, 5-HT(T), and BDNF at the site of transplantation or at lumbar enlargements (L5). Immunohistochemistry revealed that RN46A-B14, but not RN46A-V1 cells, increased 5-HT tissue staining at L5 in the dorsal white matter as well as in superficial dorsal horn laminae I and II on both ipsilateral and contralateral sides, results confirmed by ELISA. Transplantation of RN46A-B14 cells significantly reduced ipsilateral 5-HT(T), upregulated after injury. Significantly increased levels of BDNF were also observed after RN46A-B14 transplantation but were not localized to particular spinal laminae. These results are consistent with recovery of locomotor function and reductions in chronic pain behaviors observed behaviorally after RN46A-B14 transplantation and supports the pragmatic application of cell-based therapies in correcting damaged circuitry after spinal cord injury. <http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=11532245> Department of Anatomy and Neurosciences, and Marine Biomedical Institute, University of Texas Medical Branch, 77555-1043, Galveston, TX, USA

    [This message was edited by Wise Young on September 23, 2001 at 10:25 PM.]

  2. #2
    Serotonin is an important neurotransmitter that has been shown to play a critical role in locomotion. Normally, virtually all the serotonin in the spinal cord come from descending axons from the brainstem. When the spinal cord is transected, all serotonin in the lower lumbosacral spinal cord goes away within 1-2 weeks. Serotonin is also known to stimulate locomotion in rats and cats that have transected spinal cords and when the serotonin is applied to the distal spinal cord isolated from the brain. Since serotonin may be a very important neurotransmitter, Claire Hulsebosch implanted serotonin secreting cells into the spinal cord below the injury site. They found that this improved the recovery of the rats. Wise.

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