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Neural Reconnection in the Transected Spinal Cord of the Freshwater Turtle Trachemys Dorbignyi

Overview
Journal J Comp Neurol
Specialty Neurology
Date 2009 May 7
PMID 19418545
Citations 19
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Abstract

This paper provides the first evidence that freshwater turtles are able to reconnect their completely transected spinal cords, leading to some degree of recovery of the motor functions lost after injury. Videographic analysis showed that some turtles (5 of 11) surviving more than 20 days after injury were able to initiate stepping locomotion. However, the stepping movements were slower than those of normal animals, and swimming patterns were not restored. Even though just 45% of the injured turtles recovered their stepping patterns, all showed axonal sprouting beyond the lesion site. Immunocytochemical and electron microscope images revealed the occurrence of regrowing axons crossing the severed region. A major contingent of the axons reconnecting the cord originated from sensory neurons lying in dorsal ganglia adjacent to the lesion site. The axons bridging the damaged region traveled on a cellular scaffold consisting of brain lipid-binding protein (BLBP)- and glial fibrillary acidic protein (GFAP)-positive cells and processes. Serotonergic varicose nerve fibers and endings were found at early stages of the healing process at the epicenter of the lesion. Interestingly, the glial scar commonly found in the damaged central nervous system of mammals was absent. In contrast, GFAP- and BLBP-positive processes were found running parallel to the main axis of the cord accompanying the crossing axons.

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References
1.
Guest J, Hiester E, Bunge R . Demyelination and Schwann cell responses adjacent to injury epicenter cavities following chronic human spinal cord injury. Exp Neurol. 2005; 192(2):384-93. DOI: 10.1016/j.expneurol.2004.11.033. View

2.
Flores C, Ene S, Pereda A . An immunochemical marker for goldfish Mauthner cells. J Neurosci Methods. 2008; 175(1):64-9. PMC: 2582833. DOI: 10.1016/j.jneumeth.2008.08.009. View

3.
Russo R, Hounsgaard J . Burst-generating neurones in the dorsal horn in an in vitro preparation of the turtle spinal cord. J Physiol. 1996; 493 ( Pt 1):55-66. PMC: 1158950. DOI: 10.1113/jphysiol.1996.sp021364. View

4.
Talos D, Fishman R, Park H, Folkerth R, Follett P, Volpe J . Developmental regulation of alpha-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid receptor subunit expression in forebrain and relationship to regional susceptibility to hypoxic/ischemic injury. I. Rodent cerebral white matter and cortex. J Comp Neurol. 2006; 497(1):42-60. PMC: 4313670. DOI: 10.1002/cne.20972. View

5.
Feng L, Hatten M, Heintz N . Brain lipid-binding protein (BLBP): a novel signaling system in the developing mammalian CNS. Neuron. 1994; 12(4):895-908. DOI: 10.1016/0896-6273(94)90341-7. View