Neural reconnection in the transected spinal cord of the freshwater turtle Trachemys dorbignyi

Abstract

This paper provides the first evidence that fresh water turtles are able to reconnect their completely transected spinal cord leading to some degree of recovery of the motor functions lost after injury. Videographic analysis showed that some turtles (5 out 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 BLBP and 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.

‘Evorego’: Studying Regeneration to Understand Evolution, the Case of the Serotonergic System

“…Profuse sprouting and branching of numerous serotonergic axons has been also observed at the site of spinal cord injury in the freshwater turtle Trachemys dorbignyi [Rehermann et al, 2009]. Interestingly, the recent study from Silver's group has shown that aft er a thermocoagulatory lesion in the rat frontoparietal cortex, serotonergic axons persist within the lesion edge and, by the third week post-injury, sprout robustly into the lesion cavity, whereas callosal axons become dystrophic and die back [Hawthorne et al, 2011].…”

Transforming Growth Factor α Transforms Astrocytes to a Growth-Supportive Phenotype after Spinal Cord Injury

“…During development, astrocyte precursors support growing axons (Rakic, 1971; McDermott et al, 2005) and after SCI in lower vertebrates and very young mammals, astrocyte progenitors migrate from the ependymal zone to form a scaffold for regeneration (Chernoff et al, 2003; Fry et al, 2003; Rehermann et al, 2009). However, after SCI in adult mammals, astrocytes vacate the lesion core (Fitch et al, 1999) and form a cellular and molecular border at the lesion edge that is inhibitory to axon growth (Reier et al, 1983; Liuzzi and Lasek, 1987; Rudge and Silver, 1990).…”

Non-mammalian model systems for studying neuro-immune interactions after spinal cord injury

“…As in the other regenerative non-mammalian species discussed above, after SCI, glial cell processes grew parallel to the long axis of the spinal cord. At the same time, phagocytic macrophages were observed at the lesion (Rehermann et al, 2009). Studies are just beginning to explore cellular aspects of neurogenesis and molecular programs influencing regeneration in this organism (Garcia et al, 2012; Rehermann et al, 2011).…”

“…A few recent studies have also demonstrated axon regeneration after complete spinal cord transection in the turtle (Garcia et al, 2012; Rehermann et al, 2009; Rehermann et al, 2011). After injury, axon regeneration, primarily of propriospinal and sensory neurons, is followed by partial restoration of locomotion in ~50% of spinalized turtles (Rehermann et al, 2009; Rehermann et al, 2011).…”

“…After injury, axon regeneration, primarily of propriospinal and sensory neurons, is followed by partial restoration of locomotion in ~50% of spinalized turtles (Rehermann et al, 2009; Rehermann et al, 2011). In this model, histological assays demonstrated that a blood clot filled with red and white blood cells formed immediately after SCI.…”