Chapter 18 Spinal cord regeneration in adult goldfish: implications for functional recovery in vertebrates

Zottoli, Steven J.; Bentley, Adrienne P.; Feiner, Deborah G.; Hering, John R.; Prendergast, Brian J.; Rieff, Heather I.

doi:10.1016/s0079-6123(08)61138-3

Cited by 35 publications

(36 citation statements)

References 24 publications

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“…44.4%). Specifically, the mortality was 32.2% in one study (N=31; 5·months postoperatively; Zottoli et al, 1994) and 36.7% in the other (N=49; 6·months postoperatively; S. J. Zottoli and J. E. Nierman, unpublished observations). Tuge and Hanzawa (1935) reported a somewhat higher mortality (65.6%) of those fish that had spinal cord transections at the high cervical level and survived for approximately 2·months (Tuge and Hanzawa, 1937).…”

Section: Recovery Of Behavior Was Due To Morphological Regenerationmentioning

confidence: 86%

“…after spinal cord injury (Zottoli and Freemer, 1991;Zottoli et al, 1994;Zottoli and Faber, 2000). The present study provides a quantitative approach to analyze these C-start differences and also provides qualitative descriptions of the recovery of equilibrium and targeted feeding.…”

mentioning

confidence: 85%

“…The age of the fish, subtle differences in the crush wound or the wound level may limit the return of behavior. In addition, regenerating central nervous system (CNS) neurons are known to make inappropriate pathway choices into the peripheral nervous system just caudal to an SML crush (Bentley and Zottoli, 1993;Zottoli et al, 1994). This inappropriate pathway choice may limit, delay or prevent the return of behavior caudal to the wound.…”

Section: Recovery Of Behavior Was Due To Morphological Regenerationmentioning

confidence: 99%

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Recovery of C-starts, equilibrium and targeted feeding after whole spinal cord crush in the adult goldfishCarassius auratus

Zottoli

Freemer

2003

Journal of Experimental Biology

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SUMMARYCentral nervous system neurons of many adult teleost fish are capable of regrowth across spinal cord lesions, which may result in behavioral recovery of swimming. Since there have been few, if any, studies that examine the return of behaviors other than swimming, we provide a quantitative analysis of the recovery of C-starts that occur in adult goldfish after spinal cord injury. In addition, we include a qualitative analysis of the return of targeted feeding and equilibrium. Whole spinal cord crushes near the junction of the brain and spinal cord [spinomedullary level (SML)] were made in 45 experimental fish. Eight sham-operated goldfish served as controls for the effects of the surgery procedures alone. After spinal cord crush and recovery from the anesthetic, experimental fish lay on their sides with no movement caudal to the wound. The fish were monitored for the return of behaviors for up to 190 days postoperatively. Twenty-five fish survived the course of this study. Of these fish, 12 regained equilibrium and C-starts, two regained equilibrium but not C-starts, and 11 did not regain equilibrium (one of these did display a C-start). Twenty-two of the 25 experimental fish that survived the 190 days were able to target food from the water surface. Quantitative analysis of recovered C-starts in this study revealed that the probability of eliciting the response is reduced, that latencies from stimulus to response are longer and that movement parameters (i.e. angles, distance and velocity)are reduced compared with those of sham-operated control animals for up to 190 days postoperatively. The recovery of C-starts, equilibrium and targeted feeding was due to re-growth across the wound site, since re-crushing the spinal cord at the SML resulted in the loss of these behaviors. Mauthner cells are known to initiate C-starts in goldfish. Since the majority of M-axons that regrow across a crush wound associate with an inappropriate pathway (i.e. the first ventral root), it is unlikely that these cells play a major role in the return of C-starts. We propose that regeneration of Mauthner cell homologues across the wound site is responsible for the recovery of most C-starts. The identifiability of the M-cell and its homologues provides a unique opportunity to analyze the mechanisms underlying behavioral recovery at the cellular level.

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Section: Recovery Of Behavior Was Due To Morphological Regenerationmentioning

confidence: 86%

mentioning

confidence: 85%

Section: Recovery Of Behavior Was Due To Morphological Regenerationmentioning

confidence: 99%

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Recovery of C-starts, equilibrium and targeted feeding after whole spinal cord crush in the adult goldfishCarassius auratus

Zottoli

Freemer

2003

Journal of Experimental Biology

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“…In contrast to the lack of spinal cord regeneration evident in mammals, some anamniote animals, such as fish and some amphibians, regenerate damaged nerves and recover locomotor ability in a remarkably short period following SCI (Simpson, 1968;Bernstein and Gelderd, 1970;Zottoli et al, 1994;Becker et al, 1997). This difference in regenerative capacity occurs even though similar cell types are present in the spinal cords of species both capable and incapable of regeneration (Naujoks-Manteuffel and Roth, 1989;Bastmeyer et al, 1993).…”

Section: Introductionmentioning

confidence: 99%

Fgf-Dependent Glial Cell Bridges Facilitate Spinal Cord Regeneration in Zebrafish

et al. 2012

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Adult zebrafish show a remarkable capacity to regenerate their spinal column after injury, an ability that stands in stark contrast to the limited repair that occurs within the mammalian CNS post-injury. The reasons for this interspecies difference in regenerative capacity remain unclear. Here we demonstrate a novel role for Fgf signaling during glial cell morphogenesis in promoting axonal regeneration after spinal cord injury. Zebrafish glia are induced by Fgf signaling, to form an elongated bipolar morphology that forms a bridge between the two sides of the resected spinal cord, over which regenerating axons actively migrate. Loss of Fgf function inhibits formation of this "glial bridge" and prevents axon regeneration. Despite the poor potential for mammalian axonal regeneration, primate astrocytes activated by Fgf signaling adopt a similar morphology to that induced in zebrafish glia. This suggests that differential Fgf regulation, rather than intrinsic cell differences, underlie the distinct responses of mammalian and zebrafish glia to injury.

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“…Apart from tailed amphibians and fish, which retain remarkable regenerative capabilities throughout life (Zottoli et al, 1994;Clarke and Ferretti, 1998;Ferretti et al, 2003), adult vertebrates are incapable of functional repair of the spinal cord after injury. During development, however, the spinal cord of chicks and opossums is able to regenerate (Shimizu et al, 1990;Hasan et al, 1991;Nicholls and Saunders, 1996).…”

Section: Introductionmentioning

confidence: 99%

Nogo and Nogo‐66 receptor in human and chick: Implications for development and regeneration

O’Neill¹,

Whalley²,

Ferretti³

2004

Developmental Dynamics

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Antibodies to the myelin protein Nogo increase axonal regrowth after central nervous system injury. We have investigated whether Nogo expression contributes to loss of regenerative potential during development by using chick embryos, which regenerate their spinal cord until embryonic day (E) 13, when myelination begins. We show that Nogo-A and the Nogo receptor (NgR) are developmentally regulated both in chick and human embryos, are first detected at developmental stages when the chick spinal cord regenerates, and are not down-regulated after injury at permissive stages for regeneration. Therefore, expression of Nogo-A and NgR in pre-E13 chick spinal cords is not sufficient to inhibit regeneration. Nogo-A expression in the chick early embryo is primarily observed in axons, whereas NgR is mainly located on neuronal cell bodies, both in spinal cord and eye, and in striated muscle including the heart. With the onset of myelination, there is down-regulation of Nogo-A expression in neurons. Therefore, loss of regenerative potential might be linked to changes in its cellular localization. The possibility that only Nogo expressed in mature oligodendrocytes can exercise inhibitory effects would reconcile the lack of inhibition we observe in developing chick spinal cords before the onset of myelination with evidence from other laboratories on the inhibitory effects of Nogo in mature central nervous system. The distinctive and complementary patterns of Nogo-A and NgR expression and their conservation throughout evolution support the view that Nogo signaling represents a key pathway in nervous system and striated muscle development. Its putative role in target innervation and establishment of neural circuitry is discussed.

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Chapter 18 Spinal cord regeneration in adult goldfish: implications for functional recovery in vertebrates

Cited by 35 publications

References 24 publications

Recovery of C-starts, equilibrium and targeted feeding after whole spinal cord crush in the adult goldfishCarassius auratus

Recovery of C-starts, equilibrium and targeted feeding after whole spinal cord crush in the adult goldfishCarassius auratus

Fgf-Dependent Glial Cell Bridges Facilitate Spinal Cord Regeneration in Zebrafish

Nogo and Nogo‐66 receptor in human and chick: Implications for development and regeneration

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