Morphological and physiological survival of goldfish Mauthner axons isolated from their somata by spinal cord crush

Zottoli, Steven J.; Marek, Lynn E.; Agostini, Mark; Strittmatter, Sandra L.

doi:10.1002/cne.902550210

Cited by 38 publications

(29 citation statements)

References 61 publications

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“…Our biochemical data are consistent with previous morphological data (Zottoli et al, 1987) and our morphological data showing that distal segments of severed M-axons remain morphologically intact until about 77 days after severance in goldfish maintained at 15°C. Our biochemical results are also consistent with our morphological data and that of Zottoli et al ( 1987), which show that M-axons completely degenerate between 77 and 85 days after severance.…”

Section: Nfps In Severed M-axonssupporting

confidence: 94%

Long‐term survival followed by degradation of neurofilament proteins in severed Mauthner axons of goldfish

1994

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The morphology and protein composition of intact and severed Mauthner axons (M-axons) from goldfish were examined on electron micrographs, sodium dodecyl sulfate gels, and immunoblots. Neurofilaments were the most common cytoskeletal element on electron micrographs, and neurofilament proteins (NFPs) were the most intensely silver-stained bands in M-axoplasm microdissected from control M-axons. NFPs at about 235, 145, 123, 105, 80, and 60 kD in M-axoplasm were identified with four monoclonal and three polyclonal antibodies. Similar immunoblots of samples of the M-axon myelin sheath (M-sheath) showed no reactivity to antibodies against NFPs. For up to 62 days following spinal cord severance in goldfish maintained at 15 degrees C, the ultrastructure, protein banding pattern, and anti-NFP immunoreactivity of several distal segments of M-axons did not change compared with control M-axons. At 62 to 81 days after severance, novel bands appeared in many silver-stained gels and anti-NFP immunoblots of distal M-axons. NFP bands completely disappeared from distal M-axon segments of some M-axons as early as 72 days after severance. However, NFP bands persisted in some distal segments for up to 81 days after severance. The degradation of NFPs occurred equally along the entire length of a distal M-axon segment, that is, there was no indication of a proximal-to-distal or distal-to-proximal sequence of NFP degradation in distal segments of severed M-axons. These biochemical data were consistent with morphological data that showed little change in the diameter or ultrastructure of severed M-axons held at 15 degrees C for about 2 months followed by a rapid collapse of the entire distal segment at 72 to 85 days postseverance.

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Section: Nfps In Severed M-axonssupporting

confidence: 94%

Long‐term survival followed by degradation of neurofilament proteins in severed Mauthner axons of goldfish

1994

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“…In fact, LTS of anucleate axons has also been reported in a number of vertebrates, such as goldfish (Zottoli et al, 1986;Blundon et al, 1990), garfish (Cancalon, 1983), frog (Matsumoto and Scalia, 1981), and a mutant strain of mice (Lunn et al, 1989).…”

mentioning

confidence: 87%

Maintenance and degradation of proteins in intact and severed axons: implications for the mechanisms of long-term survival of anucleate crayfish axons

1995

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Protein maintenance and degradation are examined in the severed distal (anucleate) portions of crayfish medial giant axons (MGAs), which remain viable for over 7 months following axotomy. On polyacrylamide gels, the silver-stained protein banding pattern of anucleate MGAs severed from their cell bodies for up to 4 months remains remarkably similar to that of intact MGAs. At 7 months postseverance, some (but not all) proteins are decreased in anucleate MGAs compared to intact MGAs. To determine the half-life of axonally transported proteins, we radiolabeled MGA cell bodies and monitored the degradation of newly synthesized transported proteins. Assuming exponential decay, proteins in the fast component of axonal transport have an average half-life of 14 d in anucleate MGAs and proteins in the slow component have an average half-life of 17 d. Such half-lives are very unlikely to account for the ability of anucleate MGAs to survive for over 7 months after axotomy.

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“…The effectiveness of an SML crush on damaging descending axons is supported by studies in which the Mauthner axon was filled with Lucifer yellow either rostral or caudal to the wound site 30-62·days postoperatively. In all cases, the axon had separated and retracted from the crush site and no longer extended across the wound (Zottoli et al, 1987(Zottoli et al, , 1988.…”

Section: Completeness Of a Crush Woundmentioning

confidence: 99%

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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Morphological and physiological survival of goldfish Mauthner axons isolated from their somata by spinal cord crush

Cited by 38 publications

References 61 publications

Long‐term survival followed by degradation of neurofilament proteins in severed Mauthner axons of goldfish

Long‐term survival followed by degradation of neurofilament proteins in severed Mauthner axons of goldfish

Maintenance and degradation of proteins in intact and severed axons: implications for the mechanisms of long-term survival of anucleate crayfish axons

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

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