An electron microscopic study of denervated motor endplates after zinc iodide-osmium impregnation

Nickel, E.; Waser, Peter G.

doi:10.1016/0006-8993(69)90151-6

Cited by 24 publications

(9 citation statements)

References 5 publications

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“…The earliest ultrastructural signs of degeneration of terminals on cutting axons is a disintegration and lysis of vesicular material (Nickel & Waser, 1969;Manolov, 1974) but as a loss of vesicles during continual stimulation of normal terminals is not accompanied by changes in p but only in n , it is unlikely that p declines at degenerating terminals simply because of a decline in vesicle numbers. Changes in the properties of the nerve terminal membrane, more subtle than those observed with ultrastructural techniques, may be involved.…”

Section: Discussionmentioning

confidence: 99%

The formation and regression of synapses during the re‐innervation of axolotl striated muscles.

Bennett¹,

Raftos²

1977

The Journal of Physiology

102

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SUMMARY1. A study has been made of the formation and regression of synapses formed by spinal nerves 16 and 17 in axolotl hind-limb flexor muscles following the severing of nerve 16, using histological, ultrastructural and electrophysiological techniques.2. Axolotl hind-limb flexor myofibres possessed 'en plaque' end-plates from either spinal nerve 16 or 17 or both at intervals of about 1000 um along their length; the myofibre's length constant was about 700 ,m allowing electrophysiological observations of at least two of these synapses during a single impalement; transmitter release at these synapses could be described by binomial statistics and in a given set of ionic conditions the binomial statistic parameter n was directly proportional to the size of the nerve terminals whilst the binomial statistic parameter p was invariant to changes in nerve terminal size.3. The distribution of synapses formed by spinal nerves 16 and 17 in different sectors of the axolotl hind-limb flexor muscles was determined from a study of evoked end-plate potentials; the middle and proximal sectors of the flexor muscles contained myofibres which received an innervation from nerve 16 only, whereas the sectors surrounding these contained myofibres innervated either by nerve 16 or nerve 17 or by both nerves.4. Six days following the severing of spinal nerve 16, evoked transmitter release from the synapses formed by this nerve had failed; transmission was subsequently recorded at a few synapses formed by nerve 17 in the middle and proximal sectors of the flexor muscles which are not normally innervated by this nerve and these synapses had a low n; during the succeeding four weeks the value of n at the synapses increased to a size about 70 % that of the terminals normally formed by nerve 16 at these sites.II-2 M. R. BENNETT AND JULIA RAFTOS 5. Four weeks after severing nerve 16, myofibres which possessed synapses formed by nerve 17 also possessed synapses from re-innervating nerve 16 and these were sometimes formed at the same synaptic sites as those occupied by nerve 17.6. In the subsequent sixteen weeks, the n value of synapses formed by nerve 17 declined whilst the n values of synapses formed by reinnervating nerve 16 on the same myofibres matured to their control size.7. It is suggested that on severing nerve 16 collateral sprouting of nearby intact nerve 17 occurs and these collateral sprouts innervate the denervated synaptic sites, although the sprouts are not as well matched to the denervated synaptic sites as are the original nerve terminals; thus if nerve 16 returns it preferentially forms synapses at its original synaptic sites, and the collateral synapses formed by nerve 17 regress.

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Section: Discussionmentioning

confidence: 99%

The formation and regression of synapses during the re‐innervation of axolotl striated muscles.

Bennett¹,

Raftos²

1977

The Journal of Physiology

102

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“…It is also very interesting that the appositional postsynaptic membrane never showed positive reaction even when the presynaptic membrane stained black in the intermediate stage of degeneration. In the present study, we never encountered the disappearance of dark-stained axons and terminals as mentioned in degenerated endplates by Nickel and Waser (10). The increase of reactivity with ZIO in mitochondria, synaptic vesicles, synaptic membrane and matrices of degenerating terminals could be assumed to be due to the consequence of unknown biochemical alteration occurring in the degenerating terminals.…”

Section: Discussionmentioning

confidence: 62%

Zio Staining for Degenerating Terminals of Rat Spinal Cords After Transection

Ibata

Matsuura

Nojyo

et al. 1973

Acta Histochem. Cytochem

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Zinc iodide-osmium tetroxide(ZIO) staining still having an unresolved problem in its reactive mechanism as silver impregnation has been applied for the morphological investigation of synaptic endings (1, 3-9, 11, 12). Synaptic vesicles appear very electron dense with this staining. Degenerating terminals proved to be more strongly reactive to this staining than normal terminals. There have been few attempts to scrutinize degenerating terminals of mammalian central nervous system by means of this staining. The aim of the present study, therefore, is to detect the structure of degenerating terminals and to distinguish the degenerating stages using this staining method. MATERIALS AND METHODSFifteen albino rats were used in this study; 12 as experimental materials, 3 as control.Total-or hemisection was performed on the animals in this experiment at the upper thoracic segment under nembutal anaesthesia. After survival periods from 1 to 7 days, they were perfused with 4% paraformaldehyde adjusted at pH 7.4 with 0.05 M phosphate through the left ventricle. After perfusion, some parts of the spinal cord beneath the operated portion just adjacent to the portion of operation to the lumbar enlargement were removed and divided into two batches, one for ordinary electron microscopy and the other for ZIO reaction.The portion just adjacent to the operated segment in the rats surviving 7 days should show severest degenerating axons and terminals, while we should encounter axons and terminals with lightest damage in the lumbar enlargement of animals surviving for one day.

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“…The procedure used ensured that no reanastomosis of any sectioned root took place postoperatively, and that the rhabdosphincter was thereby completely and permanently deprived of this innervation. It is well known that complete somatomotor denervation of a striated muscle leads within 1-3 days to complete and irreversible degeneration of cholinergic axons innervating its motor end-plates, although their sarcoplasmic sole plates persist, often with eventual reduction of the depth and/or complexity of junctional folds [Birks et al, 1960;Slater, 1968, 1970;Nickel and Waser, 1969;Lullmann-Rauch, 19711. Loss of somatomotor innervation of the rhabdosphincter following sacral rhizotomy was confirmed by the herein observed rapid degeneration and elimination within 2 weeks postoperatively of almost all myelinated axons in its nerve bundles, and of all cholinergic axon terminals innervating its motor end-plates, with persistently nerveless sarcoplasmic sole plates.…”

Section: Discussionmentioning

confidence: 99%

Intrinsic neuromuscular defects in the neurogenic bladder: IV. Loss of somatomotor and preservation of autonomic innervation of the male feline rhabdosphincter following bilateral sacral ventral rhizotomy

Atta

Elbadawi

1985

Neurourology and Urodynamics

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Innervation of the male feline rhabdosphincter was studied ultrastructurally 1 and 2 weeks following bilateral sacral ventral rhizotomy. In all samples, there was virtual loss of myelinated axons, degeneration and loss of the axonal element of all motor end-plates, and preservation of autonomic nonrnyelinated (cholinergic, adrenergic, and probable copcptidergic) axons, as well as their nonspecialized surface contacts with myofibers of the rhabdosphincter. These observations provide solid evidence for the existence of both somatomotor and autonomic cholinergic innervation of the male feline rhabdosphincter and indicate that its potential neural control shortly after somatic denervation is exercised exclusively by autonomic axonlmyofiber surface contacts.

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An electron microscopic study of denervated motor endplates after zinc iodide-osmium impregnation

Cited by 24 publications

References 5 publications

The formation and regression of synapses during the re‐innervation of axolotl striated muscles.

The formation and regression of synapses during the re‐innervation of axolotl striated muscles.

Zio Staining for Degenerating Terminals of Rat Spinal Cords After Transection

Intrinsic neuromuscular defects in the neurogenic bladder: IV. Loss of somatomotor and preservation of autonomic innervation of the male feline rhabdosphincter following bilateral sacral ventral rhizotomy

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