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W G Hopkins

Publications and source records attributed to W G Hopkins.

88 records · Page 5Linked to original sources
PubMed1982

Short- and long-term effects of paralysis on the motor innervation of two different neonatal mouse muscles.

1. A study was made of short- and long-term effects of paralysis induced by type A botulinum toxin on the development of innervation of mouse muscles. The toxin was injected locally over the tensor fasciae latae (t.f.l.) and gluteus muscles at various times after birth, and the innervation was later examined by intracellular recording and by a histological technique using a reduced silver stain for axons.2. Paralysis induced at 0-4 days of age delayed but did not prevent the eventual elimination of nearly all focal multiple innervation in gluteus muscle fibres, whereas in t.f.l. up to 50% of the fibres remained focally innervated by more than one axon for at least 120 days. There was an associated reduction in the number of muscle fibres in t.f.l. of between 50 and 70%. The biggest reduction in the number of gluteus fibres was under 40%.3. In the t.f.l., paralysis begun at 6-9 days caused the extent of single-site polyneuronal innervation to increase above the level existing at the time of paralysis. Histologically this increase was seen to be due at least in part to the stimulation of nodal sprout growth from a limited number of nodes.4. Motor nerve terminal sprouts were evoked by paralysis at all ages. In mice injected before 4 days of age recovery from the toxin occurred rapidly and without the formation of ectopic synapses by sprouted motor terminals; however, intrafusal motor nerves also sprouted and established a permanent ectopic innervation on surrounding extrafusal muscle fibres.5. The following conclusions are drawn. (a) In some but not all muscles, neonatally induced paralysis can not only temporarily halt elimination of polyneuronal innervation but actually lead to an increase; it is suggested tentatively that this occurs only during the neonatal period because of the availability at that time of endoneurial pathways associated with normal polyneuronal innervation, rather than because of any special neuronal growth potential then. (b) Permanent establishment of focal polyneuronal innervation is due not to stability of presynaptic elements maintained past a critical developmental stage but is associated with substantial losses of muscle fibres, leading to a high ratio of nerve fibres to muscle fibres.

Aging↗
PubMed1981

Nerve growth from nodes of Ranvier in inactive muscle.

Paralysis of mouse gluteus maximus muscles with botulinum toxin not only evoked the expected sprouting from nerve terminals but also induced growth from some nodes of Ranvier close to the endplate region. This finding shows that nerve degeneration is not essential for nodal sprouting and supports the hypothesis that inactive muscle liberates a motor nerve growth factor.

Animals↗
PubMed1981

An assessment of the spread of the signal for terminal sprouting within and between muscles.

Certain muscles of the mouse and rat have been studied in order to assess how far a signal from denervated muscle can spread to elicit terminal sprouting from intact endplates. Denervation of the muscles surrounding the rat foot 4th lumbrical muscle caused no terminal sprouting in the 4th lumbrical itself. In the hemidenervated mouse gluteus maximus terminal sprouting was restricted to the central region of the muscle where innervated and denervated fibres intermingle. There was no enhancement of such sprouting if the underlying and closely apposed gluteus medius was simultaneously denervated. Hemidenervation of the mouse diaphragm and interscutularis, where intact endplates lie near to denervated muscle fibres, produced no terminal sprouting. Hemidenervation of the mouse platysma, where intact endplates often lie adjacent to denervated muscle fibres, similarly produced no significant response. However, all muscles were capable of producing extensive terminal sprouting in response to paralysis induced by botulinum toxin. The stimulus for terminal sprouting produced by an inactive muscle fibre must therefore be effective only on the fibre's own terminal or immediately adjacent terminals.

Animals↗
PubMed1981

The sequential development of nodal sprouts in mouse muscles in response to nerve degeneration.

Nodal sprouting in response to axonal degeneration was studied in silver-stained, wholemount preparations of the thin, sheet-like mouse muscles tensor faciae latae (TFL) and the inferior and superior gluteus maximus. Axon degeneration in TFL and gluteus was produced by cutting the L14 spinal nerve (partial denervation). Axon degeneration in the gluteus was also produced by superior gluteal and TFL nerve section (hemidenervation). Two days after partial or hemidenervation motor nerve nodal sprouts begin to appear in the intramuscular nerves. Sprout growth is rapid, since only a small percentage of sprouts are ever seen not to terminate at endplates. Sprouts continue to appear for at least three weeks after partial denervation, when there are up to five times as many endplates innervated by sprouts as by remaining intact axons. Sprouts arise at nodes near the denervated endplates, which they innervate by growing directly down the degenerating nerve. Sprout initiation proceeds sequentially in partly and hemidenervated muscles, since the average length of sprouts contacting endplates increases with time. Analysis of silver-stained muscles by combined light and electron microscopy shows that this sequential development is unlikely to be a consequence of slow growth and maturation of submicroscopic sprouts initiated nonsequentially throughout the intramuscular nerves. The observations are consistent with a nodal sprouting mechanism which requires a cellular or structural change in the denervated Schwann cell pathway to spread disto-proximally from the terminal ends of the nerves and thereby to permit the growth of nodal sprouts. The initiation of sprout growth may require a diffusible substance from degenerating nerve or denervated muscle.

Animals↗
PubMed1981

Restoration of focal multiple innervation in rat muscles by transmission block during a critical stage of development.

1. The soleus, extensor digitorum longus and peroneus tertius muscles of the hind leg were paralysed by botulinum toxin injection in neonatal rats varying in age from 8 to 31 days. The soleus muscle was similarly paralysed in adult rats.2. Muscles were excised after different periods of block, neuromuscular transmission was assessed in vitro, and the nerve terminal size and amount of terminal sprouting and multiple innervation determined histologically using silver (Ag) and zinc iodide-osmium (ZIO) tetroxide stains.3. Recovery from the block induced by botulinum toxin was more rapid in immature multiply-innervated muscles than in muscles of older rats in which all multiple innervation had been eliminated.4. Terminals in muscles blocked during the first month after birth grew rapidly in size and developed a characteristic granulose morphology in the first few days following the block. This change did not occur in fully adult rat solei.5. Sprouts growing from the terminals were infrequent in muscles paralysed before day 16. Terminal sprouts were more frequent in muscles paralysed between 16 and 31 days of age, but were very infrequent in adult solei.6. In confirmation of Thompson, Kuffler & Jansen (1979) paralysis begun at 10 days was followed initially by a continued fall in multiple innervation detected electrophysiologically. After 2 days the percentage of muscle fibres with more than one input rose. The extra inputs did not come from terminal sprouts. They innervated the single synaptic site on each muscle fibre as they do during normal synaptogenesis.7. The amount of multiple innervation regained 5-10 days after the start of paralysis became progressively less the later paralysis started and was approximately equal to the level existing at the time the block was begun. Thus paralysis starting on or after day 16 (when all excess inputs have normally withdrawn) caused no return of multiple innervation.8. The return of multiple inputs and the swelling of the nerve terminals are presumably responses of the motoneurone to growth stimuli from inactive muscle. It is not clear whether the return of multiple innervation in the 10-15 day old rats is due to reactivation of inputs still in close contact with the end-plate before withdrawal or to regrowth of partly retracted nerve branches.9. A parallel is drawn between the limited period when inactivity can reinstate multiple innervation, and the critical period in the developing visual cortex.

Aging↗
PubMed1981

Role of degenerating axon pathways in regeneration of mouse soleus motor axons.

1. The recovery of tension in mouse soleus was assayed 1-5 days after crushing the extramuscular nerve in muscles which had been previously either denervated by nerve crush, partly denervated by spinal nerve root section, or paralysed by I.M. injection of botulinum toxin. Recovery of tension following nerve crush in contralateral control muscles from the same mice was also measured. The muscles were then stained with zinc iodide-osmium and examined in the light microscope. 2. Recovery in control muscles began at about 50 hr after crush and was nearly complete by 5 days. Recovery began at about 50 hr after crush and was nearly complete by 5 days. Recovery began about 10 hr earlier and was more rapid in muscles denervated by crushing the muscle nerve 4 days before recrushing at the same site. 3. Paralysis 12 days earlier by intramuscular injection of botulinum toxin did not enhance recovery after nerve crush. The axons remained following partial denervation 6 days before nerve crush also regenerated at a rate similar to controls. 4. It is concluded that (1) nerves regenerate more quickly down a pre-degenerated pathway, (2) chromatolysis does not significantly enhance reinnervation, and (3) each motor axon regenerating after a crush is constrained to follow its own denervated pathway back into the muscle. 5. Histology was consistent with these conclusions, and also showed that end-plates in control muscles reinnervated after short periods of denervation were normal in appearance and possessed little "escaped' nerve growth. This was in contrast to end-plates which had been regenerated in muscle after a preceding nerve crush, botulinum toxin paralysis or partial denervation. This suggests that growth from nerve terminals is controlled locally within a muscle.

Animals↗
PubMed1979

Nerve sheaths and motoneurone collateral sprouting.

When disease or injury causes partial loss of innervation from a muscle, the remaining axons sprout and form new connections to the denervated muscle fibres. Sprouting can occur in two ways: from axon terminals (terminal sprouting) or from the intramuscular axons themselves, probably from the nodes of Ranvier (collateral sprouting). Terminal sprouting has been induced experimentally using various methods, including partial denervation, nerve conduction block and nerve transmission block. A common factor in the induction of terminal sprouting seems to be changes in the surface membrane of muscle fibres; these changes and terminal sprouting are prevented by direct stimulation of the muscle. Collateral sprouting has been induced only by partial denervation and is not prevented by direct stimulation. This has been taken as evidence for an earlier suggestion that products of nerve or axon degeneration may be a direct stimulus for collateral sprouting. We report here that axon degeneration products alone are probably not the stimulus for collateral sprouting.

Acetylcholinesterase↗
PubMed1979

Vertical plane serial sectioning of identified tissue culture cells.

Identifying marks can be made around specific cells on the culture surface of plastic tissue culture dishes. When the cultures are embedded in situ and the plastic dish is split away, the marks are reproduced around the cells. The marks permit trimming and complete serial sectioning of specific cells in the vertical plane.

Cells, Cultured↗
PubMed1969

Avena coleoptile elongation: stimulation by fluorophenylalanine.

A 100 to 150% stimulation of Avena coleoptile segment elongation by the amino acid analogue p-fluorophenylalanine (FPA) has been observed. The effect is reversed by phenylalanine and is not seen with comparable concentrations of sodium fluoride. FPA does not alter elongation of red-irradiated segments. Stimulation by FPA occurs only when the apex is intact and the segments are incubated in the absence of exogenous auxin. In the presence of FPA, (14)C-leucine uptake by coleoptile segments is reduced by 34% and protein synthesis by 42%. When pre-incubated on labeled media and subsequently transferred to unlabeled media, segments fail to incorporate into the protein fraction any of the previously absorbed label. It is therefore difficult to ascertain whether FPA results in a genuine inhibition of protein synthesis in apical coleoptile segments. Possible mechanisms for the action of FPA and its relationship to light dependent elongation are considered.

Journal Article↗
PubMed1966

Relationships between phytochrome state and photosensitive growth of Avena coleoptile segments.

Using various photostationary state light sources to obtain reproducible phytochrome conversion of from 5 to 88% P(FR), assayed by 2 wavelength in vivo spectrophotometry, relationships between initial percent P(FR) and elongation of apical Avena coleoptile segments over the succeeding 20 hours in darkness were studied. With material grown in total darkness, all P(FR) levels promote elongation, and maximal promotion requires roughly 50% P(FR). The promotion caused by an initial 5 minute red (88% P(FR)) treatment at hour 0 is partially reversible at hour 5 by sources forming less than 48% P(FR), but totally irreversible at hour 8, though less than 50% of the growth has been accomplished by this time. Direct photometric assays at hour 5 indicate a phytochrome state of roughly 45% P(FR), consistent with the reversal data. At hour 8, however, 11 to 22% of the phytochrome still assays as P(FR), an inconsistency suggesting simply that the elongation process has proceeded beyond photochemical control. Thus, in contrast with results previously reported for Pisum and Phaseolus, there is no contradiction between photometric and physiological assays of phytochrome state in Avena coleoptile segments.Attempts to expand this study by using segments from seedlings pretreated with red light showed that such pretreatment as little as 1 to 2 hours before drastically reduces subsequent elongation and photoresponse on the medium employed. This decline in growth potential can be halted at any time before its completion by either excision of the segment or far-red treatment of the intact seedling.

Journal Article↗
PubMedDate not supplied

Survival.

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Economic Competition↗