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J R Slack

Publications and source records attributed to J R Slack.

36 records · Page 2Linked to original sources
PubMed1983

Effects of contralateral denervation on quantal output and gross nerve terminal morphology in mouse muscles.

We have studied the effect of unilateral denervation on the quantal output and gross nerve terminal morphology of the contralateral tensor fascia latae (TEL) muscle in mice. Unilateral TFL denervation was achieved by resecting spinal nerves L4 and L5. We found no significant difference, in quantal output or in the percentage of nerve terminals with sprouts, between the contralateral muscles and muscles in unoperated, age-matched control mice, at 4 days, 11-12 days or 6.5 months after denervation. This finding is in contrast to marked differences between similar experimental and control muscles after unilateral denervation reported in frogs by others.

Animals↗
PubMed1983

Ability of motoneurons to regulate quantal release and terminal growth after reduction in motor unit size.

Experiments were performed to test the hypothesis that motoneurons are programmed to produce fixed amounts of growth and transmitter release substrates and are unable to regulate production to match the number of nerve terminals they support. The size of the average motor unit in mouse tensor fascia latae muscles was approximately halved by cutting out the distal half of the muscle. Surviving terminals were assessed 100-110 days later for level of quantal output and percentage of terminals with sprouts. Both quantal output and sprout percentage were the same as in contralateral control muscles. Both parameters have been reported to be elevated 1-9 days after a similar operation. We conclude that mouse motoneurons can down-regulate their production of growth and release substrates but that the process takes more than 9 days to become effective.

Animals↗
PubMed1983

Evidence for a motor nerve growth factor.

We review the evidence that a motor nerve growth factor released from muscle has wide ranging effects on the development and maintenance of muscle innervation. The actions of this putative factor on motor neurons are analogous to the actions of the well known nerve growth factor (NGF) on sympathetic and sensory neurons.

Animals↗
PubMed1983

Regulation of postnatal growth of motor end plates in rat soleus muscle.

The question of whether or not postnatal growth in the length of end-plate acetylcholinesterase plaques in rat soleus muscle is controlled by the nerve or by the muscle was studied. When muscles with intact innervation were tenotomized in young rats, the muscles failed to grow in length and diameter and the end-plate esterase plaques remained short when the animals attained adulthood. When muscles in young rats were denervated the fibers also failed to grow in diameter and end-plate esterase plaques failed to attain the length of control plaques in normal innervated muscle. We conclude that growth of postnatal muscle fiber is an important determinant of end plate and motor terminal growth.

Acetylcholinesterase↗
PubMed1982

Pruning of axonal trees results in increased efficacy of surviving nerve terminals.

The intramuscular nerve was crushed in mouse tensor fascia latae muscles so that on average motor units lost 40% of their terminals. Quantal contents at 20% of the surviving terminals had doubled in muscles examined between 17 h and 9 days later. Silver staining revealed that some surviving nerve terminals had sprouted, but too few to account for the quantal content increases. Redistribution of axoplasmically transported materials to the surviving terminals is hypothesized to explain the increase in their efficacy.

Animals↗
PubMed1982

Neuromuscular transmission at terminals of sprouted mammalian motor neurones.

Motor nerve sprouting was induced in the tensor fasciae latae muscle of mice by partial denervation produced either by cutting (to prevent reinnervation) or crushing (to allow subsequent reinnervation) spinal nerve L4 unilaterally. The quantum content (m) of endplate potentials recorded intracellularly in vitro in the presence of high-Mg2+ and low-Ca2+ ion concentrations was determined up to 400 days later in non-reinnervated, reinnervated and contralateral control muscles. The muscles were then either fixed and stained with silver and cholinesterase for light microscopy, or fixed and examined in the electron microscope. The average value of m in control muscles increased by 4-5-fold as the animals matured in the 4 months following the operations. The average value of m at terminals of sprouted motor neurones in the absence of reinnervation also increased with time after partial denervation but was always less than the value in the corresponding control muscle. In electron micrographs of muscles following L4 section the nerve terminals closely apposed on average only two-thirds of the proportion of junctional folds apposed to terminals in control muscles. When muscles were reinnervated following L4 crush the average value of m at terminals of sprouted and reinnervating motor neurones equalled and sometimes exceeded m in contralateral control muscles. A proportion of muscle fibres had endplate potentials from reinnervating and sprouted axons, and the silver stain showed that these muscle fibres were innervated at the site of the original endplate. At these endplates the fraction of the total quantum content contributed by presumed sprout terminals fell significantly in the 4 months following L4 crush. It is concluded that: (i) in the absence of reinnervation, sprout terminals grow in size but a significant number never occupy all endplate site available to them; and (ii) in the presence of reinnervation axons terminals share some endplates with sprout terminals and grow at the expense of the sprout terminals which are eventually withdrawn from some shared endplates.

Action Potentials↗
PubMed1982

Source of the stimulus for nerve terminal sprouting in partially denervated muscle.

The topological positions of nerve terminal sprouts in partially denervated rat sternocostal muscles were analysed. Sprouted nerve terminals were found only within 200 microns of a denervated muscle fibre, but were not necessarily within 200 microns of a denervated endplate. From this it was concluded that the sprout-inducing factor released from denervated muscle fibres does not necessarily arise from the denervated endplate, but may be released along the length of the muscle fibre. It is proposed that sprout factor is released during the incorporation of acetylcholine receptors into the muscle fibre membrane.

Animals↗
PubMed1981

The absence of nodal sprouts from partially denervated nerve trunks.

Nodal sprouts were absent from partially denervated, silver-stained, mouse superior gluteal (SG) nerves examined between 4 and 20 days after partial denervation. Nodal sprouts were also absent from electron micrographs of partially denervated SG nerves. We conclude that an earlier report describing profuse nodal sprouting in partially denervated nerve trunks mistakenly identified fine Schwann cell processes as nodal sprouts.

Animals↗
PubMed1981

Terminal sprouting of motoneurones is a local response to a local stimulus.

Terminal sprouting was visualized in silver stained whole mounts of rat sternocostal muscles after resecting one segmental nerve. Sprouts were only found near denervated muscle fibres. The effective diffusion range of the sprout inducing factor released by denervated fibres was 50--100 micrometers. Individual terminals of the same motoneurone sprout independently of each other and only when they intercept the sprout inducing factor.

Animals↗
PubMed1981

A method for visualizing axons and endplates throughout whole mounts of skeletal muscles using combined silver and cholinesterase stain.

A silver-cholinesterase stain is described which allows the visualization of the complete axonal tree, perineurial sheaths, motor nerve terminals and the cholinesterase at neuromuscular junctions throughout whole mounts of relatively thin muscles. The method is rapid, reliable and simple and allows the preservation of topographical information regarding both terminal and nodal sprouting in the whole muscle.

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↗
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↗
PubMed1978

The pattern of innervation of a polyneural muscle: axolotl iliotibialis.

The pattern of innervation on individual iliotibialis muscle fibres from axolotl (Ambystoma mexicanum) has been investigated histologically and electrophysiologically. These polyneural fibres were found to be innervated on average at five end plate sites. The sites were distributed irregularly along each fibre. Average end plate length was found to be approximately 70 micrometer. Most end plates were separated by less than 1000 micrometer; 26% by less than 150 micrometer; the average separation was 516 micrometer. Advantage was taken of the dual innervation of the muscle to investigate the separation between synaptic terminals from different axons. Some individual fibres were found to be innervated by axons from two different spinal nerves. End plate sites on dually innervated fibres were located by ACh iontophoresis. 30% of such sites were found to be innervated by more than one axon terminal. The average separation of such sites was found to be 9 micrometer. Four different axons were found to innervate some individual muscle fibres. It is suggested that the unusual ability of axolotl muscle fibres to accept synaptic terminals from different axons at closely adjacent sites may be a major factor underlying selective reinnervation in this animal.

Ambystoma↗