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Biomedical subjects

J B Harris

Publications and source records attributed to J B Harris.

At least 109 records · Page 6Linked to original sources
PubMed1983

Regeneration of mammalian skeletal muscle following the injection of the snake-venom toxin, taipoxin.

Taipoxin, a toxin isolated from the venom of the snake Oxyuranus scutellatus was injected subcutaneously into the anterolateral aspect of one hind limb of the rat. The toxin caused a necrotising myopathy in the underlying muscle. The ultrastructural characteristics of the regeneration that followed the administration of the myotoxin were studied. Regeneration occurred within the surviving basal lamina tubes from a population of spared satellite cells. Myotubes were formed by 3 days and small immature muscle fibres by 5 days. The regenerative response was total and very rapid. Highly activated satellite cells were found in apparently undamaged fibres in the toxin-damaged muscles. Many of these cells appeared to be motile, having cytoplasmic processes which seemed to be passing through the basal lamina of the parent muscle fibres.

Animals↗
PubMed1982

Myotoxic activity of the crude venom and the principal neurotoxin, taipoxin, of the Australian taipan, Oxyuranus scutellatus.

1 The crude venom of the Australian taipan. Oxyuranus scutellatus and its principal neurotoxin, taipoxin, were injected into the anterolateral aspect of one hind limb of the rat. 2 The effects of the venom and toxin on the morphology and physiology on the underlying soleus muscles were examined. 3 Both the crude venom and the toxin caused necrosis and degeneration of the muscle. Damage to the peripheral muscle fibres could be seen at the light microscopic level as early as 3 h after injection of the toxic compounds. 4 The necrotic response was accompanied by an infiltration of phagocytic cells and an extensive oedema. The wet weight of the damaged muscles was almost doubled by 6 h. 5 In individual muscle fibres, necrosis was associated with the disruption of the plasma membrane and the disorganization of the myofibrils. The basal lamina of the muscle fibres was left intact. 6 Denervated mammalian muscles and innervated avian muscles were also destroyed by tiapoxin, but immature avian muscle growing in tissue culture was resistant. 7 Of the 3 subunits of taipoxin, only the basic alpha-taipoxin was itself myotoxic. However, its potency was enhanced by the presence of the acid gamma subunit. The role of the neutral beta-subunit is unclear. 8 The period of necrosis and degeneration lasted for approximately 48 h, after which the muscle fibres began to regenerate. Regeneration took place within the surviving basal lamina, with the formation of myotubes by three days, and small, immature muscle fibres by five days. Regeneration was virtually complete by 21 days.

Animals↗
PubMed1981

The uptake of 99mtechnetium diphosphonate into degenerating and regenerating muscle. A correlative histological and biochemical study.

The uptake of 99mTc-methylene diphosphonate into rat skeletal muscle has been studied. Uptake did not occur in normal or denervated muscles. Muscles damaged by exposure to the myotoxin notexin did accumulate label. The toxin causes a severe inflammatory, necrotising myopathy and regeneration normally begins 2-3 days after toxin administration. The uptake of label was maximal at 12-24 h, at which time muscle wet weight and cellular infiltration were also maximal. Label was found in the muscle mitochondria, the invading inflammatory cells and the oedema fluid. Regenerating muscles did not accumulate label. The uptake of label was positively correlated with total muscle calcium up to 24 h after the onset of necrosis, but it was suggested that the changes in the two parameters are not causally related.

Animals↗
PubMed1981

Actions of the crude venom of the Sydney funnel-web spider. Atrax robustus on autonomic neuromuscular transmission.

1 The effects on mammalian autonomic neuromuscular transmission of the crude venom of the female Sydney funnel-web spider Atrax robustus, have been investigated.2 At doses of 10 mug/ml or lower the indirectly elicited twitch-like responses of the rat anococcygeus preparation were inhibited. At doses greater than 10 mug/ml there was an initial reduction in the twitch-like response followed by a sustained contracture of the tissue.3 The long-lasting contracture caused by the venom was abolished by the application of phentolamine. It was virtually non-existent in muscle preparations isolated from reserpine-treated rats.4 In the presence of tetrodotoxin the contracture was smaller and less well maintained than in its absence.5 The venom caused a small reduction in the amplitude of the indirectly elicited twitch-like response of the longitudinal muscle of the guinea-pig ileum, followed by an increase in the tone of the preparation. The increase in tone was maintained for several minutes and was rapidly abolished by the application of atropine. The presence of venom did not affect control responses to either histamine or acetylcholine.6 Inhibitory transmission in the rat anococcygeus preparation was unaffected by the venom.7 The neurally-mediated twitch-like responses of both guinea-pig and rat vas deferens were inhibited by the venom at doses below 10 mug/ml. At higher doses the inhibition was accompanied by spontaneous contractions, and at doses in excess of 100 mug/ml the inhibition of twitch-like responses was transient and was followed by a potentiation of the motor response and extensive spontaneous activity. The preparation became quiescent 20 min after the application of venom and the evoked response was abolished after 60 min.8 The venom had qualitatively similar effects on motor transmission in the human vas deferens as on the rat and guinea-pig preparations. However, the human preparations were 50 to 100 times more sensitive to the effects of the venom.

Animals↗
PubMed1981

Mechanical and electrophysiological effects of sea anemone (Anemonia sulcata) toxins on rat innervated and denervated skeletal muscle.

1 Some effects of the sea-anemone toxin ATX-II on mammalian nerve-muscle preparations have been described. 2 When ATX-II (10(-8)-10(-6) M) was applied to rat hemidiaphragm preparations, both directly and indirectly generated twitch responses were potentiated and prolonged. At the same time the resting tension of the preparations increased. 3 The increase in resting tension caused by ATX-II in innervated muscles was not prevented by curarization, but was reversed by exposure to tetrodotoxin. The increase in denervated muscles was not completely reversed by tetrodotoxin. 4 At concentrations exceeding 1 x 10(-7) M, ATX-II caused a sodium-dependent depolarization of both normal and denervated muscles. The depolarization of the denervated muscles was only partially reversed by tetrodotoxin. 5 In the presence of ATX-II repetitive endplate potentials (e.p.ps) were evoked by single shocks to the motor nerves in many fibres, and in those in which a single e.p.p. was still observed, the quantum content (m) was increased. Miniature e.p.p. frequency was not increased by ATX-II, even when muscle fibres were depolarized by 30 mV. 6 The indirectly and directly elicited action potentials of normal and denervated muscle fibres were much prolonged by ATX-II. The action potentials remained sodium-dependent. The sodium-dependent tetrodotoxin-resistant action potential of the denervated muscle fibre was also prolonged by ATX-II. 7 It is concluded that ATX-II both activates, and delays inactivation of, sodium channels in mammalian skeletal muscle fibres, probably in interacting with the channel "gate'.

Action Potentials↗
PubMed1981

The effects of the subcutaneous injection of the crude venom of the Australian common brown snake, Pseudonaja textilis on the skeletal neuromuscular system.

1 The effects of the crude venom of the Australian common brown snake on the mammalian neuromuscular system have been investigated. 2 The venom was injected subcutaneously into the dorso-lateral aspect of one hind limb of the rat. The limb was paralyzed within 90 min and remained paralysed for 2 to 3 days. 3 The exposed muscles failed to respond to indirect excitation, and individual fibres were not depolarized at the nerve-muscle junction by exposure to carbachol. 4 The wet weight, histological appearance, resting potential and input resistance of the muscle fibres and their ability to generate directly elicited action potentials were unaffected by exposure to the venom. 5 Administration of venom to isolated preparations caused a reduction in the amplitude of miniature endplate potentials, with no change in frequency. The quantal content of evoked endplate potentials was unchanged. 6 It was concluded that the crude venom was largely devoid of presynaptic activity and myotoxicity, and that its primary site of neurotoxicity was directed to the postsynaptic membrane.

Action Potentials↗
PubMed1979

Insulin secretion and carbohydrate metabolism in the dystrophic mouse.

Dystrophic mice were investigated with regard to their regulation of blood glucose and insulin secretion in vivo. The following were also measured: tissue glycogen levels, activity of the glycogenolytic hydrolase, acid amyloglucosidase, and in vitro glucose utilization by liver, muscle and adipose tissue. Basal levels of blood glucose and plasma insulin of dystrophic mice were essentially within the same range as in the clinically unaffected littermate controls. Dystrophic mice had a decreased tolerance to glucose and glibenclamide; the secretion of insulin in response to these secretagogues was moderately reduced. Insulin release following beta-adrenergic stimulation, however, was increased in the dystrophic mice. Glycogen levels and acid amyloglucosidase activity were increased in dystrophic muscles but were normal in liver. Acid amyloglucosidase activity in pancreatic islets was lower in the dystrophic mouse. Glucose utilization in vitro appeared normal in liver tissue from dystrophic mice; in dystrophic muscle there was a threefold increase in 14CO2-production with no concomitant increase in either glycogen or 14C-incorporation into glycogen. 14CO2 production and 14C-incorporation into lipid and glycogen were increased in dystrophic adipose tissue. We suggest that the decreased glucose tolerance, and the reduced insulin response to glucose in the dystrophic mouse are compensated by an increased glucose utilization in muscle and adipose tissue and an increased beta-adrenergic-mediated secretion of insulin.

Adipose Tissue↗
PubMed1979

Pharmacological aspects of neuromuscular transmission in the isolated diaphragm of the dystrophic (Rej 129) mouse.

1. Some aspects of the pharmacology of neuromuscular transmission have been studied in the isolated diaphragm of the normal and dystrophic mouse. 2. The effects of (+)-tubocurarine and atropine on the indirectly elicited twitch responses of the dystrophic diaphragm were indistinguishable from normal. 3. Intracellular recording techniques revealed no significant differences between the rise time, time to half decay, frequency and amplitude of miniature endplate potentials (m.e.p.ps) recorded in dystrophic muscle fibres, compared to those recorded in normal muscle fibres. 4. Transmitter null potential, the size of the available store of transmitter, the probability of release of the transmitter, and the characteristics of endplate potentials (e.p.ps) of dystrophic muscle fibres did not differ from normal. 5. The quantum contents of e.p.ps generated in response to nerve stimulation of 0.1 to 100 HZ were consistently larger in dystrophic muscle fibres than in normal muscle fibres, but the differences were not statistically significant under the conditions of the experiment.

Animals↗
PubMed1979

Muscular dystrophy in the mouse: neuromuscular transmission and the concept of functional denervation.

The results of recent investigations by ourselves and others indicate that no form of denervation exists to any remarkable degree in dystrophic mouse skeletal muscles. This conclusion is based on the following information: Dystrophic nerve terminals liberate normal amounts of transmitter both spontaneously and during impulse-mediated activity. The characteristics of the release process, the size of the available store of transmitter, and the probability of release of transmitter in response to the invasion of an action potential appear to be normal. The sensitivity of the postsynaptic membrane to the transmitter is normal. Action potential generation in response to both direct and indirect excitation is normal. There is no unequivocal pharmacologic evidence of denervation in dystrophic skeletal muscle, even though dystrophic muscle fibers respond to surgical denervation in a normal fashion. Nerve terminal sprouting is extensive, but there is no evidence of collateral reinnervation.

Action Potentials↗
PubMed1979

The relationship between end-plate size and transmitter release in normal and dystrophic muscles of the mouse.

1. The morphology of nerve terminals and sub-neural apparatuses was examined in the muscles of normal and dystrophic adult mice of the Bar Harbor 129 ReJ strain. Nerve terminals were larger in dystrophic muscles than in normal muscles and nerve terminal sprouting was evident in about 50% of the dystrophic muscles fibres. End-plate area was positively correlated with muscle fibre diameter in both normal and dystrophic muscles. 2. Polynueronal innervation was found in only 1% of dystrophic muscle fibres impaled with micro-electrodes. 3. Miniature end-plate potential amplitude was positively correlated with muscle fibre input resistance in both normal and dystrophic muscles. There was however, a greater than normal variation in the amplitudes of m.e.p.p.s recorded from individual dystrophic muscle fibres. 4. Quantum contents of end-plate potentials were estimated in normal and dystrophic mouse nerve-muscle preparations partially blocked with D-tubocurarine. The quantum content of e.p.p.s seemed to be related to muscle fibre diameter, and in dystrophic muscles the characteristics of evoked release were indistinguishable from normal. 5. It was concluded that the nerve terminal sprouting and the expansion of end-plate area which were observed in dystrophic muscles are not a consequence of any form of denervation, but represent an attempt by the axon to expand the area of synaptic contact in hypertrophied muscle fibres.

Animals↗
PubMed1978

The effects of a toxin isolated from Australian tiger snake (Notechis scutatus scutatus) venom on autonomic neuromuscular transmission.

1 The effects on mammalian autonomic neuromuscular transmission of a purified toxin from the crude venom of the Australian tiger snake, Notechis scutatus, have been investigated. 2 The toxin had no measurable effect on transmission in either the rat anococcygeus, the rat vas deferens, or the longitudinal muscle of the guinea-pig ileum. 3 The toxin induced a contraction of longitudinal smooth muscle of the ileum. The tissue relaxed in spite of the continued presence of the toxin, and remained insensitive to further doses. The contractile response was not mediated by either cholinergic or histaminergic mechanisms. 4 The toxin caused an inhibition of the response to field stimulation of the guinea-pig vas deferens and the guinea-pig seminal vesicle. The inhibition was spontaneously reversible, and the preparations remained insensitive to further doses fo the toxin. The effects of the toxin were not mediated by either prostaglandins or by noradrenaline. 5 The inhibitory effects of a variety of compounds known to act at presynaptic sites were also blocked by exposure to the toxin; inhibition caused by postsynaptic activity was unaffected by the toxin. 6 It is suggested that the toxin inhibits transmission in the guinea-pig vas deferens and seminal vesicle by a presynaptic mechanism. 7 The possibility that the mechanism involves phospholipase A2 activity is discussed.

Animals↗
PubMed1978

Development of a tubular apparatus in chloroplasts of ageing Cyphomandra leaves.

Ultrastructural studies of chloroplasts from leaves of the solanaceous genus Cyphomandra during maturation and early senescence showed unusual activities of the inner chloroplast membrane. Before leaf maturity, released small vesicles and saccules. During continued development these structures apparently produced narrow, irregular small tubules which by short branching, slight enlargement and slight coiling became closely associated to form a relatively small tubular apparatus. In the senescing leaf the inner membrane developed long and enlarged extensions into the matrix which branched and coiled in a few cases so as to isolate bits of matrix which were released into the cytoplasm.

Chloroplasts↗