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Biomedical subjects

A J Harris

Publications and source records attributed to A J Harris.

At least 73 records · Page 4Linked to original sources
PubMed1975

Dissociation between nerve-muscle transmission and nerve trophic effects on rat diaphragm using type D botulinum toxin.

Small doses of botulinum toxin can produce partial blockage of transmitter release at the nerve--muscle junction. 2. Subthreshold e.p.p.s, 3--10 days after poisoning, show a distribution of amplitudes that is fitted by Poisson statistics. Successive e.p.p.s. in a short train show a marked facilitation. 3. Two weeks or more after poisoning with a dose of toxin that paralyses the whole muscle, when nerve--muscle transmission is in course of recovery, subthreshold e.p.p.s have an amplitude distribution that is fitted by binomial statistics. This property of transmission is similar to those described in newly formed nerve--muscle junctions, during embryogenesis or regeneration. 4. Muscle fibres with subthreshold transmission in the 5--10 day group of muscles were all supersensitive to ACh, as were a number of fibres in which nerve stimulation still produced an action potential. 5. Two weeks or more after poisoning, muscle fibres with subthreshold transmission had lost their extrajunctional ACh-sensitivity, as had many fibres with m.e.p.p.s of roughly normal frequency but no response to nerve stimulation. 6. In diaphragm muscles poisoned with botulinum toxin between 1 and 4 days previously, the rate of fast axonal transport of radioactively labelled proteins down the phrenic nerve is not greatly affected, but the amount of materials carried is reduced to about one quarter of normal. These labelled proteins accumulate in the intramuscular portion of the phrenic nerve, in or near the nerve terminals, to a much greater extent than in controls, showing that the normal release of some of these materials has been prevented by the toxin. 7. It is concluded that the blockage of the trophic effects of nerves by botulinum toxin is due to a blockage of release of trophic factors other than ACh. 8. The muscle nerve cannot maintain a muscle in its normal state simply by activation of contraction, and a regenerating nerve terminal can restore a muscle towards its normal state before it can release enough ACh to produce muscle contraction.

Acetylcholine↗
PubMed1974

Characterization of a unique muscle cell line.

A clonal cell line derived from a mouse neoplasm is described which shares many properties with smooth muscle. The cells have electrically excitable membranes capable of generating overshooting action potentials, and they contract both spontaneously and with electrical stimulation. They respond to the iontophoretic application of acetylcholine with a depolarizing response, and to norepinephrine with a hyperpolarizing response. Electron microscopy reveals that the cells have a morphology similar in many, but not all, respects to that of smooth muscle cells in vivo. The cells secrete soluble collagen-like molecules in addition to several proteins of undefined function. Finally, there is an increase in the specific activities of creatine phosphokinase and myokinase associated with increased cell density and the cessation of cell division.

Acetylcholine↗
PubMed1973

Nerve-muscle interaction in vitro. Role of acetylcholine.

Nerve and muscle cells from clonal lines interact in vitro, resulting in the association on the muscle surface of an area of increased acetylcholine sensitivity with a site of nerve-muscle contact. This localization of acetylcholine sensitivity on the muscle cell to a site of contact between nerve and muscle was found to occur when acetylcholine receptors on the muscle had been blocked with alpha-neurotoxin. Localization was also found to occur when the nerve cell had been prevented from releasing acetylcholine. It is concluded that neither the presence of active acetylcholine receptors on the muscle, nor the release of acetylcholine from the nerve, was required for the events leading to the localization of acetylcholine sensitivity in vitro.

Acetylcholine↗
PubMed1972

A study of frog muscle maintained in organ culture.

1. Frog muscles are isolated and maintained in organ culture conditions for periods of up to 2 months. During the first 2 weeks, muscle fibres have normal resting membrane and action potentials. Subsequently the potentials decline in amplitude.2. Slow muscle fibres also survive in culture and retain their ability to give maintained contractures.3. Muscle sensory receptors continue to function in culture until the axon terminals degenerate at about 2 weeks.4. Neuromuscular transmission is normal during the first few days of culture, after which the motor endings degenerate. Transmission persists longer (up to 17 days) if a long segment of nerve is left attached to the muscle. With short-nerve preparations failure of transmission in vivo occurs at about the same time as in culture. With long-nerve preparations failure of transmission is delayed even further in culture.5. In short-nerve preparations miniature end-plate potentials disappear, in general, at about the time that transmission fails. In long-nerve preparations some end-plates continue to have miniature end-plate potential activity for a short time after nerve impulses cease to evoke any response; but eventually miniature potential activity disappears from all end-plates.6. After a few days of electrical silence, miniature end-plate potentials reappear at some of the denervated end-plates. The proportion of denervated end-plates which show miniature end-plate potentials in culture is smaller than in muscles denervated in situ.7. Electron microscopy shows that muscle structure is well preserved in culture, that the axons degenerate and that the Schwann cells move to occupy the space vacated by the axons. The Schwann cells are very probably the source of the acetylcholine which evokes miniature potentials in the denervated end-plates.

Acetylcholine↗
PubMed1971

The effect of type D botulinum toxin on frog neuromuscular junctions.

1. Botulinum toxin type D blocks neuromuscular transmission in frogs. Motor nerve impulses continue to invade the nerve terminals but cease to evoke the phasic release of transmitter normally associated with them.2. Sensory receptors in the muscle continue to generate impulses even after 4 days of continuous exposure to botulinum toxin.3. Contrary to expectations, spontaneous miniature end-plate potentials did not disappear completely after botulinum intoxication; they still occurred, although with reduced frequency, in most end-plates. These miniature potentials had a skew amplitude distribution instead of the bell-shaped distribution of normal end-plates.4. The electron-microscopic appearance of botulinum-poisoned end-plates was not obviously altered.5. Even though after botulinum nerve impulses fail to release transmitter, tetanic nerve stimulation causes an increase in the frequency of miniature end-plate potentials. Many of the unit potentials which appear during the tetanic period are of an amplitude which is larger than that of spontaneous potentials, indicating that a different class of unit is being released preferentially. Some implications of this finding are briefly discussed.

Action Potentials↗
PubMed1970

Acetylcholine sensitivity and distribution on mouse neuroblastoma cells.

Action potentials resulted from iontophoretic application of acetylcholine to cloned mouse neuroblastoma cells maintained in culture. Cell bodies were sensitive to acetylcholine, but half the cells were insensitive along one of their processes, suggesting an analogy with normal axons and dendrites. Some cells were electrically coupled via their processes, but no chemically mediated synaptic transmission was seen.

Acetylcholine↗