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Biomedical subjects

Z W Hall

Publications and source records attributed to Z W Hall.

At least 109 records · Page 6Linked to original sources
PubMed1975

Synthesis of acetylcholine receptor by denervated rat diaphragm muscle.

Acetylcholine receptor was purified by affinity chromatography from denervated rat hemidiaphragms that had been incubated in organ culture for 24 hr in medium containing [35-S] methionine. Radioactive acetylcholine receptor was identified in purified preparations by zone sedimentation in a sucrose gradient, by isoelectric focusing, and by precipitation with an antiserum to the acetylcholine receptor from electric eel. When innervated and denervated hemidiaphragms were incubated with [35-S] methionine in organ culture, and the acetylcholine receptors from each were purified separately, only the preparation from denervated muscles contained radioactive receptor as determined by zone sedimentation. We conclude that newly synthesized receptor is accumulated as a result of muscle denervation.

Acetylcholine↗
PubMed1975

Increased extrajunctional acetylcholine sensitivity produced by chronic acetylcholine sensitivity produced by chronic post-synaptic neuromuscular blockade.

1. Anaesthetized rats were paralysed for periods of up to 3 days by chronic administration of D-tubocurarine (DTC), succinylcholine or alpha-bungarotoxin. 2. After 3 days of treatment with DTC, the phrenic nerve remained active. Neuromuscular transmission and spontaneous miniature end-plate potentials (m.e.p.p.s) were restored after removal of the DTC. Resting potentials and input resistances of muscle fibres that had been paralysed for 3 days were similar to those in denervated fibers. 3. Chronic neuromuscular blockade increased the binding of [125-I]-alpha-bungarotoxin by extrajunctional regions of muscle. The time course of the increase was similar to that seen after denervation. Binding to muscles from animals that were anaesthetized and respirated, but not paralysed, was not increased. 4. Three days of paralysis increased the sensitivity of the extrajunctional muscle membrane to acetylcholine (ACh) applied by iontophoresis. 5. Approximately the same proportion of muscle fibres from muscles paralysed for 3 days gave overshooting action potentials in the presence of tetrodotoxin 10-minus 6 g/ml. as did fibres form muscles denervated for 3 days. 6. Chronic paralysis did not change the accumulation of acetylcholinesterase above a ligation in the sciatic nerve. 7. These results are consistent with the idea that extrajunctional ACh sensitivity is normally controlled by muscle activity.

Acetylcholine↗
PubMed1975

Loss of alpha-bungarotoxin from junctional and extrajunctional acetylcholine receptors in rat diaphragm muscle in vivo and in organ culture.

Acetylcholine (ACh) receptors in rat diaphragm muscle were blocked by intrathoracic injection of alpha-bungarotoxin (alpha-BuTx) or [125I]alpha-bungarotoxin ([125I]alpha-BuTx). The stability in vivo of the toxin-receptor complex formed by receptors in normal muscles and receptors in extrajunctional regions of denervated muscles was compared. Toxin was lost from junctional regions of normal muscles with a half-time of approximately 6 days. The loss of toxin was accompanied by a corresponding increase in the number of free toxin-binding sites. In contrast, 65% of the toxin bound to extrajunctional regions of denervated muscle was lost in 24 hr. 2. In a second series of experiments, animals were injected with [125I]alpha-BuTx and the muscle subsequently cultured for 24 hr. Loss of toxin again occurred more rapidly from extrajunctional receptors than from junctional receptors. The loss from extrajunctional receptors was described by a single first-order rate constant whose corresponding half-time was 8-11 hr. Loss was almost completely blocked by sodium cyanide and dinitrophenol and was inhibited by puromycin and cycloheximide. The radioactivity recovered in the medium was largely monoiodotyrosine. These results are consistent with the hypothesis that toxin loss reflects intracellular degradation of toxin-receptor complex. 3. Neonatal rats were injected with [125I]alpha-BuTx and the diaphragms cultured. Radioactive toxin was lost rapidly from extrajunctional regions of muscle and more slowly from regions containing end-plates. 4. These results could be explained by a difference in turnover rates for junctional and extrajunctional receptors.

Animals↗
PubMed1974

Fate of alpha-bungarotoxin bound to acetylcholine receptors of normal and denervated muscle.

In organ culture, alpha-[(125)I]bungarotoxin bound to extrajunctional receptors of denervated muscle is lost from the tissue at a more rapid rate than the toxin bound to the junctional receptors of normal muscle. The rapid loss of toxin from denervated muscle can be blocked by inhibitors of energy production and protein synthesis, and may reflect turnover of the toxin-receptor complex in the membrane.

Animals↗
PubMed1972

Binding of -bungarotoxin to acetylcholine receptors in mammalian muscle (snake venom-denervated muscle-neonatal muscle-rat diaphragm-SDS-polyacrylamide gel electrophoresis).

Experiments were performed to determine the specificity of [(125)I]alpha-bungarotoxin binding to skeletal muscle. In adult rat diaphragm, [(125)I]alpha-bungarotoxin was found to bind almost exclusively to those regions of the muscle that contain endplates and are known to be sensitive to acetylcholine. In contrast, chronically denervated adult muscle and muscle from neonatal rats, both of which are sensitive along their entire lengths, bound substantial amounts of toxin in all regions. Toxin binding to all muscles was inhibited by d-tubocurarine and by carbamylcholine, but not by atropine. The bound [(125)I]toxin was solubilized by homogenization of the tissue in 1% Triton X-100 and was recovered as a single band, distinct from free toxin, after zone sedimentation. Treatment of the solubilized, toxin-bound complex with 2-mercaptoethanol and sodium dodecyl sulfate resulted in the recovery of free toxin. A toxin-bound complex was also obtained when toxin was incubated directly with extracts of muscle endplate regions prepared by homogenization in Triton X-100. No such complex was observed with extracts prepared from muscle lacking endplates. These results are consistent with the interpretation that alpha-bungarotoxin binds specifically to the acetylcholine receptor of mammalian skeletal muscle.

Acrylamides↗
PubMed1970

The metabolism of gamma aminobutyric acid in the lobster nervous system. Enzymes in single excitatory and inhibitory axons.

gamma-aminobutyric acid (GABA) is the inhibitory transmitter compound at the lobster neuromuscular junction. This paper presents a comparison of the enzymes of GABA metabolism in single identified inhibitory and excitatory axons from lobster walking legs. Inhibitory axons contain more than 100 times as much glutamic decarboxylase activity as do excitatory axons. GABA-glutamic transaminase is found in both excitatory and inhibitory axons, but about 50% more enzyme is present in inhibitory axons. The kinetic and electrophoretic behavior of the transaminase activity in excitatory and inhibitory axons is similar. Succinic semialdehyde dehydrogenase is found in both axon types, as is an unknown enzyme which converts a contaminant in radioactive glutamic acid to GABA. In lobster inhibitory neurons, therefore, the ability to accumulate GABA ultimately rests on the ability of the neuron to accumulate the enzyme glutamic decarboxylase.

Aminobutyrates↗