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W D Dettbarn

Publications and source records attributed to W D Dettbarn.

108 records · Page 6Linked to original sources
PubMed1967

Cholinesterase activity of nodal and internodal regions of myelinated nerve fibers of frog.

The distribution of cholinesterase (Ch-esterase) in isolated myelinated fibers of the frog has been investigated. Quantitative microgasometric measurements have confirmed the previous histochemical observations. Both approaches indicate that in frog nerve fibers acetylcholinesterase (ACh-esterase) is the only or the predominant enzyme when selective inhibitors and different substrates are used: acetylcholine (ACh), butyrylcholine, and acetyl-B-methylcholine (Mecholyl). By means of the microgasometric technique, a significant difference in ACh-esterase activity between axons isolated from ventral (37.2 +/- 1.7 micromole x 10(-5) ACh/mm(2)/hr) and dorsal roots (2.0 +/- 0.9 micromole x 10(-5) ACh/mm(2)/hr) was found. In the region of the node of Ranvier the enzyme activity (50.4 +/- 4.4 micromole x 10(-5) ACh/mm(2)/hr) appears to be considerably higher than in the internodal area (36.6 +/- 2.1 micromole x 10(-5) ACh/mm(2)/hr). The findings are discussed in relation to the theory of saltatory conduction and the ACh system.

Acetylcholine↗
PubMed1966

Effect of ions on the efflux of acetylcholine from peripheral nerve.

The nerves from the walking leg of lobster released acetylcholine (ACh) even when the ends were tied off, although this release was significantly increased when the nerve endings were not tied. The resting nerves were kept in sea water containing physostigmine. In absence of physostigmine no ACh was found in the surrounding fluid. Removal of Ca from the sea water reduced the release of ACh, while increased concentrations of Ca had no significant effect. Removal of Mg++ or increased Mg++ concentrations in the presence of normal Ca++ concentrations increased the release of ACh. Increased K+ concentrations had a stimulating action on the efflux of ACh. Increased or reduced Na+ concentrations had only slight effects on the release of ACh in resting lobster nerve. During the 4 hr observation period the excised nerves were still able to synthesize ACh. The choline acetylase activity was stimulated by increased concentrations of Mg++ and K+. The effects of ions on the release of ACh are similar to those reported at the junction.

Acetylcholine↗
PubMed1965

Cholinesterase activity per unit surface area of conducting membranes.

According to theory, the action of acetylcholine (ACh) and ACh-esterase is essential for the permeability changes of excitable membranes during activity. It is, therefore, pertinent to know the activity of ACh-esterase per unit axonal surface area instead of per gram nerve, as it has been measured in the past. Such information has now been obtained with the newly developed microgasometric technique using a magnetic diver. (1) The cholinesterase (Ch-esterase) activity per mm(2) surface of sensory axons of the walking leg of lobster is 1.2 x 10(-3) microM/hr. (sigma = +/- 0.3 x 10(-3); SE = 0.17 x 10(-3)); the corresponding value for the motor axons isslightly higher: 1.93 x 10(-3) microM/hr. (sigma = +/- 0.41 x 10(-3); SE = +/- 0.14 x 10(-3)). Referred to gram nerve, the Ch-esterase activity of the sensory axons is much higher than that of the motor axons: 741 microM/hr. (sigma = +/- 73.5; SE = +/- 32.6) versus 111.6 microM/hr. (sigma = +/- 28.3; SE = +/- 10). (2) The enzyme activity in the small fibers of the stellar nerve of squid is 3.2 x 10(-4) microM/mm(2)/hr. (sigma = +/- 0.96 x 10(-4); SE = +/- 0.4 x 10(-4)). (3) The Ch-esterase activity per mm(2) surface of squid giant axon is 9.5 x 10(-5) microM/hr. (sigma = +/- 1.55 x 10(-5); SE = +/- 0.38 x 10(-5)). The value was obtained with small pieces of carefully cleaned axons after removal of the axoplasm and exposure to sonic disintegration. Without the latter treatment the figurewas 3.85 x 10(-5) microM/mm(2)/hr. (sigma = +/- 3.24 x 10(-5); SE = +/- 0.93 x 10(-5)). The experiments indicate the existence of permeability barriers in the cell wall surrounding part of the enzyme, since the substrate cannot reach all the enzyme even when small fragments of the cell wall are used without disintegration. (4) On the basis of the data obtained, some tentative approximations are made of the ratio of ACh released to Na ions entering the squid giant axon per cm(2) per impulse.

Acetylcholine↗
PubMedDate not supplied

Lipid peroxidation and changes in cytochrome c oxidase and xanthine oxidase activity in organophosphorus anticholinesterase induced myopathy.

A possible role of radical oxygen species (ROS) initiated lipid peroxidation in diisopropylphosphorofluoridate (DFP)-induced muscle necrosis was investigated by quantifying muscle changes in F2-isoprostanes, novel and extremely accurate markers of lipid peroxidation in vivo. A significant increase in F2-isoprostanes of 56% was found in the diaphragm of rats 60 min after DFP-induced fasciculations. As possible source of ROS initiating lipid peroxidation, the cytocrome-c oxidase (Cyt-ox) and xanthine dehydrogenase-xanthine oxidase (XD-XO) systems were investigated. Within 30 min of onset of fasciculations Cyt-ox activity was reduced by 50% from 0.526 to 0.263 mumol/mg prot/min and XO activity increased from 0.242 to 0.541 mumol/mg prot/min. Total XD-XO activity was unchanged, indicating a conversion from XD into XO. In rats pretreatment with the neuromuscular blocking agent d-tubocurarine, prevented DFP-induced fasciculations, increases in F2-isoprostanes and changes in Cyt-ox or XD-XO. The decrease in Cyt-ox and increase in XO suggest that ROS are produced during DFP induced muscle fasciculations initiating lipid peroxidation and subsequent myopathy.

Animals↗
PubMedDate not supplied

Evidence of necrosis in human intercostal muscle following inhalation of an organophosphate insecticide.

Intercostal muscle samples obtained from autopsy of a 51 year old male, exposed to an organophosphate insecticide by inhalation, were analyzed for cholinesterase (ChE) activity and muscle fiber integrity. Muscle ChE activity, five days after exposure, was still reduced to 53% of control values. Histological analysis indicated the presence of muscle fibers with subsarcolemmal grouped granular basophilic inclusions and scattered necrotic fibers. Results indicate that acute organophosphate exposure through inhalation can lead to skeletal muscle fiber damage in humans, similar to results obtained by ingestion. Furthermore, the pathology is comparable to the histological alterations observed in rats following acute injection of organophosphates.

Diazinon↗