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PubMed1983

Effect of tubocurarine and decamethonium on voluntary muscle contractions in man.

Six healthy, young male subjects performed repeated brisk maximal voluntary muscle contractions (MVC) with the knee and hip extensors. Three MVCs were performed every minute. On separate days decamethonium 0.03 mg X kg-1 and tubocurarine 0.01 mg X kg-1 were administered intravenously during repeated MVCs. While ordinary MVCs showed a slow rate of rise of tension over approximately 1 s, brisk MVCs showed a steep rate of rise of tension and a biphasic configuration appeared, as a notch was seen 370-480 ms after the initiation of the contraction curve. An arbitrary straight line was drawn connecting the starting point of the contraction curve and the notch. The tension time integral to the left and above this line (alpha component), respectively to the right and below the line (beta component) was measured during the first 600 ms of the contraction. Tubocurarine affected the beta component until 70% reduced. With further curarization, the remainder of the beta component was reduced together with the alpha component. Decamethonium, in contrast, affected the alpha component together with 30% of the beta component. Thereafter, the rest of the beta component was increasingly affected. The results suggest that the isometric mechanogram is composed of a phasically active component with a high innervation threshold primarily sensitive to decamethonium, and a tonically active component with a lower innervation threshold, and primarily sensitive to tubocurarine.

Decamethonium Compounds↗
PubMed2006

Early effects of embryonic movement: 'a shot out of the dark'.

It has long been appreciated that studying the embryonic chick in ovo provides a variety of advantages, including the potential to control the embryo's environment and its movement independently of maternal influences. This allowed early workers to identify movement as a pivotal factor in the development of the locomotor apparatus. With an increasing focus on the earliest detectable movements, we have exploited this system by developing novel models and schemes to examine the influence of defined periods of movement during musculoskeletal development. Utilizing drugs with known neuromuscular actions to provoke hyperactivity (4-aminopyridine, AP) and either rigid (decamethonium bromide, DMB) or flaccid (pancuronium bromide, PB) paralysis, we have examined the role of movement in joint, osteochondral and muscle development. Our initial studies focusing on the joint showed that AP-induced hyperactivity had little, if any, effect on the timing or scope of joint cavity elaboration, suggesting that endogenous activity levels provide sufficient stimulus, and additional mobilization is without effect. By contrast, imposition of either rigid or flaccid paralysis prior to cavity formation completely blocked this process and, with time, produced fusion of cartilaginous elements and formation of continuous single cartilaginous rods across locations where joints would ordinarily form. The effect of these distinct forms of paralysis differed, however, when treatment was initiated after formation of an overt cavity; rigid, but not flaccid, paralysis partly conserved precavitated joints. This observation suggests that 'static' loading derived from 'spastic' rigidity can act to preserve joint cavities. Another facet of these studies was the observation that DMB-induced rigid paralysis produces a uniform and specific pattern of limb deformity whereas PB generated a diverse range of fixed positional deformities. Both also reduced limb growth, with different developmental periods preferentially modifying specific osteochondral components. Changes in cartilage and bone growth induced by 3-day periods of flaccid immobilization, imposed at distinct developmental phases, provides support for a diminution in cartilage elaboration at an early phase and for a relatively delayed influence of movement on osteogenesis, invoking critical periods during which the developing skeleton becomes receptive to the impact of movement. Immobilization also exerts differential impact along the proximo-distal axis of the limb. Finally, our preliminary results support the possibility that embryonic hyperactivity influences the potential for postnatal muscle growth.

4-Aminopyridine↗
PubMed1985

Membrane potential and catecholamine secretion by bovine adrenal chromaffin cells: use of tetraphenylphosphonium distribution and carbocyanine dye fluorescence.

Changes in plasma membrane potential of isolated bovine adrenal chromaffin cells were measured independently by two chemical probe methods and related to corresponding effects on catecholamine secretion. The lipophilic cation tetraphenylphosphonium (TPP+) and the carbocyanine dye 3,3'-dipropylthiadicarbocyanine [DiS-C3-(5)] were used. The necessity of evaluating the subcellular distribution of TPP+ among cytoplasmic, mitochondrial, secretory granule, and bound compartments was demonstrated and the resting plasma membrane potential determined to be -55 mV. The relationship between membrane potential and catecholamine secretion was determined in response to variations in extracellular K+ and to the presence of several secretagogues including cholinergic receptor ligands, veratridine, and ionophores for Na+ and K+. The dependence of potential on K+ concentration fit the Goldman constant field equation with a Na/K permeability ratio of 0.1. The dependence of both K+- and veratridine-evoked catecholamine secretion on membrane potential exhibited a potential threshold of about -40 mV before a significant rise in secretion occurred. This is likely related to the threshold for opening of voltage-sensitive Ca2+ channels. Acetylcholine and nicotine evoked a large secretory response without a sufficiently sustained depolarization to be detectable by the relatively slow potential sensitive chemical probes. Decamethonium induced a detectable depolarization of the chromaffin cells. Veratridine and gramicidin evoked both membrane depolarization and catecholamine release. By contrast the K ionophore valinomycin evoked significant levels of secretion without any depolarization. This is consistent with its utilization of an intracellular source of Ca2+ and the independence of its measured secretory response on extracellular Ca2+.

Acetylcholine↗
PubMed1986

Characterization of muscarinic cholinergic receptors in the crab nervous system.

The selective muscarinic antagonist L-[3H]-quinuclidinyl benzilate (L-[3H]QNB) binds reversibly and with high affinity (KD = 0.3 nM) to a single population (Bmax = 105 fmol/mg protein) of specific sites in nervous tissue of the crab Cancer magister. The binding site is stereoselective; (-)QNB is over 200 times more potent than (+)QNB as an inhibitor of specific L-[3H]QNB binding. The muscarinic antagonists scopolamine and atropine are over 10,000 times more potent inhibitors of L-[3H]QNB binding than the nicotinic antagonists decamethonium and d-tubocurarine. The muscarinic agonists oxotremorine, pilocarpine, arecoline, and carbachol also compete effectively for the L-[3H]QNB binding site. This pharmacological profile strongly suggests the presence of classical muscarinic receptors in the crab nervous system. These receptors are localized to nervous tissue containing cell bodies and neuropil, whereas specific L-[3H]QNB binding is low or absent in peripheral nerve, skeletal muscle, and artery.

Animals↗
PubMed1988

Nicotinic agonists regulate alpha-bungarotoxin binding sites of TE671 human medulloblastoma cells.

The TE671 human medulloblastoma cell line expresses a variety of characteristics of human neurons. Among these characteristics is the expression of membrane-bound high-affinity binding sites for alpha-bungarotoxin, which is a potent antagonist of functional nicotinic acetylcholine receptors on these cells. These toxin binding sites represent a class of nicotinic receptor isotypes present in mammalian brain. Treatment of TE671 cells during proliferative growth phase with nicotine or carbamylcholine, but not with muscarine or d-tubocurarine, induced up to a five-fold increase in the density of radiolabeled toxin binding sites in crude membrane fractions. This effect was blocked by co-incubation with the nicotinic antagonists d-tubocurarine and decamethonium, but not by mecamylamine or by muscarinic antagonists. Following a 10-13 h lag phase upon removal of agonist, recovery of the up-regulated sites to control values occurred within an additional 10-20 h. These studies indicate that the expression of functional nicotinic acetylcholine receptors on TE671 cells is subject to regulation by nicotinic agonists. Studies of the murine CNS have consistently indicated nicotine-induced up-regulation of nicotinic acetylcholine receptors, thereby supporting the identification of the toxin binding site on these cells as the functional nicotinic receptor. Although a mechanism for this effect is not apparent, nicotine-induced receptor blockade does not appear to be involved.

Atropine↗
PubMed1959

The pharmacology of a molluscan smooth muscle.

The effects of a number of pharmacologically active substances on contraction and on membrane polarization of the anterior byssal retractor muscle of Mytilus edulis, L., have been studied. Tetramethylammonium bromide, trimethyl(4-oxopentyl)ammonium chloride and nicotine, like acetylcholine, produced depolarization and sustained contraction. Nicotine, on repeated application, lost acetylcholine-like activity and effectively blocked acetylcholine. In order of decreasing potency, methanthelinium, tubocurarine, benzoquinonium, tetraethylammonium, atropine, pentamethonium, and decamethonium blocked acetylcholine action. These agents did not show initial acetylcholine-like action and did not relax sustained contractions. Adrenaline, noradrenaline, tyramine, dibenamine, phentolamine, and lysergic acid diethylamide relaxed sustained contractions without reducing initial depolarization and tension development in response to acetylcholine or electrical stimuli. Adrenaline and noradrenaline often caused depolarization and contraction when first applied, and displayed relaxing action on subsequent application.

Acetylcholine↗
PubMed1960

The effect of temperature on the direct muscle twitch response and the action of drugs on the isolated denervated rat diaphragm.

The effect of temperature on the direct twitch response of the normal and denervated rat diaphragm, and the sensitivity of the contractural response of the denervated muscle to acetylcholine, suxamethonium, decamethonium, and potassium salts, was studied. Cooling the normal diaphragm from 39 to 20 degrees increased the size of the direct twitch, but below this temperature the twitch response of the muscle was progressively depressed. The denervated muscle twitch was, by contrast, maximal at 39 degrees and decreases as the temperature was lowered. This property of the denervated muscle first appeared about the third day after denervation. The contractural response of the denervated diaphragm to applied acetylcholine was enhanced by cooling, while the response to potassium salts was depressed. The depression of the contracture induced by potassium followed closely the depression of the direct muscle twitch of the denervated muscle over the same temperature range.

Acetylcholine↗