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Biomedical subjects

A C Oliveira

Publications and source records attributed to A C Oliveira.

10 recordsLinked to original sources
PubMed1992

Type I collagen synthesis by rats fed beans (Phaseolus vulgaris, L.) as the protein source.

Type I collagen synthesis was studied in 12 female Wistar rats weighing 60 +/- 5 g at the beginning of the experiment. The animals were fasted for 24 h and then injected ip with 10 microCi uniformly labeled [14C]-glycine. Two hours later, groups of 4 animals each were fed balanced diets (10.7 +/- 0.4% protein) containing raw beans (Phaseolus vulgaris, L.), cooked beans or casein (control) as the single protein source, ad libitum. The animals were killed after 4 days and collagen was extracted from the tail and calcaneal tendons. Food intake and weight gain of rats fed raw beans (22 g, 0 g) were considerably less than rats fed cooked beans (38 g, 9 g) and casein (44 g, 22 g). Collagen was quantitated on the basis of hydroxyproline and corresponded to 0.1, 0.2 and 0.2% rat body weight, with specific radioactivity of 1.2, 1.6 and 4.2 microCi/g, for the rats fed raw beans, cooked beans and casein, respectively. The results indicate that rats fed either bean protein synthesized less collagen than those fed casein (P < 0.05). Although the food intake and extractable collagen of rats fed cooked beans were similar to those of casein-fed rats, weight gain and collagen specific radioactivity were less.

Animals↗
PubMed1979

Tetraethylammonium: voltage-dependent action on endplate conductance and inhibition of ligand binding to postsynaptic proteins.

Tetraethylammonium (Et(4)N(+)) ions depressed the amplitude and accelerated the decay rate of spontaneously occurring and nerve-evoked endplate currents (EPCs) in frog sartorius muscle. The relationship between peak EPC amplitude and membrane potential became nonlinear in the presence of 100 muM Et(4)N(+), and with drug concentrations of 250 muM or greater the current-voltage relationship exhibited negative conductance in the hyperpolarized region. Et(4)N(+) modified the exponential dependence of the EPC decay on membrane potential such that the decays between -150 and -50 mV were abbreviated and voltage independent but remained near control levels at more positive membrane potentials. The minimal effective concentration of Et(4)N(+) for altering the EPC time course was 10, and maximal effects were attained with 100 muM. Little additional shortening in the EPC decay phase was detected on raising the drug concentration to 1000 muM. Acetylcholine noise analysis revealed a voltage-dependent reduction in the mean channel open time, which was comparable in magnitude to the shortening in the EPC decay, and a depression of single-channel conductance. In concomitant biochemical studies, Et(4)N(+) was found to inhibit the binding of both [(3)H]acetylcholine and [(3)H]perhydrohistrionicotoxin to receptor-rich membranes from the electric organ of Torpedo ocellata with K(i) values of 200 muM and 280 muM, respectively. These results suggest that Et(4)N(+) interacts with both the acetylcholine receptor and its associated ionic channel. The voltage-dependent actions of Et(4)N(+) are attributed to blockade of the ionic channel in closed as well as open conformation.

Acetylcholine↗
PubMed1979

Reaction of tetraethylammonium with the open and closed conformations of the acetylcholine receptor ionic channel complex.

The effect of tetraethylammonium (TEA) bromide on the neurally and iontophoretically evoked endplate current (EPC) of frog sartorius muscle was investigated using voltage-clamp and noise analysis techniques, and its binding to the acetylcholine (ACh) receptor ionic channel complex was determined on the electric organ of Torpedo ocellata. TEA (250-500 microM) produced an initial enhancement followed by a slow decline in the amplitude of the endplate potential and EPC, but caused only depression in the amplitude of the miniature endplate potential and current. In normal ringer's solution, the EPC current-voltage relationship was approximately linear, and the decay phase varied exponentially with membrane potential. Upon addition of 50-100 microM TEA, the current-voltage relationship became markedly nonlinear at hyperpolarized command potentials, and with 250-2000 microM TEA, there was an initial linear segment, an intermediate nonlinear segment, and a region of negative conductance. The onset of nonlinearity was dose-dependent, undergoing a 50 mV shift for a 10-fold increase in TEA concentration. The EPC decay phase was shortened by TEA at hyperpolarized but not depolarized potentials, and remained a single expotential function of time at all concentrations and membrane potentials examined. These actions of TEA were found to be independent of the sequence of polarizations, the length of the conditioning pulse, and the level of the initial holding potential. TEA shifted the power spectrum of ACh noise to higher frequencies and produced a significant depression of single channel conductance. The shortening in the mean channel lifetime agreed closely with the decrease in the EPC decay time constant. At the concentrations tested, TEA did not alter the EPC reversal potential, nor the resting membrane potential, and had little effect on the action potential duration. TEA inhibited the binding of both [3H] ACh (Ki = 200 microM) and [3H]perhydrohistrionicotoxin (Ki = 280 microM) to receptor-rich membranes from the electric organ of Torpedo ocellata, and inhibited the carbamylcholine-activated 22Na+ efflux from these microsacs. It is suggested that TEA reacts with the nicotinic ACh-receptor as well as its ion channel; the voltage-dependent actions are associated with blockade of the ion channel. The results are compatible with a kinetic model in which TEA first binds to the closed conformation of the receptor-ionicchannel complex to produce a voltage-depdndent depression of endplate conductance and sudsequently to its open conformation, giving rise to the shortening in the EPC decay and mean channel lifetime.

Acetylcholine↗
PubMed1979

Differential effect of perhydrohistrionicotoxin on 'intrinsic' and 'extrinsic' end-plate responses.

1. At rat and frog neuromuscular junctions, perhydrohistrionicotoxin (H12-HTX), at concentrations below 10(-6) M, blocked end-plate currents and potentials generated by ionophoretic application of ACh (extrinsic responses) more effectively than end-plate currents and potentials generated by neurotransmitter secreted from the motor nerve (intrinsic responses). 2. In contrast, (+)-tubocurarine affected both extrinsic and intrinsic responses in a parallel manner. 3. There was no change in the time course and little or no change in the amplitude of intrinsic end-plate currents when extrinsic currents were depressed by H12-HTX nor was there any change in the conductance or lifetime of channels activated by applied ACh. 4. The depressant effect of H12-HTX on extrinsic responses persisted both when carbachol was used as the agonist and when acetylcholinesterase was inhibited with diisopropylfluorophosphate. 5. Large end-plate currents elicited by nerve stimulation that presumably activate the whole end-plate area were not depressed by H12-HTX to the same degree as extrinsic end-plate currents generated by ionophoresis of ACh at the same end-plate. 6. Brief (50 microsec) pulses of ACh produced brief end-plate potentials which were depressed by concentrations of H12-HTX that had little or no effect on miniature end-plate potentials. 7. Extrinsic responses to ACh at extrajunctional regions of denervated fibres were also depressed by low concentrations of H12-HTX. 8. It was concluded that the differential effects of H12-HTX on intrinsic and extrinsic end-plate responses could be due to the existence of two populations of receptor-channel complexes or to protection of local receptor-channel complexes from the toxin by a substance secreted from motor nerve terminals.

Acetylcholine↗
PubMed1977

Perhydrohistrionicotoxin: a potential ligand for the ion conductance modulator of the acetylcholine receptor.

Histrionicotoxin from the Colombian frog Dendrobates histrionicus and its perhydro derivative reversibly block the acetylcholine-sensitive ion conductance system in frog neuromuscular preparations. The perhydro derivative and [3H]perhydrohistrionicotoxin, like histrionicotoxin, caused a significant decrease in the peak amplitude of the end-plate current and shortened its rise time and half-decay time. In membrane preparations from Torpedo electroplax, [3H]perhydrohistrionicotoxin bound reversibly to a limited number of high-affinity sites [dissociation constant, (KD) = 0.4 micronM]. The ratio of perhydrohistrionicotoxin to acetylcholine binding sites in these membrane preparations approached 2. Histrionicotoxins, local anesthetics, and certain cholinergic agonists inhibited binding of perhydrohistrionicotoxin. Binding of perhydrohistrionicotoxin to membranes was decreased by heat or treatment with proteases. Treatment of membranes with Triton X-100 solubilized acetylcholine binding proteins and apparently also perhydrohistrionicotoxin-binding proteins. However, the detergent Triton X-100 also bound [3H]perhydrohistrionicotoxin. This nonspecific binding was not saturable and complicated studies on the antagonism by drugs of binding of [3H]perhydrohistrionicotoxin. In solubilized preparations the binding protein for acetylcholine could be removed by affinity chromatography or immunoprecipitation without affecting binding of perhydrohistrionicotoxin. Sephadex chromatography also separated acetylcholine- from perhydrohistrionicotoxin-binding proteins. Perhydrohistrionicotoxin did not bind significantly to purified acetylcholine-receptor protein but presumably bound to an ion conductance modulator protein that was associated with the acetylcholine-receptor in intact membrane and readily separable from the receptor protein after solubilization.

Amphibian Venoms↗
PubMedDate not supplied

Mechanisms of hexamethonium-induced tetanic fade in the isolated rat muscle.

The action of hexamethonium on neuromuscular transmission was investigated on the rat extensor digitorum longus muscle in vitro. Hexamethonium (5 x 10(-4) M) induced a complete fade of the tetanic contraction while leaving the twitch unaffected. At the same concentration, hexamethonium induced a significant decrease in the amplitude of the endplate potentials evoked at 50 and 100 Hz. Additionally, hexamethonium (5 x 10(-4) M) significantly increased the tetanic rundown of the endplate potential trains evoked at 100 Hz. The former effect was mainly the result of a frequency-independent decrease in the quantal size of the endplate potentials. This decrease seemed to be due to a postsynaptic blocking action of hexamethonium. The increase in tetanic rundown was due to a presynaptic action of hexamethonium. Such an action led to a frequency-dependent decrease in the quantal release of transmitter during repetitive stimulation of the motor nerve. It is concluded that both pre- and postsynaptic actions are necessary for hexamethonium to induce tetanic fade without affecting the twitch; and that, if it is accepted that the presynaptic action of hexamethonium is exerted on presynaptic receptors, these are not of the ganglionic type since the presynaptic effect of hexamethonium was less pronounced than the postsynaptic one.

Animals↗