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Biomedical subjects

M V Lo

Publications and source records attributed to M V Lo.

9 recordsLinked to original sources
PubMed1987

Cholinergic regulation of impulse frequency in peripheral nerve.

Previous studies have demonstrated the existence of receptors for gamma-aminobutyric acid (GABA), beta-adrenergic catecholamines and acetylcholine in vertebrate peripheral nerve, and provided functional correlates for activation of both GABA and beta-adrenergic receptors. The present studies show that a cholinergic receptor present on the nerve can also modify impulse pattern. In frog sciatic nerve, both carbamylcholine and dibutyryl cyclic GMP increased the amplitude of the response to the second stimulus of a train at very short interstimulus intervals. The effect of carbamylcholine was blocked by 4-aminopyridine. The results are consistent with the hypothesis that cholinergic agonists mediate an increase in endogenous cyclic guanosine monophosphate (cGMP), which increases the ability of the nerve to follow closely spaced stimuli by inhibiting potassium channels.

Action Potentials↗
PubMed1983

The periaxonal space of crayfish giant axons.

The influence of the glial cell layer on effective external ion concentrations has been studied in crayfish giant axons. Excess K ions accumulate in the periaxonal space during outward K+ current flow, but at a rate far below that expected from the total ionic flux and the measured thickness of the space. At the conclusion of outward current flow, the external K+ concentration returns to normal in an exponential fashion, with a time constant of approximately 2 ms. This process is about 25 times faster than is the case in squid axons. K+ repolarization (tail) currents are generally biphasic at potentials below about -40 mV and pass through a maximum before approaching a final asymptotic level. The initial rapid phase may in part reflect depletion of excess K+. After block of inactivation and reversal of the Na+ concentration gradient, we could demonstrate accumulation and washout of excess Na ions in the periaxonal space. Characteristics of these processes appeared similar to those of K+. Crayfish glial cell ultrastructure has been examined both in thin sections and after freeze fracture. Layers of connective tissue and extracellular fluid alternate with thin layers of glial cytoplasm. A membranous tubular lattice, spanning the innermost glial layers, may provide a pathway allowing rapid diffusion of excess ions from the axon surface.

Action Potentials↗
PubMed1982

Freeze-fracture study of the Drosophila photoreceptor membrane: mutations affecting membrane particle density.

The photoreceptor membrane of Drosophila melanogaster (wild type, vitamin A-deprived wild type, and the mutants ninaAP228, ninaBP315, and oraJK84) was studied by freeze-fracture electron microscopy. The three mutations caused a decrease in the number of particles on the protoplasmic face of the rhabdomeric membrane. The ninaAP228 mutation affected only the peripheral photoreceptors (R1-6), while the ninaBP315 mutation affected both the peripheral (R1-6) and the central photoreceptors (R7). The oraJK84 mutation, which essentially eliminates R1-6 rhabdomeres, was found to drastically deplete the membrane particles in the vestigial R1-6 rhabdomeres but not in the normal rhabdomeres of R7 photoreceptors, suggesting that the failure of the oraJK84 mutant to form normal R1-6 rhabdomeres may be due to a defect in a major R1-6 photoreceptor-specific protein in the mutant. In all cases in which both the rhabdomeric particle density and rhodopsin content were studied, the mutations or vitamin A deprivation was found to reduce both these quantities, supporting the idea that at least the majority of the rhabdomeric membrane particles are closely associated with rhodopsin. Vitamin A deprivation and the mutations also reduced the number of particles in the plasma membrane as in the rhabdomeric membrane, suggesting that both classes of membrane contain rhodopsin.

Animals↗
PubMed1981

Block and inactivation of sodium channels in nerve by amino acid derivatives. I. Dependence on voltage and sodium concentration.

The side chain of arginine, n-propylguanidinium (nPG), reversibly decreases peak sodium conductance and increases the speed of sodium current decay, when perfused internally. Effects are voltage dependent and are more pronounced at high depolarizations. Results are also dependent on the sodium concentration gradient. Both the decline in peak conductance and the speeding of inactivation are greater if the sodium concentration gradient is reversed from the normal. The decrease in peak sodium current is too large to be due solely to the faster decay kinetics. The difference is not due to a change in slow inactivation of the channel. Sodium current inactivation has also been studied with a double pulse procedure. Results show that at - 70 mV, nPG leaves sodium channels rapidly (less than 500 microseconds) in normal sodium gradient, but more slowly (greater than 1 ms) in reversed sodium gradient. Several structural analogs of nPG have been tested. Shortening the alkyl chain weakens effects significantly. Arginine itself, which contains extra charged groups, is also less effective. n-Propylammonium is active but with an apparent affinity only one-fifth that of arginine. We conclude that nPG acts within the sodium channel, and has at least two modes of action.

Animals↗
PubMed1981

Block and inactivation of sodium channels in nerve by amino acid derivatives. II. Dependence on temperature and drug concentration.

The interaction of n-propylguanidinium (nPG) with sodium channels has been further characterized. From experiments at varying temperatures, the Q10 for the sodium current decay time constant in the two [Na+] gradients is 2.6-2.9 independent of drug. Testing several nPG concentrations we find that peak sodium current declines sharply with [nPG] at all levels, but the decay time constant approaches an asymptote above 4 mM. No "hooks" in sodium tail currents are seen. If the sodium current is allowed to decay completely before repolarization no tail current is observed. We have developed a kinetic model in which nPG acts at a single site within the sodium channel. Reaction of nPG with its receptor requires two steps. Fitting the temperature data shows that the first step involves diffusion of the drug to the site and close association with it. The second step may include molecular reorganization of the complex. The rate constants for the reaction are all simple exponential functions of voltage. Using them, the model successfully predicts decay time constants and peak currents, and their dependence on potential, [Na+] gradient, temperature, and nPG concentration. The results are consistent with the idea that an arginine residue may be closely associated with inactivation.

Animals↗
PubMed1981

Light-induced pigment granule migration in the retinular cells of Drosophila melanogaster. Comparison of wild type with ERG-defective mutants.

The dependence of pigment granule migration (PGM) upon the receptor potential was examined using several strains of electroretinogram (ERG)-defective mutants of Drosophila melanogaster. The mutants that have a defective lamina component but a normal receptor component of the ERG (no on-transient A [nonA] and tan) exhibited normal pigment granule migration. The mutants that have very small or no receptor potentials (certain no receptor potential A [norpA] alleles), on the other hand, exhibited no PGM. In the case of the temperature-sensitive norpA mutant, norpAH52, normal PGM was present at 17 degrees but not at 32 degrees C or above, corresponding to its electrophysiological phenotype. In the transient receptor potential (trp) mutant, whose receptor potential decays to the baseline within a few seconds during a sustained light stimulus, the pigment granules initially moved close to the rhabdomere when light was turned on but moved away after about 5 s during a sustained light stimulus. All these results lend strong support to the notion that PGM is initiated by a light-evoked depolarization of the receptor membrane, i.e., the receptor potential. However, under certain experimental conditions, the receptor potentials failed to induce PGM in the trp mutant. The depolarization of the receptor, thus, appears to be closely associated with PGM but is not a sufficient condition for PGM.

Animals↗