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R W Meech

Publications and source records attributed to R W Meech.

33 records · Page 2Linked to original sources
PubMed1979

Light induced changes of internal pH in a barnacle photoreceptor and the effect of internal pH on the receptor potential.

1. Intracellular pH (pH1) was measured in Balanus photoreceptors using pH-sensitive glass micro-electrodes. The average pH1 of twelve photoreceptors which had been dark adapted for at least 30 min was 7.3 +/- 0.07 (S.D.). 2. Illumination reduced the recorded pH1 by as much as 0.2 pH unit. The change in pH1 was graded with light intensity. 3. When the cells were exposed to CO2 in the dark, pH1 declined monophasically. Saline equilibrated with 2% CO2; 98% O2 produced a steady reduction in pH1 of about 0.25 unit in 2--3 min. The buffering capacity of the receptor cell cytoplasm calculated from such experiments is approximately 15 slykes. 4. In the presence of HCO3-1, CO2 saline produced smaller, biphasic changes in pH1. 5. The membrane depolarization produced by a bright flash (depolarizing receptor potential) was reversibly reduced in the presence of external CO2 or by injection of H+. Iontophoretic injection of HCO2- increased the amplitude of the receptor potential. 6. In individual cells there was a close correlation between the amplitude of the receptor potential and pH1. 7. Saline equilibrated with CO2 reduced the light induced current (recorded under voltage-clamp) by 40--50% without affecting its reversal potential. 8. Exposure of the receptor to 95% CO2 saline for several minutes (pH0 5.5) not only abolished the receptor potential but also reversibly decreased the K conductance of the membrane in the dark. These effects were not reproduced by pH0 5.5 buffered saline or by a 5 min exposure to saline equilibrated with N2. 9. It is suggested that changes in pH1 induced by light modulate the sensitivity of the receptor under physiological conditions.

Animals↗
PubMed1979

Membrane potential oscillations in molluscan "burster" neurones.

Membrane potential oscillations can be induced in molluscan neurones under a variety of artificial conditions. In the so-called 'burster' neurones oscillations are generated even in isolated cells. A likely mechanism for 'bursting' involves the following ionic currents: 1. A transient inward current carried by Na+ and Ca2+. This current is responsible for the upstroke of the action potentials. 2. A delayed outward current carried by K+. This current is voltage-sensitive and is responsible for the downstroke of the action potential during the early part of the burst. It becomes progressively inactivated during the burst. Its amplitude depends on the intracellular pH. 3. A rapidly developing outward current carried by K+ which is inactivated at potentials close to action potential threshold. This current tends to hold the membrane in the hyperpolarized state and is involved in spacing the action potentials. 4. A prolonged inward current which may not inactivate. It is probably carried by both Na+ and Ca2+. This current is responsible for the depolarizing phase of the burst but also contributes to the action potential. 5. A slowly developing outward current, carried by K+. This current appears as a result of a slow increase in intracellular ionized calcium and is responsible for the hyperpolarizing phase of the burst. Note that a transient increase in this current may also contribute to the falling phase of the action potential during the later stages of the burst. It is also sensitive to intracellular pH. One of the more significant features of this system of producing membrane potential oscillations is that the frequency of the bursts depends on the rate at which the intracellular ionized calcium returns to its resting level. This process depends on the metabolic state of the animal which can thereby exert a considerable influence on the electrical activity of burster neurones.

Animals↗
PubMed1977

The effect of calcium injection on the intracellular sodium and pH of snail neurones.

1. Ion-sensitive glass micro-electrodes were used to measure the intracellular pH (pHi) and the intracellular sodium ion concentration, [Na+]i, in identified Helix aspersa neurones. 2. The injection of small volumes of 0-1 McaCl2, which increased the membrane potential by 10-15 mV for 1-2 min, had little or no effect on [Na+]i. Increases of up to 1 mM in [Na+]i could be reversibly induced by larger injections. 3. Calcium injection caused an immediate decrease in pHi, which appeared to be directly proportional to the amount of calcium injected. Injections causing hyperpolarizations of 10-20 mV which recovered in 2-5 min caused pHi decreases of 0-04-0-15 units. After each of these injections both pHi and the membrane potential recovered exponentially but with different time constants. 4. The injection of calcium at a low rate could decrease pHi without affecting the membrane potential. 5. Neither membrane potential nor pHi were affected by the injection of small volumes of 0-1 M-MgCl2, Injection of CoCl2 produced a large transient decrease in pHi but no significant change in membrane potential. 6. Exposure of the cell to saline equilibrated with 2-5% CO2 greatly reduced the pHi decrease caused by calcium injection but had only small effects on the membrane potential response. 7. It is concluded that most of the injected calcium is exchanged for protons inside the cell.

Animals↗
PubMed1975

Potassium activation in Helix aspersa neurones under voltage clamp: a component mediated by calcium influx.

1. Helix aspersa neurones under voltage clamp generate prolonged outward currents (potassium currents) in response to depolarizing command pulses. 2. The potassium currents recorded from cell A were reversibly reduced 25-50% by 10 mM cobalt ions in the bathing medium; 1 mM lanthanum, 10(-6) g/ml. D-600 and 10(-6) g/ml. iproveratril had similar effects but were only partially reversible. 3. The relationship between the potassium currents and the membrane potential had an "n" shape in normal saline. In calcium-free saline (containing 25 mM magnesium) the potassium currents were reduced and the "n" shape was abolished. The effect of calcium-free saline was readily reversible. 4. The voltage-dependence of the calcium-sensitive potassium currents was similar to that of the "late" calcium channel in squid axons (Baker, Hodgkin & Ridgway, 1971). 5. When cell A was depolarents were made up of two exponentially declining components. The slower of the two components was reduced in calcium-free saline. 6. When cell A was depolarized by 150 mV for 10 msec and then repolarized the "tail" currents were made up of a single rapidly declining component. The reversal potential of this component changed by 58 mV for a tenfold change in the external potassium concentration as predicted by the Nernst equation. 7. The reversal potential of "tail" currents having both components was less sensitive to changes in the external potassium concentration. 8. Tetraethylammonium (TEA) ions blocked both calcium dependent and voltage sensitive potassium currents. Each receptor was found to bind a single molecule of TEA. The dissociaton constant was about 10 mM in each case. 9. The intracellular concentration of ionized calcium was estimated from the potential at which there was no apparent calcium influx (the null point). It was between 3 x 10(-8) M and 8 x 10(-8) M with 10(-2) M calcium in the bathing medium. 10. The null point changed 30 mV for a tenfold change in the external calcium concentration as predicted by the Nernst equation. 11. It is concluded that depolarization of Helix neurones activates two typesof potassium channel. One channel is voltage dependent and highly selective for potassium. Activation of the other channel is dependent on the influx (or injection, see Meech, 1972, 1974a) of calcium. This calcium mediated potassium activation system saturates at high external calcium concentrations and is inhibited by external magnesium ions.

Animals↗
PubMed1974

The sensitivity of Helix aspersa neurones to injected calcium ions.

1. When calcium chloride was injected into Helix aspersa neurones there was a fall in membrane resistance and the membrane potential became hyperpolarized.2. The reversal potential of the response was dependent on the concentration of potassium in the external solution.3. Injection of a calcium-EGTA buffer containing 9 x 10(-7)M free calcium reduced the membrane resistance by 25%. When calcium chloride was injected it was necessary to increase the total intracellular calcium concentration by about 10(-3)M to produce similar change of resistance.4. In sodium-free (Tris) solution there was a slow fall of membrane resistance as if the intracellular calcium concentration had increased. There was a similar resistance change in the presence of 2,4-dinitrophenol and iodoacetate.5. A series of repetitive depolarizing pulses produced a long lasting reduction in membrane resistance which was enhanced by 2,4-dinitrophenol and iodoacetate.6. It is concluded that (a) injection of calcium causes an increase in potassium permeability, (b) the injected calcium is rapidly pumped from the cytoplasm by a sodium-dependent mechanism and by mitochondria, and (c) 1-2 msec depolarizing pulses stimulate an influx of calcium. This influx is rapid enough to trigger potassium activation during an action potential.

Action Potentials↗
PubMed1969

Current-voltage relations during illumination: photoreceptor membrane of a barnacle.

In voltage clamped photoreceptor cells of the barnacle, light-induced membrane current varied nonlinearly with membrane potential and changed sign at about + 27 millivolts (reversal potential) independently of light intensity. Instantaneous current-voltage relations were linear and intersected the voltage axis at the reversal potential. Illumination increased membrane conductance that was dependent on membrane potential, light intensity, and time.

Animals↗
PubMedDate not supplied

Separate sodium and calcium spikes in the same axon.

Aglantha digitale is a jellyfish (order Hydromedusae) capable of two distinct kinds of locomotion; 'slow' swimming which is generated endogenously and is used in fishing behaviour, and 'fast' swimming which is evoked by predators and serves for escape. Both forms of swimming are produced by contraction of the bell-shaped body wall and expulsion of a jet of water from an opening at the base of the animal. During slow swimming, the contractions are weak and the animal moves about 15 mm, roughly one body length, but during a fast swim there is a more violent contraction which can propel the animal five times as far. Both forms of contraction depend on impulses in the eight giant motor axons that synapse directly with the muscle sheet making up the inner surface of the body wall. We report here that the giant motor axons are able to mediate both kinds of activity because they can conduct two different sorts of impulse. Fast swimming requires a rapidly conducted Na+-dependent action potential whereas slow swimming depends on a low amplitude Ca2+ 'spike'. This is the first report of an axon capable of two kinds of impulse propagation and it provides a physiological function for low potential Ca2+ activation.

Action Potentials↗
PubMedDate not supplied

Ionic basis of membrane potential in outer hair cells of guinea pig cochlea.

Mammalian hearing involves features not found in other species, for example, the separation of sound frequencies depends on an active control of the cochlear mechanics. The force-generating component in the cochlea is likely to be the outer hair cell (OHC), one of the two types of sensory cell through which current is gated by mechano-electrical transducer channels sited on the apical surface. Outer hair cells isolated in vitro have been shown to be motile and capable of generating forces at acoustic frequencies. The OHC membrane is not, however, electrically tuned, as found in lower vertebrates. Here we describe how the OHC resting potential is determined by a Ca2+-activated K+ conductance at the base of the cell. Two channel types with unitary sizes of 240 and 45 pS underlie this Ca2+-activated K+ conductance and we suggest that their activity is determined by a Ca2+ influx through the apical transducer channel, as demonstrated in other hair cells. This coupled system simultaneously explains the large OHC resting potentials observed in vivo and indicates how the current gated by the transducer may be maximized to generate the forces required in cochlear micromechanics.

Animals↗