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R W Meech

Publications and source records attributed to R W Meech.

At least 19 recordsLinked to original sources
PubMed2000

Potassium inhibition of sodium-activated potassium (K(Na)) channels in guinea-pig ventricular myocytes.

N(a+)-activated potassium channels (K(Na) channels) were studied in inside-out patches from guinea-pig ventricular myocytes at potentials between -100 and +80 mV. External K(+) (K(+)(o)) was set to 140 mM. For inwardly directed currents with 105 mM internal K(+) (K(+)(1)), the unitary current-voltage relationship was fitted by the constant field equation with a potassium permeability coefficient, P(K), of 3.72 x 10(-13) cm(3) s(-1). The slope conductance (-100 to -10 mV) was 194 +/- 4.5 pS (mean +/- s.d., n = 4) with 105 mM K(+)(i) (35 mM Na(+)(i)) but it decreased to 181 +/- 5.6 pS (n = 5) in 70 mM K(+)(i) (70 mM Na(+)(i)). K(Na) channels were activated by internal Na(+) in a concentration-dependent fashion. With 4 mM K(+)(i), maximal activation was recorded with 100 mM Na(+)(i) (open probability, P(o), about 0.78); half-maximal activation required about 35 mM Na(+)(i). When K(+)(i) was increased to 70 mM, half-maximal activation shifted to about 70 mM Na(+)(i). With Na(+)(i) set to 105 mM, channel activity was markedly inhibited when K(+)(i) was increased from 35 to 105 mM. Channel openings were abolished with 210 mM K(+)(i). The inhibitory effect of internal K(+) was also observed at more physiological conditions of osmolarity, ionic strength and chloride concentration. With 35 mM Na(+)(i) and 4 mM K(+)(i), P(o) was 0.48 +/- 0.10 (n = 6); when K(+)(i)was increased to 35 mM, P(o) was reduced to 0.04 +/- 0.05 (n = 7, P < 0.001). The relationship between P(o) and Na(+)(i) concentration at different levels of K(+)(i) is well described by a modified Michaelis-Menten equation for competitive inhibition; the Hill coefficients were 4 for the P(o)-Na(+)(i) relationship and 1.2 for the P(o)-K(+)(i) relationship. It is suggested that Na(+) and K(+) compete for a superficial site on the channel's permeation pathway. K(Na) channels would be most likely to be activated in vivo when an increase in Na(+)(i) is accompanied by a decrease of K(+)(i).

Adenosine Triphosphate↗
PubMed2000

Central circuitry in the jellyfish Aglantha digitale. III. The rootlet and pacemaker systems.

Tactile stimulation of the subumbrella of Aglantha digitale was found to evoke an escape swimming response similar to that evoked by stimulation of the outer surfaces of the margin but that does not involve the ring giant axon. Evidence is presented that conduction around the margin takes place via an interconnected system of rootlet interneurones. Confocal microscopy of carboxyfluorescein-filled axons showed that the rootlet neurones run out from the bases of the motor giant axons within the inner nerve ring and come into close contact with those of the neighbouring motor giant axons on either side. Transmission between the rootlet neurones has the properties of chemical synaptic transmission. A distinct type of fast excitatory postsynaptic potential (rootlet PSP) was recorded in motor giant axons following stimulation of nearby axons in 3-5 mmol l(-)(1) Mn(2+), which lowered the PSP below spike threshold. Immune labelling with anti-syntaxin 1 showed structures tentatively identified as synapses in the inner nerve ring, including some on the rootlet neurones. Neuromuscular junctions were not labelled. A secondary consequence of stimulating motor giant axons was the triggering of events in the pacemaker system. Triggering was blocked in 105 mmol l(-)(1) Mg(2+), indicating a synaptic link. Activity in the pacemaker system led indirectly to tentacle contractions (as described in earlier papers in this series), but the contractions were not as sudden or as violent as those seen when escape swimming was mediated by the ring giant axon. Events triggered in the pacemaker system fed back into the motor giants, producing postsynaptic potentials that appeared as humps in the spike after-potential. The conduction velocity of events propagating in the relay system was increased when the rootlet pathway was simultaneously excited (piggyback effect). With the addition of the rootlet pathway, the number of identified systems concerned with locomotion, feeding and tentacle contractions comes to fourteen, and the list is probably nearly complete.

Animals↗
PubMed1999

Evidence that the product of the human X-linked CGD gene, gp91-phox, is a voltage-gated H(+) pathway.

Expression of gp91-phox in Chinese hamster ovary (CHO91) cells is correlated with the presence of a voltage-gated H(+) conductance. As one component of NADPH oxidase in neutrophils, gp91-phox is responsible for catalyzing the production of superoxide (O(2).(2)). Suspensions of CHO91 cells exhibit arachidonate-activatable H(+) fluxes (Henderson, L.M., G. Banting, and J.B. Chappell. 1995. J. Biol. Chem. 270:5909-5916) and we now characterize the electrical properties of the pathway. Voltage-gated currents were recorded from CHO91 cells using the whole-cell configuration of the patch-clamp technique under conditions designed to exclude a contribution from ions other than H(+). As in other voltage-gated proton currents (Byerly, L., R. Meech, and W. Moody. 1984. J. Physiol. 351:199-216; DeCoursey, T.E., and V.V. Cherny. 1993. Biophys. J. 65:1590-1598), a lowered external pH (pH(o)) shifted activation to more positive voltages and caused the tail current reversal potential to shift in the manner predicted by the Nernst equation. The outward currents were also reversibly inhibited by 200 microM zinc. Voltage-gated currents were not present immediately upon perforating the cell membrane, but showed a progressive increase over the first 10-20 min of the recording period. This time course was consistent with a gradual shift in activation to more negative potentials as the pipette solution, pH 6.5, equilibrated with the cell contents (reported by Lucifer yellow included in the patch pipette). Use of the pH-sensitive dye 2'7' bis-(2-carboxyethyl)-5(and 6) carboxyfluorescein (BCECF) suggested that the final intracellular pH (pH(i)) was approximately 6.9, as though pH(i) was largely determined by endogenous cellular regulation. Arachidonate (20 microM) increased the amplitude of the currents by shifting activation to more negative voltages and by increasing the maximally available conductance. Changes in external Cl(-) concentration had no effect on either the time scale or the appearance of the currents. Examination of whole cell currents from cells expressing mutated versions of gp91-phox suggest that: (a) voltage as well as arachidonate sensitivity was retained by cells with only the NH(2)-terminal 230 amino acids, (b) histidine residues at positions 111, 115, and 119 on a putative membrane-spanning helical region of the protein contribute to H(+) permeation, (c) histidine residues at positions 111 and 119 may contribute to voltage gating, (d) the histidine residue at position 115 is functionally important for H(+) selectivity. Mechanisms of H(+) permeation through gp91-phox include the possible protonation/deprotonation of His-115 as it is exposed alternatively to the interior and exterior faces of the cell membrane (see Starace, D.M., E. Stefani, and F. Bezanilla. 1997. Neuron. 19:1319-1327) and the transfer of protons across an "H-X-X-X-H-X-X-X-H" motif lining a conducting pore.

Animals↗
PubMed1999

Impulse conduction in a sponge.

All-or-none propagated electrical impulses were recorded from the hexactinellid sponge Rhabdocalyptus dawsoni using suction electrodes attached to lumps of aggregated sponge tissue grafted onto the surface of pieces of the same sponge. Impulses were normally evoked by means of externally applied electrical shocks. Recorded externally using an a.c.-coupled amplifier, the electrical event was triphasic and lasted approximately 30 s; integration gave a diphasic waveform. A further integration to give the form of the membrane action potential produced a monophasic signal. Impulses propagated at 0.27+/-0.1 cm s-1 with an absolute refractory period of 29 s and a relative refractory period of approximately 150 s. Concurrent thermistor flow meter recordings confirmed that water flow through the sponge was arrested following the passage of an impulse, presumably as result of the cessation of beating of the flagella in the flagellated chambers. Tactile stimuli also evoked impulses, as did addition of particulate material to the incoming water stream. Impulses continued to propagate through the sponge during arrests, indicating that the conduction and effector systems were independent. Sponges lack nerves, and a variety of evidence indicates that the conducting tissues are the syncytial trabecular reticulum and pinacoderm layers. Na+-deficient solutions had little effect on the action potential, but propagation was blocked by 10 mmol l-1 Co2+, 1 mmol l-1 Mn2+ or 24 micromol l-1 nimodipine. Tetraethylammonium ions at 1-5 mmol l-1 also blocked propagation without prolonging the action potential. Impulse conduction in the sponge is discussed in relation to excitability and conduction in the protozoa and in plants and to non-nervous conduction in more advanced animals.

Journal Article↗
PubMed1998

The effect of polyamines on KATP channels in guinea-pig ventricular myocytes.

1. The effect of natural polyamines on KATP channels was studied using inside-out patches from guinea-pig ventricular myocytes. 2. At a holding potential of +40 mV, spermine at the intracellular membrane surface reduced the KATP channel open probability (Popen) in a dose-dependent manner. Half-maximal inhibition occurred at 29 microM with a Hill coefficient of 1.2. 3. The effect of spermine on Popen was not greatly influenced by the membrane potential but there appeared to be a small reduction in unitary current amplitude during strong depolarizations. 4. Analysis of KATP single channel kinetics showed that spermine inhibited the channel by decreasing the mean open time and introducing transitions to a long closed state. 5. Spermidine (0.1 mM) was found to have a similar effect to spermine. Putrescine (10 mM) was found to block more effectively at positive membrane potentials. Up to 20 mM arginine had no significant effect on KATP channels. 6. Our results indicate that natural polyamines influence native KATP channel gating in cardiac myocytes.

Adenosine Triphosphate↗
PubMed1995

Synaptic potentials and threshold currents underlying spike production in motor giant axons of Aglantha digitale.

1. Motor giant axons that excite swimming muscles in the jelly-fish Aglantha digitale interface with units of the inner and outer nerve rings in the margin at the base of the bell. External recording electrodes were used to monitor electrical activity at different sites within the nerve ring while events in the motor giant axon were recorded with intracellular micropipettes placed within 100 microns of the synaptic area. In some experiments, 4- to 6-micron-diam patch pipettes were used to record in situ from ion channel clusters at different locations along the axon. 2. Independently propagating calcium and sodium spikes in the motor giant axon were found to arise from different excitatory postsynaptic potentials (EPSPs). Two separate inputs were identified; one EPSP class represented an input from the pacemaker system in the inner nerve ring, whereas another represented an input from the giant axon in the outer nerve ring. EPSPs from the two nerve rings had significantly different time courses and amplitudes. EPSPs from the ring giant axon reached a peak in little more than 1 ms, whereas EPSPs from the pacemaker system reached a maximum in approximately 7 ms. These slower EPSPs may be compound events composed of postsynaptic potentials from multiple synapses excited in series by the passage of the pacemaker neuron signal. 3. The threshold for the production of calcium spikes by the slow EPSPs of the pacemaker system (-51 +/- 2.2 mV, mean +/- SD; n = 5) corresponded well with the voltage at which a net inward "T"-type calcium current first appeared in recordings from axon membrane patches (-55 to -50 mV); the threshold for the initiation of the sodium spike by the fast EPSPs of the ring giant system (-32 +/- 1.2 mV, mean +/- SD; n = 6) corresponded well with the voltage at which a net inward sodium current first appeared (-35 to -30 mV). 4. Inward currents were rarely observed in membrane patches formed using pipettes with tips of < 1 micron OD. Even with 4-micron pipettes, patches of membrane were sometimes obtained with a channel population consisting exclusively of potassium channels; calcium and sodium currents were found in highly discrete areas ("hot spots"). Preliminary findings on the undersurface of the axon, which makes synaptic contact with the myoepithelium, are consistent with a similar distribution. 5. The pathway by which the ring giant excites the motor giant axon is not definitely known. The synaptic delay between the peak of the ring giant action potential (monitored externally) and the initial rise of the fast EPSP (1.64 +/- 0.15 ms, mean +/- SD; n = 21) would allow for transmission at two synapses, because single synaptic delays at neuromuscular junctions in Aglantha are approximately 0.7 ms at 12 degrees C. The mean synaptic delay at the slow EPSP synapse was 0.88 +/- 0.09 (SD) ms (n = 12). 6. The delay between the impulse in the ring giant axon and the subsequent excitation of the motor giant axon may permit the animal to withdraw its tentacles and so lower the drag that would otherwise reduce the effectiveness of any escape swim and might induce tentacle autotomy.

Action Potentials↗
PubMed1993

Ionic currents in giant motor axons of the jellyfish, Aglantha digitale.

1. In the motor system of the jellyfish, Aglantha digitale, there are eight giant axons connected by chemical synapses to a muscle epithelium. The simplicity of this structure makes it possible to assess the contribution of different ion conductances in the axon membrane to the two forms of swimming that provide the behavioral output of the system. In situ recordings from large clusters of ion channels provide a means of studying these membrane conductances in isolation so that the features that permit them to perform their behavioral function may be identified. 2. In Aglantha motor axons, low-amplitude, low-threshold spikes are associated with slow swimming, whereas escape swimming depends on a higher-threshold, overshooting action potential. The action potential was abolished by a sodium-free (choline-containing) bathing medium but was resistant to tetrodotoxin (0.09 mM; 3 x 10(-5) g/ml). It was prolonged by tetraethylammonium (TEA) ions (50 mM) but little affected by changes in holding potential in the range of -51 to -82 mV. The low-threshold spikes were unaffected by sodium-free saline containing TEA (30 mM). They were inactivated by holding the membrane potential at -51 mV. Average axon resting potentials were -63 +/- 6 (SD) mV (n = 17). 3. Shortened axons studied with the two-electrode voltage-clamp technique had a transient inward current with a low threshold for activation (about -60 mV). The inward current was fully inactivated at -51 mV; it was present in sodium-free saline and abolished by Mg2+ (120 mM) just like the low-threshold spike. 4. Calcium-dependent low-threshold spikes and sodium action potentials coexist in the same axons but may be elicited separately because an outward current limits the peak of the low-threshold spike to a level below the threshold of the action potential (about -20 mV). 5. Analysis of ensemble currents showed that axon-attached membrane patches contained clusters of different voltage-dependent potassium channels. Three channel classes were distinguished by prepulse inactivation experiments. All three channels were found to inactivate, but they had different voltage-dependencies and different inactivation kinetics (fast, intermediate, or slow). Recovery from inactivation was slow in each case (time constant 2-10 s). 6. All axon-attached membrane patches were found to contain one or two of the three classes of potassium channel. Channels with intermediate kinetics were found less frequently and may have been present at lower density.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1993

Potassium channel family in giant motor axons of Aglantha digitale.

1. The simplicity of the jellyfish nervous system makes it an ideal preparation to assess the contributions of different ion channels to behavior. In the giant motor axons of the jellyfish Aglantha digitale, low-threshold spikes elicit slow swimming, whereas escape swimming depends on a higher-threshold, overshooting sodium-dependent action potential. At least three kinetically distinct transient potassium channels (fast, intermediate, and slow) are concerned with spike management in this preparation. 2. In situ recording with patch-clamp micropipettes from clusters of potassium channels provides a means of studying their properties in isolation. The three classes of ion channel were identified in ensemble current averages by their kinetics, their response to a conditioning prepulse and their voltage dependence. All three were highly selective for potassium, and the reversal potential of their unitary currents depended on the level of potassium used to fill the patch pipette. 3. A single potassium permeability coefficient (PK) calculated from the Goldman, Hodgkin, Katz "constant field" equation was used to fit unitary current data from all three channels in concentrations of external potassium < or = 500 mM. 4. Data from ensemble tail currents in seawater indicated that the sodium permeability coefficient (PNa) of channels with either intermediate or slow kinetics was < or = 0.015 PK; preliminary data from channels with fast kinetics suggested that they too had a PNa/PK selectivity of approximately 0.01. 5. We propose that spike management in the giant motor axons of Aglantha depends on three members of a family of potassium-selective ion channels that seem likely to be structurally related.

Animals↗
PubMed1988

Membrane currents that govern smooth muscle contraction in a ctenophore.

Ctenophores are transparent marine organisms that swim by means of beating cilia; they are the simplest animals with individual muscle fibres. Predatory species, such as Beroe ovata, have particularly well-developed muscles and are capable of an elaborate feeding response. When Beroe contacts its prey, the mouth opens, the body shortens, the pharynx expands, the prey is engulfed and the lips then close tightly. How this sequence, which lasts 1 s, is accomplished is unclear. The muscles concerned are structurally uniform and are innervated at each end by a neuronal nerve net with no centre for coordination. Isolated muscle cells studied under voltage-clamp provide a solution to this puzzle. We find that different groups of muscle cells have different time-dependent membrane currents. Because muscle contraction depends upon calcium entry during each action potential, these different currents produce different patterns of contraction. We conclude that in a simple animal such as a ctenophore, a sophisticated set of membrane conductances can compensate for the absence of an elaborate system of effectors.

4-Aminopyridine↗
PubMed1987

Voltage-dependent intracellular pH in Helix aspersa neurones.

1. The intracellular pH (pHi) of large nerve cells from the mollusc, Helix aspersa, was measured with pH-sensitive micro-electrodes. Cells were held under voltage clamp and the effect on pHi of different holding potentials was determined. 2. Depolarization of the cell from the resting potential (about -50 mV) to -10 mV produced a fall in pHi that could be reduced by bathing the cell in nominally Ca2+-free saline. 3. At positive holding potentials pHi increased to a steady level that depended upon the electrochemical gradient for H+ across the cell membrane; it shifted by about 1 unit when the external pH was increased from 7 to 8 (or when the membrane potential increased by 58 mV, Thomas & Meech, 1982). 4. The depolarization-induced increase in H+ permeability was insensitive to SITS (4-acetamido-4'-isothiocyanostilbene-2,2'-disulphonic acid, 20 microM), which blocks pHi regulation at the resting potential in these cells (Thomas, 1976). When pHi was displaced from a steady level by ionophoretic injection of HCl, there was a rapid recovery at depolarized potentials even in the presence of SITS. The H+ pathway appeared to be little affected by prolonged periods at positive membrane potentials. 5. The depolarization-induced H+ efflux was insensitive to the metabolic inhibitor CCmP (carbonyl cyanide-m-chlorophenylhydrazone, 20 microM) and persisted in cells bathed in pH-buffered n-methyl glucamine-gluconate. It was also insensitive to DCCD (N, N'-dicyclohexylcarbodiimide, 10-100 microM) and oligomycin (2-10 micrograms/ml). 6. The H+ pathway could be fully blocked by 1 mM-ZnCl2, 1 mM-LaCl3, 1 mM-CuCl2, 2 mM-CdCl2 or 10 mM-CoCl2. Other divalent ions such as BaCl2 (10 mM) produced a block at membrane potentials near 0 mV but the block was released at more positive potentials. Low levels of LaCl3 (0.1 mM), the organic Ca2+ channel antagonist D600 (100 mg/ml) and high levels of the K+ channel blocker TEA (50 mM) all had similar effects to Ba2+. 7. The K+ channel blocker 4-aminopyridine (10 mM), which blocks H+ currents in perfused Lymnaea neurones (Byerly, Meech & Moody, 1984), has a complex action.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗
PubMed1985

Neuromuscular transmission in the jellyfish Aglantha digitale.

In the jellyfish Aglantha digitale escape swimming is mediated by the nearly synchronous activity of eight giant motor axons which make direct synaptic contact with contractile myoepithelial cells on the under-surface of the body wall. The delay in transmission at these synapses was 0.7 +/- 0.1 ms (+/- S.D.;N = 6) at 12 degrees C as measured from intracellular records. Transmission depended on the presence of Ca2+ in the bathing medium. It was not blocked by increasing the level of Mg2+ to 127 mmol l-1. The myoepithelium is a thin sheet of electrically coupled cells and injection of current at one point was found to depolarize the surrounding cells. The potential change declined with distance from the current source as expected for two-dimensional current spread. The two-dimensional space constant (lambda) was 770 micron for current flow in the circular direction and 177 micron for radial flow. The internal resistance of the epithelium (178-201 omega cm) and the membrane time constant (5-10 ms) were direction independent. No propagated epithelial action potentials were observed. Spontaneous miniature synaptic potentials of similar amplitude and rise-time were recorded intracellularly at distances of up to 1 mm from the motor giant axon. Ultrastructural evidence confirms that neuro-myoepithelial synapses also occur away from the giant axons. It is likely that synaptic sites are widespread in the myoepithelium, probably associated with the lateral motor neurones as well as the giant axons. Local stimulation of lateral motor neurones generally produced contraction in distinct fields. We suppose that stimulation of a single motor giant axon excites a whole population of lateral motor neurones and hence a broad area of the myoepithelium.

Action Potentials↗
PubMed1982

Hydrogen ion currents and intracellular pH in depolarized voltage-clamped snail neurones.

Until now the only reported effect of depolarization on the intracellular pH (pHi) of excitable cells in an acidification of the cell cytoplasm. It seems unlikely that this could be a direct effect of membrane potential because pHi is known to be regulated by an electroneutral mechanism and in most cells H+ ions are not in equilibrium with the membrane potential (Em). In any case the membrane conductance to H+ ions would be expected to be small because they are at such low concentrations on either side of the cell membrane. But it is possible that the H+ ion permeability of the membrane increases on depolarization just like that of other ions in the bathing medium depolarization just like that of other ions in the bathing medium (Na+, K+ and Ca2+ for example). To test this idea we have made pHi measurements on molluscan neurones under voltage-clamp. Our findings, presented here, provide evidence for a large increase in H+ ion permeability in depolarized cells. We suggest that this increase in proton conductance may be the basis for the "nonspecific' currents previously described in perfused molluscan neurones and we assess the physiological significance of this newly discovered pathway.

Animals↗
PubMed1980

Giant smooth muscle cells of Beroë. Ultrastructure, innervation, and electrical properties.

Beroë muscle fibers are single cells which may be 20-40 micrometer in diameter in mature specimens. Longitudinal muscles may be 6 cm or more long. There is no striation pattern and the muscles were observed to contract in a tonic fashion when stretched. They are innervated by a nerve net, and external recording revealed what are probably nerve net impulses. Intracellular stimulation of the muscles themselves was found to initiate large propagating action potentials which were recorded intracellularly. The action potentials were insensitive to tetrodotoxin (10(-5) g/ml), tetraethylammonium ions (50 mM), MnCl2 (25 mM), and low concentrations of verapamil (2 X 10(-6) g/ml). Full-size action potentials were recorded in sodium- or calcium-deficient salines, but were small and graded in salines deficient in both sodium and calcium. Cable analysis yielded mean values for lambda (1.95 mm), Ri (154 omega cm), Rm (9,253 omega cm2), and tau m (13.9 ms). The conduction velocity depended primarily on fiber diameter and maximum rate of rise of the action potential and could be predicted from the theoretical analysis of Hunter et al. (1975 Prog. Biophys. Mol. Biol. 30: 99-144). The calculated membrane capacity (less than microF/cm2) indicates little infolding of the surface membrane, a conclusion which is in agreement with anatomical studies.

Animals↗
PubMed1980

Effect of measured calcium chloride injections on the membrane potential and internal pH of snail neurones.

1. Ion-sensitive micro-electrodes were used to measure changes in intracellular pH (pHi) and internal chloride which resulted from the pressure injection of calcium chloride into identified Helix aspersa neurones. The internal chloride measurement allowed the quantity of calcium chloride injected to be estimated. 2. Application of the metabolic inhibitor carbonyl cyanide m-chlorophenyl hydrazone (CCmP) to a calcium-loaded cell caused an increase in the membrane potential comparable to the effect of injecting calcium itself. The effect was not observed in normal cells. 3. When injected in the presence of CCmp, calcium caused a much larger and longer-lasting effect on the membrane potential than that observed in untreated cells. 4. The injection of ruthenium red can increase and/or prolong the hyperpolarization caused by a given quantity of injected calcium. The pHi changes following calcium injection were biphasic and slower than normal. 5. In seven experiments, both hydrogen chloride and calcium chloride were injected into the same cell. The relative changes in pHi corresponded to the production of one hydrogen ion for each calcium ion injected. 6. The relationship between the quantity of calcium injected and the size of the induced hyperpolarization suggested that at least three calcium ions acting cooperatively are required to activate a potassium 'channel'. 7. Injection of barium chloride hyperpolarized the membrane after a delay of about 1 min. After several injections of barium the cell lost this response while retaining its normal response to calcium injection. Injection of barium also caused a slowly developing (biphasic) fall in pHi. 8. We conclude that injected calcium is normally rapidly taken up by mitochondria in exchange for hydrogen ions. If this uptake process is blocked by ruthenium red or CCmP, the calcium is taken up by a second, slower, process which also releases hydrogen ions. When pre-loaded, but not otherwise, the mitochondria will release calcium ions on treatment with CCmP. Injection of barium does not directly affect the membrane conductance, but causes the release of calcium from intracellular binding sites.

Animals↗
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↗