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PubMed1991

Injection of RNA from carp retina induces the formation of a membrane potassium channel in Xenopus oocytes.

Total RNA was purified from freshly isolated retinas of adult carp and injected into oocytes of Xenopus laevis (stages 5-6). Two to six days after injection, depolarizing voltage-clamp steps evoked a slowly activated outward current as large as 3 microA. This current inactivated slowly with a single time constant (tau = 3.1 +/- 0.24 S.E.M., for Vm = +30 mV). The current was inhibited by tetraethylammonium (3.8 mM for half-maximal inhibition). In the presence of Co2+ (1 mM) or barium methanesulfonate (40 mM), the current-voltage relationship shifted to slightly more depolarized values (5-10 mV); the maximal value of the current that was sensitive to Co2+ or Ba2+ treatments was only a small fraction (about 10%) of the TEA-sensitive current, and its current-voltage relationship was similar to that for uninjected oocytes. The reversal potential of the membrane current was studied with [K+]0 of 1-77 mM. For [K+]0 greater than 20 mM, the reversal potential changed with a slope of 63 mV (+/- 2 mV S.E.M.) per 10-fold change in [K+]0. The conductance was induced half-maximally at 17 mV (+/- 0.9 mV S.E.M.). The depolarization required for an e-fold increase in conductance was 13 mV (+/- 0.6 mV S.E.M.). From these results, we conclude that the injection of total RNA from carp retinas induces the formation of a membrane K+ channel in Xenopus oocytes. The channel formed has many of the properties reported for the maintained outward current of goldfish horizontal and bipolar cells.

Animals↗
PubMed1978

Demineralization in organic solvents by alkylammonium salts of ethylenediaminetetra-acetic acid.

1. Insoluble salts of alklaine earth metals (e. g. calcium phosphate) dissolve in non-aqueous solvents containing EDTA salts of organic cations (e.g. tetraethylammonium). 2. Bone is efficiently demineralized in ethanolic trimethylammonium EDTA. Retention in the matrix of water-soluble materials (e.g. proteoglycan) is much better than in standard aqueous EDTA demineralization procedures.

Animals↗
PubMed1991

On the interaction of bovine pancreatic trypsin inhibitor with maxi Ca(2+)-activated K+ channels. A model system for analysis of peptide-induced subconductance states.

Bovine pancreatic trypsin inhibitor (BPTI) is a 58-residue basic peptide that is a representative member of a widely distributed class of serine protease inhibitors known as Kunitz inhibitors. BPTI is also homologous to dendrotoxin peptides from mamba snake venom that have been characterized as inhibitors of various types of voltage-dependent K+ channels. In this study we compared the effect of DTX-I, a dendrotoxin peptide, and BPTI on large conductance Ca(2+)-activated K+ channels from rat skeletal muscle using planar bilayer methodology. As previously found for DTX-I (1990. Neuron. 2:141-148), BPTI induces the appearance of distinct subconductance events when present on the internal side of maxi K(Ca) channels. The single channel kinetics of substate formation follow the predictions of reversible binding of the peptide to a single site or class of sites with a Kd of 4.6 microM at 0 mV and 50 mM symmetrical KCl. The apparent association rate of BPTI binding decreases approximately 1,000-fold per 10-fold increase in ionic strength, suggestive of a strong electrostatic interaction between the basic peptide and negative surface charge in the vicinity of the binding site. The equilibrium Kd for BPTI and DTX-I is also voltage dependent, decreasing e-fold per 30 mV of depolarization. The unitary subconductance current produced by BPTI binding exhibits strong inward rectification in the presence of symmetrical KCl, corresponding to 15% of open channel current at +60 mV and 70% of open state at -40 mV. In competition experiments, the internal pore-blocking ions, Ba2+ and TEA+, readily block the substate with the same affinity as that for blocking the normal open state. These results suggest that BPTI does not bind near the inner mouth of the channel so as to directly interfere with cation entry to the channel. Rather, the mechanism of substate production appears to involve a conformational change that affects the energetics of K+ permeation.

Amino Acid Sequence↗
PubMed1993

Giant GABAB-mediated synaptic potentials induced by zinc in the rat hippocampus: paradoxical effects of zinc on the GABAB receptor.

The interaction of zinc with pre- and postsynaptic GABAB receptors was studied in adult rat hippocampal slices using intracellular recording in CA1 and CA3 pyramidal neurons. Zinc (50-300 microM) antagonized baclofen responses with a variable potency, whereas CGP-35348 (100 microM) or barium (300 microM) produced a more substantial and consistent inhibition. Zinc also induced giant GABAA-mediated depolarizing potentials (GDP) in these neurons. After blocking GABAA and excitatory synaptic transmission, monosynaptic hyperpolarizing inhibitory postsynaptic potentials (IPSP) mediated by GABAB receptors (IPSPB) were inhibited by CGP-35348 or barium; however, zinc increased the latency and prolonged the duration of the IPSPB and also induced the appearance of spontaneous giant GABAB-mediated hyperpolarizing potentials (GHP). In some cells, IPSPBs in zinc exhibited a multiphasic appearance. The early component was partially inhibited by 300 microM zinc and was followed by a late GHP. CGP-35348 at 100 microM inhibited the early monosynaptic IPSPB but not the GHP; however, at 300 microM both components were blocked. Paired-pulse inhibition of the IPSPB was used to assess the effect of zinc on presynaptic GABAB receptors. Neither the zinc-chelating agent CP94 (400 microM) nor zinc affected this phenomenon. CGP-35348, barium and polyvalent cations, such as cadmium, copper, cobalt, manganese, iron and aluminum, failed to induce giant potentials in hippocampal neurons. It is concluded that zinc is apparently unique in synchronizing the release of GABA to produce GDPs and GHPs.

Animals↗
PubMed1971

The mechanism of acetylcholine release from parasympathetic nerves.

1. The output of acetylcholine from the plexus of the guinea-pig ileum longitudinal strip has been used to study the mechanism of acetylcholine release. From the effects of hexamethonium and tetrodotoxin, it was inferred that 60% of the normal resting output is due to propagated activity in the plexus, and 40% to spontaneous release. Tetrodotoxin virtually abolishes the increase in output in response to electrical stimulation.2. Resting acetylcholine output is increased when the bathing medium is changed in the following ways:(a) sodium replacement by sucrose, trometamol or lithium;(b) addition of ouabain or p-hydroxymercuribenzoate (PHMB), or withdrawal of potassium;(c) the combination of PHMB and partial sodium replacement;(d) addition of potassium; this increase in output becomes greater in the absence of sodium.3. The resting output is virtually abolished by calcium withdrawal, and is restored by barium substitution for calcium. It is also reduced by raising the magnesium concentration.4. The enhanced resting output in response to sodium withdrawal also occurs in the absence of calcium.5. Cooling to 5 degrees C greatly reduces both the resting output and the output in response to raised potassium concentration or to electrical stimulation.6. The increase in resting output due to potassium excess is slight up to 25 mM [K(+)](o), but increases thereafter with about the fourth power of the potassium concentration; it is resistant to tetrodotoxin.7. Synthesis of acetylcholine by the longitudinal strip is increased when output is enhanced by electrical stimulation, by potassium excess or by addition of barium, so that the acetylcholine content of the strip is maintained approximately normal. Synthesis is reduced, in relation to output, by potassium lack or by treatment with ouabain, and is virtually abolished by sodium withdrawal.8. The theory is discussed that acetylcholine release depends on inhibition of the activity of a (Na(+) + K(+) + Mg(2+))-activated ATPase at the axonal membrane.

Acetylcholine↗
PubMed1976

Control of the delayed outward potassium currents in bursting pace-maker neurones of the snail, Helix pomatia.

The net outward current in bursting pace-maker neurones of the snail (Helix pomatia) during sustained and repeated voltage clamp pulses was studied. The properties of currents remaining in cobalt-Ringer or after TEA injection were compared with those in untreated cells. 2. With sustained voltage clamp depolarizations the net outward current first increases to a maximum at 150 msec and then declines to 60% or less of its peak intensity. This depression, which is greater during repetition of short pulses (e.g. 100 msec pulses at 0-5 sec intervals), represents a true decrease in the outward flow of K (designated IK) and is not due to a decreased driving force resulting from extracellular K accumulation. The steady-state current-voltage (I-V) relationship for IK is N-shaped (Heyer & Lux, 1976). 3. A component of IK persists when Ca and Mg in the medium are replaced by Co (ICo-res). With voltage clamp depolarizations ICo-res increases rapidly to a maximum and then partially inactivates with voltage dependent time constants of hundredths or tenths of seconds. Repolarization removes the inactivation. Thus, repeated stimulation with short pulses does not increase the depression of ICo-res-ICo-res (e.g. measured during voltage steps from holding potentials of -50 to near 0 mV) is smaller in test pulses preceded by depolarization and larger in pulses preceded by hyperpolarization. The steady state I-V relationship is not N-shaped. ICo-res is blocked by intracellular injection of tetraethylammonium (TEA). 4. Repeated voltage clamp depolarization to near 0 mV with 100 msec pulses for neurones with large Ca currents in normal Ringer produces a long-term depression which is maximal with 300-400 msec repolarizations (to -50 mV) between pulses. This corresponds with stimulus parameters for the maximum Ca current (Heyer & Lux, 1976). Intracellular injection of Ca2+ (also Ba2+ and Co2+) likewise reduces the total net outward current and especially the delayed outward current under voltage clamp. 5. The component of IK which is removed by Co is identified as Ca dependent and designated IK(Ca). With single voltage clamp pulses IK(Ca) follows the approximate time course and voltage dependence of the slow inward Ca current (Iin slow; Heyer & Lux, 1976). Several lines of evidence suggest that Ca ions moving through the membrane activate IK(Ca). 6. Part of IK cannot be blocked by intracellular TEA injection. In different neurones the magnitude of the IK component resistant to TEA (ITEA-res) is approximately proportional to the relative magnitudes of Iin slow.ITEA-res does not inactivate with sustained depolarization and shows pronounced long-term depression with repetitive stimulation at intermediate intervals and an increased outward current at the onset of the second and subsequent pulses following short repolarizations. The steady-state I-V relationship is N-shaped. ITEA-res is abolished by extracellular Co. 7. A net inward current with low depolarizations can be measured after TEA injection...

Animals↗
PubMed1982

Stimulation of calcium-dependent release of labelled protein from pulse-labelled mouse pituitary intermediate lobe tissue.

1. The effect of K depolarization on the release of labelled protein from pulse-labelled intermediate lobe tissue of mouse pituitaries has been studied.2. Depolarization briefly stimulated Ca-dependent release of labelled protein. Co (2.5 mM) and verapamil (0.08 mM) reversibly blocked stimulation. Efflux of (45)Ca was also briefly stimulated by depolarization, but not in the presence of Co or verapamil, nor in the absence of Ca.3. The response to maintained depolarization quickly inactivated. Inactivation probably resulted from Ca-channel inactivation rather than exhaustion of available labelled protein, since responses different in magnitude but of constant time course could be obtained by depolarization in different concentrations of Ca. In addition, much more labelled protein could be released by exposure to Ba.4. Depolarization did not cause a response if the Ca concentration was 0.4 mM or less; neither did inactivation occur in these conditions, and a response occurred as soon as the Ca concentration was raised. Two separate responses could be generated by a stepwise increase in the Ca concentration during maintained depolarization. The magnitude of the two responses together was similar to the magnitude of one response at the higher Ca concentration.5. Recovery from inactivation was complete after about 20 min in normal K. However, recovery also occurred during maintained depolarization provided the Ca concentration was reduced sufficiently. Recovery was complete at 0.4 mM-Ca or less, and at higher concentrations the extent of recovery depended on the Ca concentration selected.6. It is concluded that depolarization opened potential-dependent Ca channels permitting Ca entry and causing the release of labelled products. The response was brief probably because the Ca channels were inactivated. Since the channels were not inactivated by depolarization in low Ca, inactivation may result from Ca entry.

Animals↗
PubMed1983

Ionic currents of solitary horizontal cells isolated from goldfish retina.

Solitary horizontal cells, dissociated from papain-treated goldfish retinas, produce action potentials and show a non-linear current-voltage relationship. Underlying ion-conductance mechanisms were analysed by a single-micro-electrode voltage-clamp technique. Pharmacological and ion-substitution experiments revealed that ionic currents could be separated into at least four voltage-dependent currents: a Ca current and three types of K currents. The Ca current was activated by membrane depolarization beyond -45 mV, reached a maximal value near 0 mV, and became smaller at more positive potentials. By extrapolation, the reversal potential was estimated to be approximately +50 mV. The Ca current was inactivated by accumulation of intracellular Ca ions but not by membrane depolarization. Co ions (4mM) blocked this current. The first type of K current showed anomalous (inward-going) rectification near the resting potential (congruent to -60 mV). Hyperpolarization from the resting level produced a large, almost steady inward current, while depolarization evoked only a small, steady outward current. The current-voltage relationship revealed a shallow negative resistance region at membrane potentials beyond -50 mV. The current was blocked by Cs (10 mM) or Ba (1 mM) ions. The second type of K current (the transient outward current) was activated by membrane depolarization beyond -25 mV. The peak amplitude increased almost exponentially as the membrane was depolarized. During steady depolarization this current decayed exponentially (time constant congruent to 500 ms at +20 mV). The current was inactivated by conditioning depolarization (greater than 10 s) beyond -30 mV and blocked by 4-aminopyridine (10 mM). The third type of K current was the maintained outward current which was activated by membrane depolarization beyond -20 mV, increased to a steady level in a few hundred milliseconds, and showed little inactivation. The amplitude increased as the membrane was depolarized. The current was blocked by tetraethylammonium ions (20 mM). A Ca-mediated K current was not detected. Action potentials and the non-linear current-voltage relationship of solitary horizontal cells can be explained qualitatively by the combination of the four ionic currents.

4-Aminopyridine↗
PubMed1993

Tetraethylammonium-sensitive apical K+ channels mediating K+ secretion by turtle colon.

1. Apical membrane K+ channels in turtle colon were identified and characterized using current fluctuation analysis. 2. Under short-circuit conditions in NaCl-Ringer solution, the power density spectrum (PDS) of the short-circuit current (Isc) sometimes exhibited a clearly discernible Lorentzian component, indicating spontaneous fluctuations produced by a population of apical ion channels. The Lorentzian component had a characteristic corner frequency (fc) which averaged 10.2 +/- 0.9 Hz (mean +/- S.E.M., n = 20). 3. The power of the spontaneous fluctuations was enhanced (So increased) by manoeuvres that depolarize the apical membrane electrical potential (Va). Discernible fluctuations were enhanced or induced by raising the serosal K+ concentration ([K+]s = 50-115 mM, Na+ replacement), by clamping the transepithelial potential (Vt) to serosa-positive values, or by blocking basolateral K+ channels with Ba2+. 4. Mucosal amiloride (100 microM) attenuated the spontaneous fluctuations observed in NaCl-Ringer solution but had no effect in the presence of serosal high K+, indicating that amiloride did not block the K(+)-permeable channels but these channels resided in the same cells as the amiloride-sensitive Na+ channels. 5. Raising the mucosal K+ concentration attenuated spontaneous fluctuations. 6. In the presence of serosal high K+ and mucosal amiloride, the spontaneous fluctuations were often accompanied by a reversed Isc consistent with K+ secretion. These conditions were used to test the effects of putative channel blockers. 7. Mucosal Ba2+ and tetraethylammonium (TEA+) were effective inhibitors of the spontaneous fluctuations and the reversed Isc. At a concentration of 10 mM, TEA+ was maximally effective but the TEA+ analogues tetramethylammonium (TMA+) and tetrapropylammonium (TPrA+) were much less effective. Mucosal Rb+ or Cs+ did not inhibit at a concentration of 10 mM. 8. Mucosal lidocaine (200 microM), quinidine (200 microM), or diphenylamine-2-carboxylate (DPC, 1 mM) had little or no effect on the spontaneous fluctuations and reversed Isc. Quinine (100 microM), 4-aminopyridine (1 mM), and apamin (100 nM) were also without effect. 9. Mucosal TEA+ (10 mM) abolished the active secretory K+ flux measured in the presence of serosa-positive transepithelial potentials. 10. These experiments identified a population of TEA(+)-sensitive, apical K+ channels which mediate active K+ secretion in turtle colon. Sensitivity to external TEA+ distinguishes these channels from basolateral K+ channels in turtle colon and demonstrates similarity to apical K+ channels in mammalian colon.

Amiloride↗
PubMed1993

Regulation of K secretion across the porcine gallbladder epithelium.

Porcine gallbladder epithelium from the neck and the fundus of the organ was stripped of serosal muscle and mounted in Ussing chambers to investigate the mechanisms of K secretion. The sensitivity to K channel blockers and regulation by norepinephrine (NE), adenosine 3',5'-cyclic monophosphate (cAMP), and increases in intracellular Ca concentration ([Ca]) were studied. The porcine gallbladder secretes K (approximately 0.8 mu eq/cm2.h) under basal conditions. Mucosal tetraethylammonium (TEA) produced a concentration-dependent increase in short-circuit current (Isc) and inhibited the unidirectional serosal-to-mucosal 86Rb flux JsmRb, resulting in a > 60% reduction in net Rb secretion. In contrast, serosal Ba produced a concentration-dependent decrease in Isc and stimulated JsmRb, resulting in a > 200% increase in net Rb secretion. NE inhibited JsmRb and net Rb secretion in both regions. In the fundic region the mucosal-to-serosal Rb flux (JmsRb) was also significantly increased, suggesting that active K absorption was activated. Exogenous cAMP increased JsmRb and net Rb secretion by > 85% in both regions. This increase in net Rb secretion was blocked by mucosal TEA but unaffected by NE. The Ca ionophore ionomycin also increased JsmRb and net Rb secretion and reduced the Isc by approximately 50%. Neither mucosal TEA nor Ba blocked changes in steady-state Rb secretion induced by ionomycin. Although both serosal Ba and ionomycin produced significant reductions in Isc, the effects of Ba were blocked by ionomycin pretreatment. These findings indicate that basal K secretion occurs through TEA-sensitive apical K channels and is regulated by intracellular cAMP. NE likely reduces K secretion by decreasing intracellular concentration of cAMP.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

Biophysical and pharmacological characterization of inwardly rectifying K+ currents in rat spinal cord astrocytes.

1. Whole cell and cell-attached patch-clamp recordings were obtained from rat spinal cord astrocytes maintained in culture for 6-14 days. It was found that the resting conductance in these astrocytes is primarily due to inwardly rectifying K+ (Kir) channels. 2. Two types of astrocytic Kir channels were identified with single-channel conductances of approximately 28 and approximately 80 pS, respectively. Channels displayed some voltage dependence in their open probability, which was largest (0.8-0.9) near the K+ equilibrium potential (Ek) and decreased at more negative potentials. The resting potential closely followed Ek, so it can be assumed that Kir channels have a high open probability at the resting potential. 3. The conductance of inwardly rectifying K+ currents (Kir) depended strongly on [K+]o and was approximately proportional to the square-root of [K+]o. 4. Kir currents inactivated in a time- and voltage-dependent manner. The Na+ dependence of inactivation was studied with ion substitution experiments. Replacement of [Na+]o with choline or Li+ removed inactivation. This dependence of current inactivation on [Na+]o resembles the previously described block of Kir channels in other systems by [Na+]o. 5. Kir currents were also blocked in a dose-dependent manner by Cs+ (Kd = 189 microM at -140 mV), Ba2+ (Kd = 3.5 microM), and tetraethylammonium (TEA; 90% block at 10 mM) but were insensitive to 4-aminopyridine (4-AP; 5 mM). In the current-clamp mode, Ba2+ and TEA inhibition of Kir currents was associated with a marked depolarization, suggesting that Kir channel activity played a role in the establishment of the negative resting potential typical of astrocytes. 6. These biophysical features of astrocyte inwardly rectifying K+ channels are consistent with those properties required for their proposed involvement in [K+]o clearance: 1) high open probability at the resting potential, 2) increasing conductance with increasing [K+]o, and 3) rectification, e.g., channel closure, at positive potentials. It is proposed, therefore, that the dissipation of [K+]o following neuronal activity is mediated primarily by the activity of astrocytic Kir channels.

4-Aminopyridine↗
PubMed1976

Action potentials in chick atria. Ontogenetic changes in the dependence of tetrodotoxin-resistant action potentials on calcium, strontium, barium.

Action potentials were recorded from chick embryo atrial muscle cells bathed in Tyrode's solution. Tetrodotoxin (TTX), 3.1 muM, was added to block the early, transient, Na+-dependent conductance system. Rectangular stimuli were used to evoke action potentials the peak amplitude (Ep) of which depend on the external concentration of divalent cations, [Me2+]0. The relationship between Ep and [Me2+]0 shifted to the right with increasing age. For example, the slope of Ep was 33 +/- 2,22 +/- 1 and 11 +/- 3 mV per 10-fold change in [Ca2+]0 on the 9th, 12th, and 18th incubation days, respectively. In solutions with reduced [Ca2+]0, Ep increased when Ba2+ or Sr2+ was added to the bath. The potency of Me2+ in generating action potentials was Ba2+ greater than Sr2+ greater than Ca2+ and this sequence did not change during development. Action potential amplitude, which was reduced in 18-day preparations, was increased by isoproterenol (increased Ca2+ conductance, gCa2+) and by tetraethylammonium (TEA) ion (decreased K+ conductance, gK). The results show that (1) Me2+-dependent action potentials support membrane excitation in chick atrial cells treated with TTX, and (2) the ability of Me2+ to support action potentials decreases during ontogenesis. We conclude from these experiments that the ontogenetically related decrease in Me2+-induced action potentials is the result of a reduction in gMe2+/gK+ during stimulation.

Action Potentials↗
PubMed1987

The effect of oral magnesium-containing bowel preparation agents on mucosal coating by barium sulphate suspensions.

Alteration in the quality of mucosal coating by barium sulphate suspension observed during double-contrast barium enema (DCBE) examinations when an oral magnesium-containing purgative (Picolax) was used as sole bowel preparation has been investigated in vivo. Small amounts of Picolax were found to produce a linear increase in apparent viscosity and thixotropy, due to flocculation. The effect of equivalent concentrations of acid was significantly less (p less than 0.01), and of magnesium chloride was significantly greater (p less than 0.05), whereas magnesium citrate was comparable to Picolax, demonstrating the deflocculating effect of citrate on the flocculating action of magnesium ions. It is suggested that colonic residue from orally ingested magnesium-containing purgatives may contain sufficient magnesium ions to increase viscosity of the barium suspension and visibly affect its coating during DCBE.

Barium Sulfate↗
PubMed1996

Technetium-99m-HMPAO labelled leucocytes in the detection and monitoring of inflammatory bowel disease in children.

This study was a retrospective evaluation of the use of technetium-99m hexamethylpropyleneamineoxime (HMPAO) labelled leucocytes in the investigation of suspected inflammatory bowel disease in children. The images were analysed in 35 children and the findings were compared with the results of endoscopy/biopsy, barium studies and antinuclear cytoplasm antibody (ANCA) serology. The sensitivity of the white cell scan was 83% and the specificity 81%. This compares well with other studies in adults and is superior to barium investigations. The technique is recommended as a first line investigation to detect inflammatory bowel disease with a resultant reduction in the use of endoscopy and barium imaging.

Adolescent↗
PubMed1992

An analysis of post-contracture potentiation in frog twitch skeletal muscle.

Post-tetanic potentiation (PTP) was mimicked by post-contracture potentiation (PCP) in the twitch muscle of frog. A marked PCP was observed in small bundles of semitendinosus muscle in tetrodotoxin (TTX)-containing solution under current clamp condition. Contractures were induced by a constant depolarizing current pulse of 1 s every 5 min. Each contracture (C) was preceded and followed by a twitch-corresponding short contracture, T1 and T2, with an interval of 2 s. The ratio of twitch height, T2/T1, was measured and compared under various conditions. In TTX-containing Ringer solution, T2/T1 depended on magnitude of both T and C. When T2/T1 was plotted against C/T1 a quasi-linear relationship was found. The slope of the curve was 0.076 and was found to decrease when the duration of T was increased to 1 s. In TTX-containing solution, addition of 2 mM Ba2+ or 1 mM caffeine potentiated T as well as C but decreased T2/T1 markedly. Similar effects were observed when Na+ was replaced with TEA+ or when bath temperature was lowered from 20 to 8 degrees C. In all cases T2/T1 vs. C/T1 curve was shifted to the left and downwards. It was considered that these results could be attributable to an elevation of the resting Ca2+ concentration in the sarcoplasm. Thus the phenomenon of PCP probably reflects the time course of Ca2+ transients in the conditioning contracture C.

Action Potentials↗