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PubMed2001

Diversity of K+ channels in circular smooth muscle of opossum lower esophageal sphincter.

We previously demonstrated that a balance of K+ and Ca2+-activated Cl- channel activity maintained the basal tone of circular smooth muscle of opossum lower esophageal sphincter (LES). In the current studies, the contribution of major K+ channels to the LES basal tone was investigated in circular smooth muscle of opossum LES in vitro. K+ channel activity was recorded in dispersed single cells at room temperature using patch-clamp recordings. Whole-cell patch-clamp recordings displayed an outward current beginning to activate at -60 mV by step test pulses lasting 400 ms (-120 mV to +100 mV) with increments of 20 mV from holding potential of -80 mV ([K+]I = 150 mM, [K+]o = 2.5 mM). However, no inward rectification was observed. The outward current peaked within 50 ms and showed little or no inactivation. It was significantly decreased by bath application of nifedipine, tetraethylammonium (TEA), 4-aminopyridine (4-AP), and iberiotoxin (IBTN). Further combination of TEA with 4-AP, nifedipine with 4-AP, and IBTN with TEA, or vice versa, blocked more than 90% of the outward current. Ca2+-sensitive single channels were recorded at asymetrical K+ gradients in cell-attached patch-clamp configurations (100.8+/-3.2 pS, n = 8). Open probability of the single channels recorded in inside-out patch-clamp configurations were greatly decreased by bath application of IBTN (100 nM) (Vh = -14.4+/-4.8 mV in control vs. 27.3+/-0.1 mV, n = 3, P < 0.05). These data suggest that large conductance Ca2+-activated K+ and delayed rectifier K+ channels contribute to the membrane potential, and thereby regulate the basal tone of opossum LES circular smooth muscle.

Animals↗

PubMed2000

Low-affinity block of cardiac K(+) currents by nifedipine.

Nifedipine inhibits a variety of K(+) currents with IC(50) between 4 and 40 microM. Among the more sensitive of these are two types (transient outward and ultrarapid hKv1.5) found in the heart. To evaluate the actions of the drug on other prominent cardiac K(+) currents, guinea-pig ventricular myocytes were voltage-clamped for measurement of inwardly rectifying K(+) current (I(K1)), rapidly activating delayed-rectifier K(+) current (I(Kr)), and slowly activating delayed-rectifier K(+) current (I(Ks)). The currents were unaffected by < or =10 microM nifedipine, but inhibited by higher concentrations; IC(50) values were 260 microM for I(K1), 275 microM for I(Kr), and 360 microM for I(Ks). The time- and voltage-dependent properties of I(Ks) were unaffected by the drug, and full block was attained on the first depolarisation after a rest. The results establish that the sensitivity of I(Kr) and I(Ks) to inhibition by nifedipine is approximately 50 times lower than the sensitivity of other cardiac delayed-rectifier K(+) currents.

Animals↗

PubMed1997

A novel slow hyperpolarization-activated potassium current (IK(SHA)) from a mouse hippocampal cell line.

1. A slow hyperpolarization-activated inwardly rectifying K+ current (IK(SHA)) with novel characteristics was identified from the mouse embryonic hippocampus x neuroblastoma cell line HN9.10e. 2. The non-inactivating current activated negative to a membrane potential of -80 mV with slow and complex activation kinetics (tau act approximately 1-7 s) and a characteristic delay of 1-10 s (-80 to -140 mV) that was linearly dependent on the membrane potential. 3. Tail currents and instantaneous open channel currents determined through fast voltage ramps reversed at the K+ equilibrium potential (EK) indicating that primarily K+, but not Na+, permeated the channels. 4. IK(SHA) was unaffected by altering the intracellular Ca2+ concentration between approximately 0 and 10 microM, but was susceptible to block by 5 mM extracellular Ca2+, Ba2+ (Ki = 0.42 mM), and Cs+ (Ki = 2.77 mM) 5. In cells stably transformed with M2 muscarinic receptors, IK(SHA) was rapidly, but reversibly, suppressed by application of micromolar concentrations of muscarine. 6. At the single channel level K(SHA) channel openings were observed with the characteristic delay upon membrane hyperpolarization. Analysis of unitary currents revealed an inwardly rectifying I-V profile and a channel slope conductance of 7 pS. Channel activity persisted in the inside-out configuration for many minutes. 7. It is concluded that IK(SHA) in HN9.10e cells represents a novel K+ current, which is activated upon membrane hyperpolarization. It is functionally different from both classic inwardly rectifying IKir currents and other cationic hyperpolarization-activated IH currents that have been previously described in neuronal or glial cells.

Animals↗

PubMed2001

Potassium outward currents in freshly dissociated rabbit corpus cavernosum myocytes.

PURPOSE: Cavernous smooth muscle cells have a key role in the control of penile erection and detumescence. In this study the types of smooth muscle cells and currents present in isolated rabbit corpus cavernosum myocytes were characterized. MATERIALS AND METHODS: Immunohistochemical methods were used to identify cavernous smooth muscle cells. Currents were recorded from freshly dissociated myocytes using the whole cell and amphotericin perforated patch clamp techniques. RESULTS: Cavernous myocytes were identified by alpha-smooth muscle actin and smooth muscle myosin immunoreactivity. Based on electrical properties at least 2 types of myocytes were present. Type I cells showed more depolarized membrane potentials, lower capacitance, higher input resistance and increased current densities at positive potentials than type II cells. In types I and II cells at voltages positive to 30 mV, maxi K+ channel (Ca2+ activated large conductance K+ channel or BK) blockade with iberiotoxin or charybdotoxin reduced outward currents by approximately 40% to 80% at 80 mV. Maxi K+ channel blocking did not affect cell membrane potential. Type II cells showed delayed rectifier K+ channel-type outward currents that were not detected in type I cells. Delayed rectifier K+ channel-type currents were resistant to iberiotoxin or charybdotoxin, activated at approximately -50 to -40 mV. and inactivated weakly. CONCLUSIONS: The data suggest that cavernous smooth muscle cells are heterogeneous with at least 2 subtypes identified based on membrane potential, capacitance, input resistance, current density and delayed rectifier K+ channel expression. The activation threshold suggests that delayed rectifier K+ channels are open at the resting membrane potential and, therefore, contribute to control and regulation of the cavernous myocyte excitability.

Animals↗

PubMed1988

Voltage- and calcium-activated potassium currents in mouse neuroblastoma x rat glioma hybrid cells.

1. Membrane currents were recorded from voltage-clamped, microelectrode-impaled cells of the NG108-15 mouse neuroblastoma x rat glioma clonal cell line, differentiated with prostaglandin E1. 2. A slow outward tail current reversing at post-pulse potentials between -80 and -90 mV was evoked by depolarizing pre-pulses to near 0 mV. The tail current was inhibited by Cd2+ ions (0.2-1 mM) and hence attributed to activation of a Ca2+-dependent K+ current by a priming voltage-activated Ca2+ current. 3. Two components to this tail current could be distinguished pharmacologically: an early (less than or equal to 50 ms) component inhibited by 1-5 mM-tetraethylammonium (TEA), and a late component lasting several hundred milliseconds inhibited by apamin (0.1-0.4 microM) or d-tubocurarine (0.1-0.5 mM). 4. Ionophoretic injection of Ca2+ ions evoked a transient outward current with an apparent reversal potential (from ramped current-voltage curves) of -70 mV. This current was succeeded or sometimes replaced by an inward current with an apparent reversal potential between -20 and -10 mV. 5. The outward current induced by Ca2+ injections was unaffected or partly inhibited by TEA (1-5 mM), but was strongly inhibited by apamin or d-tubocurarine. 6. Hyperpolarizing voltage steps from between -30 and -40 mV induced inward current relaxations reversing at between -80 and -90 mV. These were considered to result from deactivation of the voltage-dependent sustained K+ current, IM. 7. Application of methacholine, muscarine or Ba2+ ions produced an inward current, reduced input conductance and reduced IM deactivation relaxations. 8. It is concluded that differentiated NG108-15 cells possess several of the K+ currents present in sympathetic neurones, including a delayed rectifier current, two species of Ca2+-activated K+ current and the M-current.

Action Potentials↗

PubMed1993

Two types of 4-aminopyridine-sensitive potassium current in rabbit Schwann cells.

1. Delayed rectifier K+ currents were studied in Schwann cells cultured from neonatal rabbit sciatic nerves with the whole-cell patch-clamp technique. 2. Depolarizing voltage steps (40 ms duration) activated two types of K+ current: type I, whose apparent activation threshold was about -60 mV (half-maximal conductance at -40 +/- 1 mV, n = 10); and type II, whose apparent activation threshold was about -25 mV (half-maximal conductance at + 11 +/- 1 mV, n = 9). 3. Type I current was blocked by alpha-dendrotoxin (alpha-DTX) with an apparent equilibrium dissociation constant (KD) of 1.3 nM, whereas the type II current was unaffected by exposure to 500 nM toxin. The action of alpha-DTX on the type I current was reversible. 4. Most cells exhibited both types of current, but occasionally some cells displayed just type I or just type II. 5. Type I current activated rapidly and then showed a much slower fade, which became more noticeable with larger depolarizations. Activation of type II current was slower than that of type I and depended less steeply on voltage. The time constants of activation for type I and type II currents were derived with a Hodgkin-Huxley formalism (based on second-power activation and deactivation kinetics). The longest activation time constant for type II gating was more than twice the corresponding time constant for type I; however, the time constants determined from tail current decays at potentials more negative than -60 mV were shorter for the type II currents than for the type I currents. 6. Both type I and type II currents were sensitive to micromolar concentrations of 4-aminopyridine (4-AP). The KD for 4-AP blockade of type II current was 630 microM (pH 7.2, membrane potential (Em) = -10 mV), which is about 6 times higher than the corresponding value for 4-AP blockade of type I current at negative membrane potentials. The differential sensitivity of the type I and type II currents to 4-AP may account for the apparent voltage dependence of 4-AP block of delayed rectifier K+ currents. 7. In addition to types I and II, a third type of outward K+ current (type III) was generated in most cells at positive membrane potentials. This latter current was insensitive to millimolar concentrations of 4-AP. 8. Similarities between Schwann cell and neuronal potassium channels are discussed.

4-Aminopyridine↗

PubMed1995

Effects of n-dodecylguanidine on A-type potassium channels: role of external surface charges in channel gating.

n-Dodecylguanidine (C12-G) is an amphipathic compound with a guanidine moiety, which is positively charged at physiological pH, and a hydrophobic side chain. Its effects on an A-type K+ channel clone (rKv1.4) expressed in Xenopus oocytes were examined. C12-G caused a concentration-dependent (1-20 microM) positive shift in the voltage dependences of the following channel properties: activation, inactivation, rate of decay during depolarization, and rate of recovery from inactivation. C12-G was effective when added to the bath solution but was without effect when applied to the cytoplasm of oocytes, indicating an extracellular site of action. The effects of C12-G were antagonized by elevation of the extracellular Mg2+ concentration and by external guanidine ions but were augmented by lowering of the ionic strength of the external solution. C12-G did not affect the instantaneous current-voltage relationship for rKv1.4 or the time constant of decay during strong depolarizations, when the voltage dependence of channel activation approached a plateau. Our observations suggest that C12-G exerts its actions by causing a positive shift in the external surface potential around rKv1.4, without altering the ion permeation process or voltage-independent transition steps. In canine ventricular myocytes, C12-G caused changes in the function of a native A-type K+ channel similar to those seen with rKv1.4. However, C12-G had negligible effects on the voltage dependence of the slow delayed-rectifier K+ channel in the same cell type, suggesting that the actions of C12-G are not nonspecific.

Animals↗

PubMed1999

Mechanisms of verapamil inhibition of action potential firing in rat intracardiac ganglion neurons.

The effects of verapamil and related phenylalkylamines on neuronal excitability were investigated in isolated neurons of rat intracardiac ganglia using whole-cell perforated patch-clamp recording. Verapamil (>/=10 microM) inhibits tonic firing observed in response to depolarizing current pulses at 22 degrees C. The inhibition of discharge activity is not due to block of voltage-dependent Ca2+ channels because firing is not affected by 100 microM Cd2+. The K+ channel inhibitors charybdotoxin (100 nM), 4-aminopyridine (0.5 mM), apamin (30-100 nM), and tetraethylammonium ions (1 mM) also have no effect on firing behavior at 22 degrees C. Verapamil does not antagonize the acetylcholine-induced inhibition of the muscarine-sensitive K+ current (M-current) in rat intracardiac neurons. Verapamil inhibits the delayed outwardly rectifying K+ current with an IC50 value of 11 microM, which is approximately 7-fold more potent than its inhibition of high voltage-activated Ca2+ channel currents. These data suggest that verapamil inhibits tonic firing in rat intracardiac neurons primarily via inhibition of delayed outwardly rectifying K+ current. Verapamil inhibition of action potential firing in intracardiac neurons may contribute, in part, to verapamil-induced tachycardia.

4-Aminopyridine↗

PubMed1990

Potassium channel blockers and the effects of cromakalim on the smooth muscle of the guinea-pig bladder.

1. The K+ channel blocking drugs tetraethylammonium Cl (TEA), procaine, 4-aminopyridine (4AP) and quinidine all produced concentration-dependent contractions of strips of smooth muscle from the guinea-pig urinary bladder. Apamin and glibenclamide caused little increase in the mechanical activity, and tolbutamide inhibited it. 2. TEA, procaine, 4AP, quinidine and apamin all increased the frequencies of spontaneous action potentials recorded with microelectrodes. TEA, quinidine and procaine all caused prolongation of the falling phase of the spike, and procaine and apamin completely abolished the after-hyperpolarization. 3. TEA and procaine increased K+ efflux from the tissue, an effect blocked by nifedipine. TEA and apamin increased, whereas quinidine, procaine and 4AP decreased K+ uptake. 4. Cromakalim caused a concentration-dependent hyperpolarization of the membrane, abolished spike activity, increased K+ fluxes and relaxed the smooth muscle. The relaxant effect of cromakalim was unaffected by apamin, and in its presence the effects of cromakalim on membrane potential and K+ fluxes were unchanged. Procaine abolished all the effects of cromakalim, and TEA at high concentrations reduced but did not abolish these effects. Quinidine reduced the effects of cromakalim on tension and membrane potential, but its actions were surmounted by higher concentrations of cromakalim. The effects of 4AP on tension and membrane properties were transitory, but it had some effects on the actions of cromakalim. Glibenclamide and tolbutamide reversed the relaxant effects of submaximal cromakalim concentrations, tolbutamide only transiently. 5. It is concluded that the channels opened by cromakalim are not those involved in generating the spike after-hyperpolarization. They have properties similar to the delayed rectifier K+ channels responsible for spike repolarization, and also are similar to the ATP-dependent K channels in vascular smooth muscle.

4-Aminopyridine↗

PubMed2000

Inhibition of KCNQ1-4 potassium channels expressed in mammalian cells via M1 muscarinic acetylcholine receptors.

1. KCNQ1-4 potassium channels were expressed in mammalian Chinese hamster ovary (CHO) cells stably transfected with M1 muscarinic acetylcholine receptors and currents were recorded using the whole-cell perforated patch technique and cell-attached patch recording. 2. Stimulation of M1 receptors by 10 microM oxotremorine-M (Oxo-M) strongly reduced (to 0-10%) currents produced by KCNQ1-4 subunits expressed individually and also those produced by KCNQ2 + KCNQ3 and KCNQ1 + KCNE1 heteromers, which are thought to generate neuronal M-currents (IK,M) and cardiac slow delayed rectifier currents (IK,s), respectively. 3. The activity of KCNQ2 + KCNQ3, KCNQ2 and KCNQ3 channels recorded with cell-attached pipettes was strongly and reversibly reduced by Oxo-M applied to the extra-patch membrane. 4. It is concluded that M1 receptors couple to all known KCNQ subunits and that inhibition of KCNQ2 + KCNQ3 channels, like that of native M-channels, requires a diffusible second messenger.

Animals↗

PubMed1993

Voltage-gated currents in muscle cells of Schistosoma mansoni.

Three morphologically distinct types of muscle fibres isolated from the platyhelminth Schistosoma mansoni have been studied with whole cell current- and voltage-clamp techniques. Fibres showed a marked time-dependent decrease in membrane resistance in response to depolarizing current injections. Voltage-clamp experiments revealed the presence of two distinct voltage-gated outward currents. The most prominent current is a slowly activating, slowly and incompletely inactivating potassium current similar to delayed rectifier currents which have been described in a variety of cell types from a variety of organisms. Also present is a faster activating, quickly and completely inactivating potassium current that shares functional characteristics with 'A'-currents. All three of the cell types studied possess a delayed rectifier current, but only two of the three types have 'A'-currents. Though depolarization with high K+ leads to contraction of the dispersed fibres, no voltage-gated inward currents could be detected by whole cell voltage-clamp under any of our conditions.

Animals↗

PubMed1998

Resting potentials and potassium currents during development of pulmonary artery smooth muscle cells.

The pulmonary circulation changes rapidly at birth to adapt to extrauterine life. The neonate is at high risk of developing pulmonary hypertension, a common cause being perinatal hypoxia. Smooth muscle K+ channels have been implicated in hypoxic pulmonary vasoconstriction in adults and O2-induced vasodilation in the fetus, channel inhibition being thought to promote Ca2+ influx and contraction. We investigated the K+ currents and membrane potentials of pulmonary artery myocytes during development, in normal pigs and pigs exposed for 3 days to hypoxia, either from birth or from 3 days after birth. The main finding is that cells were depolarized at birth and hyperpolarized to the adult level of -40 mV within 3 days. Hypoxia prevented the hyperpolarization when present from birth and reversed it when present from the third postnatal day. The mechanism of hyperpolarization is unclear but may involve a noninactivating, voltage-gated K+ channel. It is not caused by increased Ca2+-activated or delayed rectifier current. These currents were small at birth compared with adults, declined further over the next 2 wk, and were suppressed by exposure to hypoxia from birth. Hyperpolarization could contribute to the fall in pulmonary vascular resistance at birth, whereas the low K+-current density, by enhancing membrane excitability, would contribute to the hyperreactivity of neonatal vessels. Hypoxia may hinder pulmonary artery adaptation by preventing hyperpolarization and suppressing K+ current.

Aging↗

PubMed1984

The effects of the replacement of K+ by Tl+, Rb+, and NH+4 on the muscle membrane potential.

The resting membrane potential (RMP) of mouse diaphragm muscle was measured in solutions containing several concentrations of K+ (0.4 to 5 mmol/l) or one of the following cations: Tl+ (0.4, 1 or 2 mmol/l), Rb+ (1, 2 or 5 mmol/l), or NH+4 (4, 8 or 16 mmol/l). In terms of controlling the RMP, the ratios of the efficacies were Tl+:K+:Rb+:NH+4 = 2.5:1.0:1.0:0.12. These ratios are similar to those of the selectivities of the voltage dependent K+ channel (delayed rectifier) in frog nerve and muscle, and this similarity suggests that the resting membrane potential may be controlled by this channel.

Ammonia↗

PubMed1997

The effects of catechol on various membrane conductances in lumbar sympathetic postganglionic neurones of the guinea-pig.

The effects of catechol on membrane properties in lumbar sympathetic postganglionic neurones isolated from guinea-pigs were studied in vitro in current and voltage clamp using single intracellular microelectrodes. Neurones with properties characteristic of two previously described classes of neurone (phasic and tonic) were studied. Catechol (3-12 mM) produced a few mV depolarization and a dose-dependent increase in membrane resistance which were both larger in tonic than in phasic neurones. In the presence of catechol, both phasic and tonic neurones fired only a single action potential at the beginning of a maintained depolarizing current step. In both neurone types, catechol reduced action potential amplitude and slowed its time course. The peak of the afterhyperpolarization became delayed and reduced in amplitude, particularly in tonic neurones. The time constant of inactivation of IA was reduced by catechol without change in the voltage sensitivity of activation or inactivation: IC50 was 3 mM in phasic and 4 mM in tonic neurones. Catechol also blocked a slow voltage-activated K+ current (resembling ID) that was present in many tonic neurones. Catechol did not modify the slow calcium-activated potassium current (gKCa1) or the anomalous rectifier; neither did it appear to affect the fast calcium-activated potassium current (IC) or the delayed rectifier. Catechol did not change the overall rate of spontaneous synaptic activity nor enhance the release of quanta of ACh from preganglionic terminals evoked by nerve stimulation. We conclude that, in addition to blocking IA, catechol blocks the slow ID-like current in sympathetic neurones. It also has a profound effect on the action potential probably by increasing inactivation of voltage-dependent Na+ channels. The change from tonic to phasic discharge in tonic neurones cannot be attributed solely to its effects on IA.

Action Potentials↗

PubMed2005

Effects of hyperthyroidism on delayed rectifier K+ currents in left and right murine atria.

Hyperthyroidism has been associated with atrial fibrillation (AF); however, hyperthyroidism-induced ion channel changes that may predispose to AF have not been fully elucidated. To understand the electrophysiological changes that occur in left and right atria with hyperthyroidism, the patch-clamp technique was used to compare action potential duration (APD) and whole cell currents in myocytes from left and right atria from both control and hyperthyroid mice. Additionally, RNase protection assays and immunoblotting were performed to evaluate the mRNA and protein expression levels of K(+) channel alpha-subunits in left and right atria. The results showed that 1) in control mice, the APD was shorter and the ultra-rapid delayed rectifier K(+) conductance (I(Kur)) and the sustained delayed rectifier K(+) conductance (I(ss)) were larger in the left than in the right atrium; also, mRNA and protein expression levels of Kv1.5 and Kv2.1 were higher in the left atrium; 2) in hyperthyroid mice, the APD was shortened and I(Kur) and I(ss) were increased in both left and right atrial myocytes, and the protein expression levels of Kv1.5 and Kv2.1 were increased significantly in both atria; and 3) the influence of hyperthyroidism on APD and delayed rectifier K(+) currents was more prominent in right than in left atrium, which minimized the interatrial APD difference. In conclusion, hyperthyroidism resulted in more significant APD shortening and greater delayed rectifier K(+) current increases in the right vs. the left atrium, which can contribute to the propensity for atrial arrhythmia in hyperthyroid heart.

Action Potentials↗

PubMed1999

Effects of melatonin on ionic currents in cultured ocular tissues.

The effects of melatonin on ionic conductances in a cultured mouse lens epithelial cell line (alpha-TN4) and in cultured human trabecular meshwork (HTM) cells were measured using the amphotericin perforated patch whole cell voltage-clamp technique. Melatonin stimulated a voltage-dependent Na+-selective current in lens epithelial cells and trabecular meshwork cells. The effects of melatonin were observed at 50 pM and were maximal at 100 microM. Melatonin enhanced activation and inactivation kinetics, but no change was observed in the voltage dependence of activation. The results are consistent with an increase in the total number of ion channels available for activation by membrane depolarization. Melatonin was also found to stimulate a K+-selective current at high doses (1 mM). Melatonin did not affect the inwardly rectifying K+ current or the delayed rectifier type K+ current that has been described in cultured mouse lens epithelial cells. The results show that melatonin specifically stimulated the TTX-insensitive voltage-dependent Na+ current by an apparently novel mechanism.

Animals↗

PubMed1988

Ion channel expression by white matter glia: I. Type 2 astrocytes and oligodendrocytes.

White matter is a compact structure consisting primarily of neuronal axons and glial cells. As in other parts of the nervous system, the function of glial cells in white matter is poorly understood. We have explored the electrophysiological properties of two types of glial cells found predominantly in white matter: type 2 astrocytes and oligodendrocytes. Whole-cells and single-channel patch-clamp techniques were used to study these cell types in postnatal rat optic nerve cultures prepared according to the procedures of Raff et al. (Nature, 303:390-396, 1983b). Type 2 astrocytes in culture exhibit a "neuronal" channel phenotype, expressing at least six distinct ion channel types. With whole-cell recording we observed three inward currents: a voltage-sensitive sodium current qualitatively similar to that found in neurons and both transient and sustained calcium currents. In addition, type 2 astrocytes had two components of outward current: a delayed potassium current which activated at 0 mV and an inactivating calcium-dependent potassium current which activated at -30 mV. Type 2 astrocytes in culture could be induced to fire single regenerative potentials in response to injections of depolarizing current. Single-channel recording demonstrated the presence of an outwardly rectifying chloride channel in both type 2 astrocytes and oligodendrocytes, but this channel could only be observed in excised patches. Oligodendrocytes expressed only one other current: an inwardly rectifying potassium current that is mediated by 30- and 120-pS channels. Because these channels preferentially conduct potassium from outside to inside the cell, and because they are open at the resting potential of the cell, they would be appropriate for removing potassium from the extracellular space; thus it is proposed that oligodendrocytes, besides myelinating axons, play an important role in potassium regulation in white matter. The conductances present in oligodendrocytes suggest a "modulated Boyle and Conway mechanism" of potassium accumulation.

Animals↗

PubMed1995

Activation and deactivation of membrane currents in human fibroblasts following infection with human cytomegalovirus.

The whole cell patch clamp technique was used to study the effects on membrane currents of infection of cultured human embryonic lung (HEL) fibroblasts with human cytomegalovirus (CMV). Four types of membrane currents were found in uninfected HEL cells, namely: Ca(2+)-activated potassium current, inward rectifier potassium current, delayed rectifier potassium current and voltage-dependent CMV. Voltage-dependent sodium current was detected in 30% of uninfected HEL cells whenever they were examined up to 72 h after seeding; however this current had completely disappeared by 18 h after infection with CMV. The delayed rectifier potassium current was detectable in 8% of uninfected HEL cells but, after infection, the proportion of cells expressing this current gradually increased from 20% at 18-24 h post-infection to 100% at 48 h and 72 h. Pharmacological agents known to regulate the activity of ion channels, via cellular secondary messengers, did not alter the frequency at which either current was detected in uninfected and infected cells. Phosphonoformate, an inhibitor of CMV DNA polymerase, caused 95% block of expression of CMV 'late' proteins in infected cells but did not prevent the switching off of the sodium current or the increased expression of the potassium current. The results indicate an association between the expression of CMV 'immediate-early' or 'early' proteins and the down-regulation of the sodium current and up-regulation of the potassium current.

Cells, Cultured↗