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At least 1,603 records · Page 89Linked to original sources
PubMed1992

Initial characterization of whole-cell currents from freshly dissociated corneal keratocytes.

The perforated patch technique was utilized to obtain whole-cell currents from freshly dissociated rabbit corneal keratocytes. We describe and provide the initial characterization of two distinct whole cell currents in rabbit keratocytes: a K(+)-selective delayed rectifier and a voltage-sensitive, tetrodotoxin blockable Na+ current. The voltage-sensitive Na+ current is of sufficient magnitude to allow us to initiate action potentials when current-clamping the cells. This is the first detailed electrophysiological study of corneal keratocytes.

Action Potentials↗
PubMed1995

Biophysical, pharmacological and developmental properties of ATP-sensitive K+ channels in cultured myotomal muscle cells from Xenopus embryos.

Unlike mammalian muscle cells in culture, cultured myotomal muscle cells of Xenopus embryos express ATP-sensitive K+ (KATP) channels. The KATP channels are blocked by internal ATP (half-maximal inhibition K0.5 = 16 microM) and to a lesser extent by internal ADP, are voltage independent, have an inward rectification at positive potentials and are inhibited by glibenclamide (K0.5 = 2 microM). Surprisingly, these KATP channels are not sensitive to K+ channel openers such as cromakalim. Opening of these KATP channels does not occur under normal physiological conditions. It is elicited by metabolic exhaustion of the muscle cell and it precedes the development of an irreversible rigor state. Neither intracellular acidosis nor an increase of intracellular Ca2+ are involved in KATP channel opening. Different types of K+ channels are successively expressed after plating of myotomal muscle cells: (1) sustained delayed-rectifier K+ channels; (2) KATP channels; (3) inward-rectifier K+ channels; (4) transient delayed-rectifier K+ channels. The current density associated with KATP channels far exceeds that of voltage-dependent K+ channels. Innervation controls the expression of these KATP channels. Co-culture of muscle cells with neurons from the neural tube decreases the number of active KATP channels per patch. Similarly, in situ innervated submaxillaris muscle of tadpoles at stage 50-55 has a very low density of KATP channels.

Acidosis↗
PubMed2002

Functional and clinical characterization of KCNJ2 mutations associated with LQT7 (Andersen syndrome).

Andersen syndrome (AS) is a rare, inherited disorder characterized by periodic paralysis, long QT (LQT) with ventricular arrhythmias, and skeletal developmental abnormalities. We recently established that AS is caused by mutations in KCNJ2, which encodes the inward rectifier K(+) channel Kir2.1. In this report, we characterized the functional consequences of three novel and seven previously described KCNJ2 mutations using a two-microelectrode voltage-clamp technique and correlated the findings with the clinical phenotype. All mutations resulted in loss of function and dominant-negative suppression of Kir2.1 channel function. In mutation carriers, the frequency of periodic paralysis was 64% and dysmorphic features 78%. LQT was the primary cardiac manifestation, present in 71% of KCNJ2 mutation carriers, with ventricular arrhythmias present in 64%. While arrhythmias were common, none of our subjects suffered sudden cardiac death. To gain insight into the mechanism of arrhythmia susceptibility, we simulated the effect of reduced Kir2.1 using a ventricular myocyte model. A reduction in Kir2.1 prolonged the terminal phase of the cardiac action potential, and in the setting of reduced extracellular K(+), induced Na(+)/Ca(2+) exchanger-dependent delayed afterdepolarizations and spontaneous arrhythmias. These findings suggest that the substrate for arrhythmia susceptibility in AS is distinct from the other forms of inherited LQT syndrome.

Adolescent↗
PubMed2001

Nitrooxy alkyl apovincaminate activates K+ currents in rat neocortical neurons.

The effects of nitrooxy alkyl apovincaminate VA-045 ((+)-eburunamenine-14-carboxylic acid(2-nitroxy-ethyl ester), VA) were investigated in acutely dissociated rat neocortical neurons by using a nystatin-perforated patch recording configuration. VA activated a steady-state outward current in a concentration-dependent manner, with an EC50 of 0.65 microM. The reversal potential for the current shifted 56.5 mV with tenfold changes in the extracellular K+ concentration, suggesting that the current was carried by K+. The VA-induced current was not suppressed by apamin (1 microM), charybdotoxin (1 microM), Cs+ (3 mM), Ba2+ (3 mM), 4-aminopyridine (10 mM) or glibenclamide (10 microM), whereas tetraethylammonium suppressed the current with an IC50 of 1.4 mM. These pharmacological properties of the VA-induced current were compatible with a slowly inactivating delayed rectifier current (I(K)). It was suggested that the current activated by VA was I(K). The VA-induced current was not affected by Ca2+ depletion or by staurosporine (0.1 microM), quinacrine (10 microM), wortmanin (1 microM) or genistein (1 microM). The intracellular perfusion of GDPbetaS (0.4 mM) also had no significant effect. Thus, VA may directly activate the K+ channels.

Animals↗
PubMed1997

Molecular physiology of cardiac delayed rectifier K+ channels.

Delayed rectifier K+ current in cardiac myocytes is the sum of two distinct currents, IKr and IKs. The molecular basis of these channels has recently been defined. HERG subunits coassemble to form IKr channels. KvLQT1 and minK subunits coassemble to form IKs channels. Mutations in HERG or KVLQT1 genes predispose affected individuals to ventricular arrhythmias and sudden death.

Action Potentials↗
PubMed1991

Bursting electrical activity in pancreatic beta cells caused by Ca(2+)- and voltage-inactivated Ca2+ channels.

We investigate the hypothesis that two classes of Ca2+ currents, one quickly inactivated by Ca2+ and one slowly inactivated by voltage, contribute to bursting electrical activity in pancreatic islets. A mathematical model of these currents is fit to the experimental whole-cell current-voltage and inactivation profiles, thereby fixing the Ca2+ conductance and all activation and inactivation parameters. Incorporating these currents into a model that includes delayed rectifier K+ channels and ATP-sensitive K+ channels, we show that only abnormal bursting is obtained. Modification of activation parameters to increase Ca2+ channel open times, as suggested by experiment, yields a more robust bursting similar to that observed in intact islets. This reinforces the suggestion that in addition to ATP-sensitive K+ channels, Ca2+ channels may serve as glucose sensors in the beta cell.

Calcium↗
PubMed1997

Potassium currents in presynaptic hair cells of Hermissenda.

Apart from their primary function as balance sensors, Hermissenda hair cells are presynaptic neurons involved in the Ca(2+)-dependent neuronal plasticity in postsynaptic B photoreceptors that accompanies classical conditioning. With a view to beginning to understand presynaptic mechanisms of plasticity in the vestibulo-visual system, a locus for conditioning-induced neuronal plasticity, outward currents that may govern the excitability of hair cells were recorded by means of a whole-cell patch-clamp technique. Three K+ currents were characterized: a 4-aminopyridine-sensitive transient outward K+ current (IA), a tetraethyl ammonium-sensitive delayed rectifier K+ current (IK,V), and a Ca(2+)-activated K+ current (IK,Ca). IA activates and decays rapidly; the steady-state activation and inactivation curves of the current reveal a window current close to the apparent resting voltage of the hair cells, suggesting that the current is partially activated at rest. By modulating firing frequency and perhaps damping membrane oscillations, IA may regulate synaptic release at baseline. In contrast, IK,V and IK,Ca have slow onset and exhibit little or no inactivation. These two K+ currents may determine the duration of the repolarization phase of hair-cell action potentials and hence synaptic release via Ca2+ influx through voltage-gated Ca2+ channels. In addition, IK,Ca may be responsible for the afterhyperpolarization of hair cell membrane voltage following prolonged stimulation.

4-Aminopyridine↗
PubMed2002

Genes responsible for native depolarization-activated K+ currents in neurons.

Depolarization-activated, Ca2+-independent K+ currents can be largely divided into delayed rectifiers and transient A-type currents. In mammals, each of these subtypes exhibits large variations in voltage dependence and kinetics according to cell types. At the molecular level, the principal subunits of depolarization-activated K+ channels are thought to be coded by genes from nine subfamilies, Kv1 through Kv9, of which members within each of the Kv1-Kv4 subfamilies can form either homomeric or heteromeric, functional tetrameric channels. The variations in current properties and the large number of genes make it difficult to identify genes responsible for native K(+) channels in mammalian neurons. Nevertheless, progress has been made in recent years, in which the single cell/reverse transcription/polymerase chain reaction (scRT-PCR) protocol combined with patch clamp recording played important roles. With this technique, it has been shown in a number of neuronal phenotypes that mammalian neurons create diversity of channel function by coexpression of members of different Kv subfamilies, coexpression of multiple members of a Kv subfamily, and coexpression of multiple principal and auxiliary subunits. Some genes appear to be expressed at higher levels than others. In the somatodendritic domain, evidence is accumulating that Kv4 subfamily is a major contributor for the typical A-type current, while delayed rectifiers are often attributable to Kv2 and Kv3 subfamily genes. It thus appears that mammalian neurons express some particular Kv genes at higher levels while coexpress multiple genes for the composition of depolarization-activated K+ channels. In addition to the evolution of a large number of K+ channel genes, coexpression of multiple members of the genes in a single neuron also appears to be a strategy for mammalian neurons to create channel diversity.

Action Potentials↗
PubMed1991

Further characterization of the effects of imipramine on plateau membrane currents in guinea-pig ventricular myocytes.

The effects of imipramine, a tricyclic antidepressant, on action potential characteristics and plateau membrane currents were studied in isolated guinea-pig ventricular myocytes, using the whole cell configuration of the patch-clamp technique. Imipramine (1, 5 and 15 mumols/l) decreased in a concentration-dependent manner the amplitude and shortened the duration of the action potential, but it had no effect on resting membrane potential. At all three concentrations tested, imipramine decreased the delayed outward potassium current, this effect being apparently voltage-independent since it did not modify the activation curve. Imipramine, 5 and 15 mumols/l, also produced an inhibition of the peak high threshold calcium current, but did not change the shape of the current-voltage relationship or the apparent reversal potential of this current. Therefore, imipramine probably decreased the maximum available calcium conductance. However, the inward rectifying potassium current was not affected by any concentration of imipramine tested. Imipramine, 1 and 5 mumols/l, shortened the duration of the action potentials elicited in the presence of the inorganic calcium channel blocker cobalt chloride, and at 5, but not at 1 mumol/l, also shortened the action potentials obtained in the presence of the sodium channel blocker tetrodotoxin. Washout of imipramine completely reversed all its effects within 15 minutes. All these results suggest that imipramine at a concentration of 1 mumol/l produced a shortening in action potential duration by inhibiting the late sodium current flowing during the plateau phase of the action potential. At concentrations of 5 and 15 mumols/l the effect of imipramine on action potential duration can also be explained by a blocking effect on the high threshold calcium current.

Action Potentials↗
PubMed1992

Grafted neostriatal neurons express a late-developing transient potassium current.

Previous anatomical and physiological studies of neostriatal grafts have suggested that transplanted neurons do not develop beyond an early postnatal stage. We have tested whether this hypothesis can be generalized by characterizing the developmentally regulated Ca-independent potassium currents in graft neurons. These currents were studied using a combination of the whole-cell voltage-clamp technique with acutely-dissociated neurons and intracellular recording in slices. In all of the graft neurons examined with voltage-clamp techniques (n = 13), evidence was found for a slowly-inactivating potassium current that is seen only beyond the third or fourth postnatal week in normal rats. A current resembling the delayed rectifier was also seen in all sample neurons. The rapidly inactivating A-current which dominates recordings from nearly all immature neurons was seen in only about half (54%, 7/13) of the graft neurons; in a sample of normal adult striatal neurons, the A-current was detected in a similar percentage of neurons (41%, 25/62). Recordings of graft neurons in slices corroborated the voltage-clamp findings in revealing a slowly inactivating outward current that acts in the subthreshold potential range. These findings suggest that graft neurons express the normal complement of depolarization-activated potassium channel proteins seen in adult neurons.

Animals↗
PubMed1997

Outward currents in smooth muscle cells isolated from sheep mesenteric lymphatics.

1. The patch-clamp technique was used to measure membrane currents in isolated smooth muscle cells dispersed from sheep mesenteric lymphatics. Depolarizing steps positive to -30 mV evoked rapid inward currents followed by noisy outward currents. 2. Nifedipine (1 microM) markedly reduced the outward current, while Bay K 8644 (1 microM) enhanced it. Up to 90% of the outward current was also blocked by iberiotoxin (Kd = 36 nM). 3. Large conductance (304 +/- 15 pS, 7 cells), Ca(2+)- and voltage-sensitive channels were observed during single-channel recordings on inside-out patches using symmetrical 140 mM K+ solutions (at 37 degrees C). The voltage required for half-maximal activation of the channels (V1/2) shifted in the hyperpolarizing direction by 146 mV per 10-fold increase in [Ca2+]i. 4. In whole-cell experiments a voltage-dependent outward current remained when the Ca(2+)-activated current was blocked with penitrem A (100 nM). This current activated at potentials positive to -20 mV and demonstrated the phenomenon of voltage-dependent inactivation (V1/2 = -41 +/- 2 mV, slope factor = 18 +/- 2 mV, 5 cells). 6. Tetraethylammonium (TEA; 30 mM) reduced the voltage-dependent current by 75% (Kd = 3.3 mM, 5 cells) while a maximal concentration of 4-aminopyridine (4-AP; 10 mM) blocked only 40% of the current. TEA alone had as much effect as TEA and 4-AP together, suggesting that there are at least two components to the voltage-sensitive K+ current. 7. These results suggest that lymphatic smooth muscle cells generate a Ca(2+)-activated current, largely mediated by large conductance Ca(2+)-activated K+ channels, and several components of voltage-dependent outward current which resemble 'delayed rectifier' currents in other smooth muscle preparations.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed2000

Sodium nitroprusside increases pacemaker rhythm of sinoatrial nodes via nitric oxide-cGMP pathway.

Effects of sodium nitroprusside (SNP), a nitric oxide donor, on the action potential in isolated guinea-pig sinoatrial nodes and ventricular papillary muscles were investigated. In the driven ventricular papillary muscle, SNP (10(-10)-10(-3) M) decreased the twitch tension in a concentration-dependent manner without significantly changing the configuration of action potential and the maximal velocity of depolarizing upstroke. In isolated sinoatrial nodes, SNP (10(-8)-10(-3) M) increased the pacemaker rhythm in a concentration-dependent manner. At 10(-5) M SNP, the pacemaker activity increased from 197.2+/-6.1 to 221.4+/-9.7 bpm. Changes of configuration of the action potential included a decrease of the duration of repolarization, i.e., from peak to the maximal diastolic potential (MDP), from 141.4+/-6.4 to 130.0+/-7.0 ms and an increase of the slope of the diastolic membrane potential from 101.6+/-5.3 to 116.5+/-7.3 mV/s (n=6, p<0.05). However, MDP and threshold potential were not significantly changed. Methylene blue (MB, 10(-5) M), a guanylate cyclase inhibitor, significantly decreased the pacemaker activity of the sinoatrial node by increasing the durations of repolarization and diastolic depolarization. After pretreatment with 10(-5) M MB, the effect of SNP was inhibited. The results indicate that nitric oxide, released from SNP, increases the pacemaker activity by enhancing the rates of repolarization and diastolic depolarization. These effects are possibly due to increases in delayed-rectifier K+ and diastolic slow inward currents, which are involved in a mechanism associated with the NO-cGMP pathway.

Action Potentials↗
PubMed2002

Patch-clamp recordings from white matter glia in thin longitudinal slices of adult rat spinal cord.

We developed a technique of whole cell patch-clamp recordings from white matter oligodendrocytes and astrocytes in 200-250 microm-thick horizontal slices of adult (>2 months, 240-260 g) rat thoracic spinal cord. The viability of the white matter, sectioned in Na(+)-free, low Ca(2+) media, and the function of axons were preserved for >8 h, as demonstrated by the propagation of TTX-sensitive compound action potentials (CAPs) and the sensitivity of their refractory period to K(+) channel blocker 4-aminopyridine (1 microM). Glial cells were visually identified within the slices with a 40 x water immersion objective using infra-red differential interference contrast (IR-DIC) video microscopy, and the details of their morphology were further elucidated after filling the cells with Lucifer Yellow or Alexa 350 fluorescent dyes during whole-cell recording. Using voltage steps and ramps, we revealed pronounced non-linearity of I-V relationships in both oligodendrocytes and astrocytes. Both types of cells expressed TEA-sensitive outward delayed rectifier-type currents activated at positive voltages but showed little, if any, signs of inward rectification at voltages up to -140 mV. At -70 mV holding voltage, bath-applied kainic acid (100 microM) activated inward currents in both types of cells. This novel horizontal slice preparation of adult rat thoracic cord will facilitate the examination of mature glial cell physiology, glial-axonal signaling and the pathophysiology of spinal cord trauma and ischemia.

4-Aminopyridine↗
PubMed1993

Ionic basis for OPC-8212-induced increase in action potential duration in isolated rabbit, guinea pig and human ventricular myocytes.

Changes in transmembrane ionic currents induced by OPC-8212 (3,4-dihydro-6-[4-(3,4-dimethoxybenzoyl)-1-piperazinyl]-2(1H)-quinoline) , a recently introduced positive inotropic agent which lengthens cardiac action potential duration, were examined using whole-cell voltage-clamp techniques in single rabbit, guinea pig and human ventricular myocytes. In rabbit, OPC-8212 (12 mumol/l) significantly increased membrane action potential duration measured at 90% of repolarization by an average of 88 ms (from 462 +/- 25 to 550 +/- 35 ms, n = 4; P < 0.05). In rabbit this increase in duration was not associated with significant changes in either the inward rectifier or transient outward K+ currents. The magnitude of the secondary inward current evoked from a holding potential of -50 mV was significantly increased by 97 +/- 8% (n = 6; P < 0.01) while a demonstrable delayed rectifier outward current could not be identified in the rabbit myocytes examined at room temperature. In guinea pig ventricular myocytes, where the delayed rectifier was large, 12 mumol/l OPC-8212 significantly depressed the current by 58 +/- 10% (n = 6; P < 0.01). The effects of OPC-8212 in human ventricular myocytes obtained from the explanted heart of a single patient having an idiopathic cardiomyopathy most closely resembled those observed in isolated rabbit ventricular myocytes. Thus, in rabbit and a few human ventricular myocytes examined at room temperature, OPC-8212 appeared to lengthen cardiac membrane action potential duration primarily by increasing the amplitude of the secondary inward current believed to primarily represent current through L-type Ca2+ channels. In guinea pig preparations, OPC-8212 also decreased the delayed rectifier outward K+ current which also would account for an increase in action potential duration. OPC-8212 could not be demonstrated to affect Na+ current inactivation in a manner similar to that produced by 1 mg/l veratrine, a recognized Na+ channel agonist, which dramatically slowed this process.

Action Potentials↗
PubMed2006

Transient expression of A-type K channel alpha subunits Kv4.2 and Kv4.3 in rat spinal neurons during development.

A-type K(+) currents (I(A)s) have been detected from the ventral horn neurons in rat spinal cord during embryonic day (E) 14 to postnatal day (P) 8 but not in adulthood. It is not known which types of neurons and which A-type K(+) channel alpha subunits express the I(A)s and what the possible function might be. Here, we examined the expression of two A-type K(+) channel alpha subunits, Kv4.2 and Kv4.3, in rat spinal cord at various developmental stages by immunohistochemistry. We found a transient expression of Kv4.2 in somatic motoneurons during E13.5-P8 with a peak around E17.5, which coincides temporally with the natural selection of motoneurons. Transient expression of Kv4.2 and Kv4.3 was also observed in the intermediate gray (IG) interneurons. During E19.5-P14, some IG interneurons express Kv4.2, some express Kv4.3 and a subset co-express Kv4.2 and Kv4.3. Peak expression of Kv4.2 and Kv4.3 in the IG interneurons was detected around P1, which coincides temporally with the developmental selection of IG interneurons. In contrast to the I(A)-expressing subunits Kv4.2 and Kv4.3, a delayed-rectifier K(+) channel alpha subunit Kv1.6 is persistently expressed in somatic motoneurons and IG interneurons. Together, these data support the hypothesis that expression of I(A)s may protect I(A)-expressing somatic motoneurons, and possibly also IG interneurons, from naturally occurring cell death during developmental selection.

Animals↗
PubMed1991

Novel form of long-term potentiation produced by a K+ channel blocker in the hippocampus.

Long-term potentiation (LTP) of synaptic transmission in the hippocampus is a widely studied model of memory processes. In the CA1 region, LTP is triggered by the entry of Ca2+ through N-methyl-D-aspartate (NMDA) receptor channels and maintained by the activation of Ca2(+)-sensitive intracellular messengers. We now report that in CA1, a transient block by tetraethylammonium of IC, IM and the delayed rectifier (IK) produces a Ca2(+)-dependent NMDA-independent form of LTP. Our results suggest that this new form of LTP (referred as to LTPK) is induced by a transient enhanced release of glutamate which generates a depolarization by way of the non-NMDA receptors and the consequent activation of voltage-dependent Ca2+ channels.

Animals↗
PubMed1995

[Ca2+]i inhibition of K+ channels in canine renal artery. Novel mechanism for agonist-induced membrane depolarization.

The patch-clamp technique was used to examine the inhibition of delayed rectifier K+ channels by agents that release intracellular Ca2+. During voltage-clamp experiments on isolated myocytes with 4-aminopyridine (4-AP, 10 mmol/L) and niflumic acid (100 mumol/L) present to inhibit delayed rectifier K+ current (IK(dr)) and Ca(2+)-activated Cl- current (ICl(Ca)), angiotensin II (Ang II) and caffeine increased Ca(2+)-activated K+ current (IK(Ca)) between -25 and 80 mV (n = 5). Conversely, with charybdotoxin (ChTX, 100 nmol/L) and niflumic acid (100 mumol/L) present to inhibit IK(Ca) and ICl(Ca), Ang II and caffeine only caused inhibition of IK(dr). Block was achieved within 15 seconds of drug application and was reversible upon washout (n = 5). The effects of Ang II on IK(Ca) and IK(dr) were inhibited by the specific Ang II receptor antagonist losartan (1 mmol/L, n = 3). Intracellular BAPTA (10 mmol/L) also abolished the effects of Ang II and caffeine on both IK(Ca) and IK(dr). In current-clamp experiments, the application of ChTX (100 nmol/L) and niflumic acid (100 mumol/L) caused little change in resting membrane potential; however, subsequent application of caffeine (10 mmol/L) caused a 26 +/- 2.9 mV depolarization from -54 +/- 3.1 to -28 +/- 1.7 mV (n = 6). 4-AP (10 mmol/L) blocked the caffeine-induced depolarization. When isolated cells were loaded with the Ca2+ indicator indo 1 (100 mumol/L), Ang II, caffeine, and 4-AP increased [Ca2+]i and depolarized the cells. Both Ang II and caffeine caused an increase in [Ca2+]i that preceded membrane depolarization, whereas 4-AP depolarized the cell first and then caused an increase in [Ca2+]i (n = 4). In inside-out patches, with 200 nmol/L ChTX in the patch pipette to block large-conductance Ca(2+)-activated K+ channels, a 45 +/- 7-picosiemen 4-AP-sensitive K+ channel was identified that was sensitive to cytoplasmic Ca2+ (n = 6). Increasing intracellular Ca2+ decreased channel opening probability [NxP(open), where N is the number of functional channels in a patch and P(open) is the opening probability] at all membrane potentials examined. At 0 mV, increasing Ca2+ from < 5 to 200 and 600 nmol/L free Ca2+ decreased NxP(open) by 52 +/- 3% and 73 +/- 7%, respectively (n = 6). The decrease in opening probability of the delayed rectifier K+ channel resulted from a concentration- and voltage-dependent decrease in mean open time. The decrease in mean open time reflected significant decreases and increases in open and closed time constants, respectively.(ABSTRACT TRUNCATED AT 400 WORDS)

Angiotensin II↗
PubMed1995

Potassium currents in isolated CA1 neurons of the rat after kindling epileptogenesis.

Daily tetanic stimulation of the Schaffer collaterals generates an epileptogenic focus in area CA1 of the rat hippocampus, ultimately leading to generalized tonic-clonic convulsions (kindling). Potassium currents were measured under voltage-clamp conditions in pyramidal neurons, acutely dissociated from the focus of fully kindled rats, one day and six weeks after the last generalized seizure. Their amplitude, kinetics, voltage dependence and calcium dependence were compared with controls. With Ca2+ influx blocked by 0.5 mM Ni2+, the sustained current (delayed rectifier) and the transient current (A-current) were not different after kindling. Calcium influx evoked an additional fast transient current component. This transient calcium-dependent current component was increased by 154%, but only immediately after the seizure. A second, slow calcium-dependent potassium current component was dependent on the intracellular calcium level, set by the pipette as well as on calcium influx. The peak amplitude of this slow calcium-dependent current was under optimal calcium conditions not different after kindling, but we found indications that either calcium homeostasis or the calcium sensitivity of the potassium channels was affected by the kindling process. In contrast to the previously described enhancement of calcium current, kindling epileptogenesis did not change the total potassium current amplitude. The minor changes that were observed can be related either to changes in calcium current or to changes in intracellular calcium homeostasis.

Animals↗