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PubMed2002

Characterization of the A-type potassium current in murine gastric antrum.

A-type currents are rapidly inactivating potassium currents that operate at subthreshold potentials. A-type currents have not been reported to occur in the phasic muscles of the stomach. We used conventional voltage-clamp techniques to identify and characterize A-type currents in myocytes isolated from the murine antrum. A-type currents were robust in these cells, with peak current densities averaging 30 pA pF(-1) at 0 mV. These currents underwent rapid inactivation with a time constant of 83 ms at 0 mV. Recovery from inactivation at -80 mV was rapid, with a time constant of 252 ms. The A-type current was blocked by 4-aminopyridine (4-AP) and was inhibited by flecainide, with an IC(50) of 35 microM. The voltage for half-activation was -26 mV, while the voltage of half-inactivation was -65 mV. There was significant activation and incomplete inactivation at potentials positive to -60 mV, which is suggestive of sustained current availability in this voltage range. Under current-clamp conditions, exposure to 4-AP or flecainide depolarized the membrane potential by 7-10 mV. In intact antral tissue preparations, flecainide depolarized the membrane potential between slow waves by 5 mV; changes in slow waves were not evident. The effect of flecainide was not abolished by inhibiting enteric neurotransmission or by blocking delayed rectifier and ATP-sensitive K(+) currents. Transcripts encoding Kv4 channels were detected in isolated antral myocytes by RT-PCR. Immunocytochemistry revealed intense Kv4.2- and Kv4.3-like immunoreactivity in antral myocytes. These data suggest that the A-type current in murine antral smooth muscle cells is likely to be due to Kv4 channels. This current contributes to the maintenance of negative resting membrane potentials.

4-Aminopyridine↗
PubMed2001

Effects of the antiarrhythmic agent EGIS-7229 (S 21407) on calcium and potassium currents in canine ventricular cardiomyocytes.

Based on earlier pharmacological studies performed using conventional microelectrodes EGIS-7229 (S 21407), the novel antiarrhythmic candidate, was suggested to have a combined mode of action in cardiac tissues isolated from various mammalian species. In order to characterize the electrophysiological effects of the compound, its effects on calcium and potassium currents of isolated canine ventricular cardiomyocytes were studied in the present work using the whole cell configuration of the patch clamp technique. L-type Ca current (ICa) was significantly depressed by EGIS-7229 at concentrations of 3 microM or higher with no concomitant changes in the voltage-dependence of activation and time course of inactivation of ICa. The drug reversibly suppressed the rapid component of the delayed rectifier K current (IKr) in a concentration-dependent manner, having a K0.5 value of 1.1+/-0.1 microM and a slope factor of close to unity (1.23+/-0.16), indicating that probably one single binding site of high affinity may be involved in binding of EGIS-7229 to the IKr channel. In contrast, no changes in the slow component of the delayed rectifier K current (IKs) was observed with the compound up to the concentration of 100 microM, even if the current was fully activated by 8-bromo-cAMP. At a concentration of 10 microM or higher, EGIS-7229 caused also a moderate but significant reduction in the inward rectifier K current (IK1) and the transient outward K current (Ito) with no change in the voltage-dependence of activation and steady-state inactivation of Ito. Present results indicate that EGIS-7229 can be considered as a selective IKr blocker at low (1 microM) concentration; however, its combined (class III + IV) mechanism of action is evident at concentrations of 3 microM or higher. Suppression of ICa may explain the lack of development of early afterdepolarizations in the presence of EGIS-7229, predicting a relatively safe clinical application in contrast to pure class III compounds.

Analysis of Variance↗
PubMed1997

Reversible inhibition of IK, IAHP, Ih and ICa currents by internally applied gluconate in rat hippocampal pyramidal neurones.

Previously, we reported that the spike frequency adaptation and slow afterhyperpolarizations (sAHP) in hippocampal pyramidal neurones are best preserved during whole-cell recording with a methylsulfate (MeSO4-)- based internal solution, but undergo a fast rundown when gluconate- (Gluc-)- based internal solution is used. Here we show, with internal perfusion of patch pipettes, the reversibility of the inhibitory effects of Gluc- on spike frequency adaptation and sAHP, and extend these observations to fast and medium-duration AHPs. Contrary to what might be expected based on Gluc- binding of Ca2+, the sAHP and its underlying current could be temporarily enhanced by adding 1-3 mM of the calcium chelator BAPTA to the internal solution in the presence of Gluc-. Replacement of internal MeSO4- with Gluc- did not affect the membrane resting potential or the amplitude and duration of action potentials, but reversibly increased the cell input resistance and decreased the threshold current for spike generation. Gluc- reversibly inhibited the hyperpolarization-activated non-selective cationic current (Ih), the depolarization-activated delayed rectifier K+ current (IK), the high-voltage-activated Ca2+ current and the Ca2+-activated K+ current that underlies the sAHP. The combination of these effects of Gluc- significantly alters the electrophysiological "fingerprint" of the neurone.

Animals↗
PubMed2004

Ionic currents in single smooth muscle cells of the human vas deferens.

PURPOSE: Smooth muscle cells of the vas deferens have an important role in carrying sperms to the exterior but little is known of their electrophysiological properties. We characterized the voltage-gated ion channel currents in single smooth muscle cells of the human vas deferens (HVSMCs). MATERIALS AND METHODS: We observed contractile responses of 8 circular smooth muscle strips of the human vas deferens to a high concentration (10 mM) of tetraethylammonium. HVSMCs were isolated using proteolytic enzymes (collagenase and papain), and were used for an electro-physiological study using whole cell and inside-out patch clamp configurations. RESULTS: The application of 10 mM tetraethylammonium induced rhythmic contractions of the strips. When HVSMCs were dialyzed with a KCl solution, step depolarizations of membrane potential evoked oscillatory outward K currents that were not inactivated. The large conductance Ca activated K (BKCa) and delayed rectifier components of the outward current were identified. The BKCa channel showed a large single channel conductance (162.7 +/- 13.2 pS with 5 mM K in the patch pipette). Two types of Ca currents were identified in the whole cell configuration. With a cell held at -50 mV an L-type Ca current was present during a depolarizing step pulse. From a holding potential of -90mV L-type and T-type Ca currents were elicited by depolarizing step pulses. CONCLUSIONS: HVSMCs have 2 (L and T) types of Ca channels and 2 types of K (BKCa and delayed rectifier) channels. Voltage dependent changes of these ion channels and their interactions may be important in regulating vas contractility.

Adult↗
PubMed1985

Ionic conductances in frog short skeletal muscle fibres with slow delayed rectifier currents.

Short (0.8-1.6 mm) lumbricalis fibres of Rana pipiens were voltage clamped by a two-micro-electrode technique at 5 degrees C in sucrose hypertonic Ringer solution (SHR). Terminated linear cable analysis suggests that if the current electrode is placed near the centre of the fibre length and the voltage-sensing electrode is placed 0.19 times the fibre length from the current electrode, the fibre can be adequately voltage clamped and the conductance may be simply calculated as I/V for fibre length constants from 1.0 to 0.15 mm. In SHR solution lumbricalis fibres have action potentials with peak amplitudes of only +2 to 7 mV and a slow, gradual repolarization, distinct from the action potentials observed in sartorius muscle. In 60 mM-Na+ SHR the inward Na current could be adequately controlled over the fibre length, providing an estimated Na conductance (GNa) of 8.9 mS/cm2. The magnitude of GNa and GK (delayed rectifier) in lumbricalis fibres was approximately 20% of that reported for sartorius and semitendinosus, although the resting conductances were similar. Fibres demonstrated delayed rectifier currents with complex patterns of activation suggesting two components of conductance (fast, GK,f and slow, GK,s) which were combined together in varied amounts: (a) GK,f activated rapidly to a maximum within 80 ms at 0 mV as previously described (Adrian, Chandler & Hodgkin, 1970a); (b) GK,s activated gradually with depolarizations below -50 mV and achieving peak currents at about 400 ms at 0 mV. In about 10% of lumbricalis fibres studied, GK,s occurred in isolation with a peak magnitude of 1.4 +/- 0.4 mS/cm2 (+/- S.D.). GK,s activation kinetics and tail currents are described by a squared two-state (l2) Hodgkin-Huxley model and have a Q10 of 2.8. These currents inactivated with a time constant of 5-7 s at 0 mV. Isolated GK,s with identical kinetics was also observed in certain sartorius fibres studied with the three-electrode voltage clamp. The fractional amount of GK,s in the combined delayed rectifier (GK,s + GK,f) currents could be estimated from analysis of the late activation phase with depolarization. Combined delayed currents were described by summing GK,f currents using a n4 model with GK,s currents defined by the l2 model.

Action Potentials↗
PubMed1990

Sustained and transient potassium currents of cultured horizontal cells isolated from white bass retina.

1. Horizontal cells (HCs) are second-order neurons in the retina that receive direct photoreceptor input. They rest at around -20 mV in the dark, because of the continuous release of neurotransmitter from photoreceptors. HCs respond to light with graded hyperpolarizations, which can reach -70 to -80 mV in the presence of very bright stimuli. 2. HCs from the retinas of white bass were isolated and maintained in culture. Potassium currents in three morphological types of HCs--H1, H2, and H4--were studied in culture with whole-cell, patch-clamp techniques, when sodium and calcium currents were blocked. 3. A transient outward potassium current (IA), with many characteristics of the A-current, was found in all H2s and H4s but only occasionally in H1s. The threshold for activation of this current was around -40 mV, a value more depolarized than usual for the A-current. The peak IA was typically smaller than 300 pA when the membrane was stepped from a holding potential of -70 mV to a command potential of -10 mV, the upper limit of the in vivo range of HC membrane potentials. Steady-state inactivation is expected to reduce the magnitude of IA in vivo. 4. A sustained outward potassium current (IK) was found in all types of HCs. This sustained potassium current did not activate until the membrane was stepped to potentials above -10 mV, a value much more depolarized than those reported for the delayed rectifier current in other neurons. As a result, IK is absent over the in vivo operating range of these cells. 5. No calcium-dependent potassium current was found in any cells.(ABSTRACT TRUNCATED AT 250 WORDS)

Aminopyrine↗
PubMed1993

Cloning and expression of a Kv1.2 class delayed rectifier K+ channel from canine colonic smooth muscle.

A cDNA (CSMK1) encoding a delayed rectifier K+ channel of the Kv1.2 class was cloned from canine colonic circular smooth muscle and expressed in Xenopus oocytes. These channels appear to be uniquely expressed in gastrointestinal muscles and may participate in the electrical slow wave activity. Functional expression of CSMK1 in Xenopus oocytes demonstrated a K+ current that activated in a voltage-dependent manner upon depolarization. This current was highly sensitive to 4-aminopyridine (IC50, 74 microM). A low-conductance K+ channel was identified in inside-out patches from oocytes injected with CSMK1. This channel displayed a linear current-voltage relation with a slope conductance of 14 pS. The channels were blocked in a concentration-dependent manner by 4-aminopyridine. Northern blot analysis demonstrated that CSMK1 is expressed in a wide variety of gastrointestinal smooth muscles. Portal vein, renal artery, and uterus do not express CSMK1, suggesting that, among smooth muscles, expression of this K+ channel may be restricted to gastrointestinal smooth muscles. CSMK1 is 91% homologous to RAK, a delayed rectifier K+ channel cloned from rat heart, but displays unique pharmacological properties and tissue distribution.

4-Aminopyridine↗
PubMed1990

Pharmacology of the Ca2(+)-dependent K+ channel in corn protoplasts.

We investigated the sensitivity of the Ca2(+)-dependent K+ current, IK(Ca), present in corn protoplasts, to different K+ channel blockers. IK(Ca) was inhibited by external Cs+ (10 mM), Ba2+ (10 mM), and quinine (0.5 mM): reagents which block many types of outward-rectifying K+ channels. In contrast 4-aminopyridine (5 mM), an inhibitor of delayed rectifier or inactivating K+ currents, had no effect. Neither of the peptide toxins, apamin or charybdotoxin, specific for Ca2(+)-dependent K+ channels in animal cells, inhibited currents when used in the nanomolar concentration range. However, higher levels of charybdotoxin (10 microM) caused marked reduction of IK(Ca).

Barium↗
PubMed1999

Activation of vascular smooth muscle K+ channels by endothelium-derived relaxing factors.

1. Endothelium-derived relaxing factors (EDRF), including nitric oxide (NO), prostacyclin (PGI2) and an as yet uncharacterized endothelium-derived hyperpolarizing factor (EDHF), are now recognized to induce relaxation of vascular smooth muscle, in part via the activation of K+ channels. 2. Experiments using selective K+ channel blockers, including iberiotoxin (IbTX), glibenclamide, apamin and 4-aminopyridine (4-AP) to inhibit endothelium-induced relaxation suggest that more than one type of K+ channel may be involved, depending on the species and tissue, including: (i) large conductance Ca(2+)-activated (BKCa) channels; (ii) ATP-sensitive (KATP) channels; (iii) small conductance Ca(2+)-activated (SKCa) channels; and (iv) voltage-gated (Kv) K+ channels. 3. Recent observations suggest a role for Kv channels in some vessels based on a sensitivity of NO- and PGI2-mediated relaxations to 4-AP, as well as a complete suppression of EDHF-dependent relaxation by a combination of charybdotoxin (ChTX) and apamin but not IbTX and apamin. 4. The molecular identity of the K+ channels affected by EDRF is not well characterized. Recently, findings indicate that the pore-forming alpha-subunit tetramers of vascular smooth muscle BKCa channels are due to the expression of the so-called Slo channel gene. The identities of the KATP, SKCa and Kv channels involved in endothelium-dependent vasodilation are not known. 5. The component of whole-cell Kv current affected by PGI2 may be due to slowly inactivating, 4-AP-sensitive, 15 pS delayed-rectifier K+ channels (KDR); the activity of these channels in vascular myocytes is increased by forskolin and protein kinase A (PKA) and rabbit portal vein Kv1.5 pore-forming alpha-subunits, which appear to be a component of native KDR current and possess consensus phosphorylation sequences for PKA.

Animals↗
PubMed1991

Calcium-activated potassium conductance in presynaptic terminals at the crayfish neuromuscular junction.

Membrane potential changes that typically evoke transmitter release were studied by recording intracellularly from the excitor axon near presynaptic terminals of the crayfish opener neuromuscular junction. Depolarization of the presynaptic terminal with intracellular current pulses activated a conductance that caused a decrease in depolarization during the constant current pulse. This conductance was identified as a calcium-activated potassium conductance, gK(Ca), by its disappearance in a zero-calcium/EGTA medium and its block by cadmium, barium, tetraethylammonium ions, and charybdotoxin. In addition to gK(Ca), a delayed rectifier potassium conductance (gK) is present in or near the presynaptic terminal. Both these potassium conductances are involved in the repolarization of the membrane during a presynaptic action potential.

Action Potentials↗
PubMed1995

Segmental specialization of calcium-activated potassium conductances in an identified leech neuron.

1. Retzius (R) neurons of the fifth and sixth segmental ganglia of the leech, called R(5,6) neurons are specialized to innervate the adjacent reproductive organs and are morphologically and functionally distinct from R neurons of standard ganglia [R(x) cells]. In this study the electrical properties of the R(x) and R(5,6) neurons were compared under current-clamp and voltage-clamp conditions. 2. The action-potential waveforms of R(x) and R(5,6) cells were similar except for the presence in the R(5,6) cells of a long afterhyperpolarization (AHP) following action potentials arising from the resting membrane potential but not from more depolarized potentials. Its role may thus be to inhibit firing of the R(5,6) neurons at rest or in response to weak depolarizing stimuli. 3. In the presence of the Ca2+ channel blocker Cd2+, the long AHP of the R(5,6) was abolished, and the action potentials of all R cells were identical. 4. Under voltage clamp, current kinetics and densities were similar between R(x) and R(5,6) cells for Ca2+ currents, delayed and inward rectifier K+ currents, and a rapid Ca(2+)-activated K+ current (IKc) that is common to the two cell types. The R(5,6) cells, however, expressed a second Ca(2+)-activated K+ current that was not observed in the R(x) cells. This current, called IKAHP, activated and inactivated more slowly than IKC, with a time course similar to that of the AHP observed under physiological conditions. 5. Neither IKC nor IKAHP was blocked by high concentrations of charybdotoxin or apamin, which block vertebrate Ca(2+)-activated K+ channels.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗
PubMed2004

Characterization of a hyperpolarization-activated time-dependent potassium current in canine cardiomyocytes from pulmonary vein myocardial sleeves and left atrium.

Cardiomyocytes from the pulmonary vein sleeves (PVs) are known to play an important role in atrial fibrillation. PVs have been shown to exhibit time-dependent hyperpolarization-induced inward currents of uncertain nature. We observed a time-dependent K(+) current upon hyperpolarization of PV and left atrial (LA) cardiomyocytes (I(KH)) and characterized its biophysical and pharmacological properties. The activation time constant was weakly voltage dependent, ranging from 386 +/- 14 to 427 +/- 37 ms between -120 and -90 mV, and the half-activation voltage averaged -93 +/- 4 mV. I(KH) was larger in PV than LA cells (e.g. at -120 mV: -2.8 +/- 0.3 versus-1.9 +/- 0.2 pA pF(-1), respectively, P < 0.01). The reversal potential was approximately -84 mV with 5.4 mm[K(+)](o) and changed by 55.7 +/- 2.4 mV per decade [K(+)](o) change. I(KH) was exquisitely Ba(2+) sensitive, with a 50% inhibitory concentration (IC(50)) of 2.0 +/- 0.3 microm (versus 76.0 +/- 17.9 microm for instantaneous inward-rectifier current, P < 0.01), and showed similar Cs(+) sensitivity to instantaneous current. I(KH) was potently blocked by tertiapin-Q, a selective Kir3-subunit channel blocker (IC(50) 10.0 +/- 2.1 nm), was unaffected by atropine and was significantly increased by isoproterenol (isoprenaline), carbachol and the non-hydrolysable guanosine triphosphate analogue GTPgammaS. I(KH) activation by carbachol required GTP in the pipette and was prevented by pertussis toxin pretreatment. Tertiapin-Q delayed repolarization in atropine-exposed multicellular atrial preparations studied with standard microelectrodes (action potential duration pre- versus post-tertiapin-Q: 190.4 +/- 4.3 versus 234.2 +/- 9.9 ms, PV; 202.6 +/- 2.6 versus 242.7 +/- 6.2 ms, LA; 2 Hz, P < 0.05 each). Seven-day atrial tachypacing significantly increased I(KH) (e.g. at -120 mV in PV: from -2.8 +/- 0.3 to -4.5 +/- 0.5 pA pF(-1), P < 0.01). We conclude that I(KH) is a time-dependent, hyperpolarization-activated K(+) current that likely involves Kir3 subunits and appears to play a significant role in atrial physiology.

Action Potentials↗
PubMed1999

Characterization of the K+ channel opening effect of the anticonvulsant retigabine in PC12 cells.

Retigabine (D-23129) is a new anticonvulsant compound which acts as a K+ channel opener in neuronal cells. The aim of the present study was to further characterize the retigabine induced K+ current. In nerve growth factor treated PC12 cells and in rat cortical neurones the application of retigabine activated a K+ current. In contrast, however, no K+ current activation was observed in untreated PC12 and in glial cells which were cultivated together with the neuronal cells. To characterise the retigabine activated K+ current, K+ channel blockers were used. The retigabine induced current was not affected by 1 and 10 mM 4-aminopyridine (4AP). Ba2+ 1 mM resulted in a reduction of 88.6+/-3.0% (n = 5); 10 mM abolished the current. Tetraetylamonium (TEA), 1 and 10 mM, reduced the current by 23.6+/-3.1 and 61.6+/-3.7%, respectively. To investigate the current/voltage (I/V) relation of the current initiated by retigabine (10 microM), cells were clamped to a holding potential of -80 mV and a ramp stimulation protocol (-120 to +60 mV in 5 s) was applied prior to and during application of retigabine. Subtraction of the two traces yielded the current induced by retigabine. A nearly linear relationship was determined between - 120 and -40 mV. At potentials positive to - 40 mV, the response was variable. This was due to the additionally observed weak blocking effect of retigabine on delayed rectifier (Kdr) currents. If the ramp was applied in the presence of 10 mM 4AP to block Kdr, a nearly linear I/V-relationship was present from -120 to +60 mV. The comparison of the I/V relation and pharmacology with published K+ channel subtypes gives evidence that an unknown neuronal K+ channel subtype may be involved.

Animals↗
PubMed1991

Voltage-dependent inactivation of the potassium current of embryonic chick hepatocytes.

The whole-cell patch electrode voltage clamp technique was used to study the inactivation properties of the delayed rectifying potassium current of single cultured embryonic chick hepatocytes at 20 degrees C. The potassium current activates maximally within 250-500 ms of membrane depolarization, after which it decays with a monoexponential time course. Both steady-state activation and inactivation are voltage dependent. Steady-state inactivation declines from 100% at -5 mV to 0 near -70 mV. with half inactivation at -41 mV. At the resting potential (EM) of these cells (-21.5 +/- 6.0 mV, n = 36) 6-18% of the IK channels are not inactivated and less than 5% are open. Development and removal of inactivation follow single exponential time courses. The inactivation time constant attains a maximum of around 30 s at -35 mV and is sharply voltage dependent at the EM of these cells. Measurement of EM under current clamp shows random oscillations of 5-10 mV amplitude. We suggest that the voltage- and time-dependent properties of IK, in tandem with a time- and voltage-independent, non-selective current also seen here, would provide the mechanism for a fluctuating EM.

Animals↗
PubMed1997

Model of a thalamocortical neurone with dendritic voltage-gated ion channels.

To investigate the functional role of dendrites of thalamocortical neurones, we have used our one-compartmental model to construct a multi-compartmental model with dendritic regions chosen according to a representative soma-to-dendritic terminal path of an X cell of the cat dorsal lateral geniculate nucleus. The multi-compartmental model with dendritic low-threshold CA2+ and delayed rectifier K+ channels yields more accurate results than the one-compartmental model when simulating tonic firing and oscillatory activities, and provides a useful means for the study of propagation of excitation on the dendrites.

Action Potentials↗
PubMed1999

Endothelial cells freshly isolated from resistance-sized pulmonary arteries possess a unique K(+) current profile.

We have, for the first time, developed a reliable method for freshly isolating viable endothelial cells from resistance-sized rat pulmonary arteries. The endothelial origin of these cells was confirmed using indirect immunofluorescence, utilizing fluorescently labeled low-density lipoprotein. Biophysical and pharmacological patch-clamp experiments conducted under quasiphysiological cationic gradients revealed that these cells had a mean resting membrane potential of approximately -38 mV and displayed a delayed-rectifying K(+) current. Immunohistochemical staining of rat lung cross-sections revealed an abundance of K(V)1.5 channel protein in pulmonary endothelium. This is the first report of a delayed-rectifying K(+) current in endothelial cells of resistance-sized pulmonary arteries. Since changes in membrane potential associated with K(+) channel activity affect release of vasoactive substances from endothelial cells, this finding has important implications for understanding the mechanisms underlying control of pulmonary vascular tone.

Animals↗
PubMed1996

Spectrum of HERG K+-channel dysfunction in an inherited cardiac arrhythmia.

Long QT syndrome (LQT) is an autosomal dominant disorder that can cause sudden death from cardiac arrhythmias. We recently discovered that mutations in HERG, a K+-channel gene, cause chromosome 7-linked LQT. Heterologous expression of HERG in Xenopus oocytes revealed that HERG current was similar to a well-characterized cardiac delayed rectifier K+ current, IKr, and led to the hypothesis that mutations in HERG reduced IKr, causing prolonged myocellular action potentials. To define the mechanism of LQT, we injected oocytes with mutant HERG complementary RNAs, either singly or in combination with wild-type complementary RNA. Some mutations caused loss of function, whereas others caused dominant negative suppression of HERG function. These mutations are predicted to cause a spectrum of diminished IKr and delayed ventricular repolarization, consistent with the prolonged QT interval observed in individuals with LQT.

Animals↗
PubMed1998

Potassium currents and excitability in second-order auditory and vestibular neurons.

Potassium channels are involved in the control of neuronal excitability by fixing the membrane potential, shaping the action potential, and setting firing rates. Recently, attention has been focused on identifying the factors influencing excitability in second-order auditory and vestibular neurons. Located in the brainstem, second-order auditory and vestibular neurons are sites for convergence of inputs from first-order auditory or vestibular ganglionic cells with other sensory systems and also motor areas. Typically, second-order auditory neurons exhibit two distinct firing patterns in response to depolarization: tonic, with a repetitive firing of action potentials, and phasic, characterized by only one or a few action potentials. In contrast, all mature vestibular second-order neurons fire tonically on depolarization. Already, certain fundamental roles have emerged for potassium currents in these neurons. In mature auditory and vestibular neurons, I(K), the delayed rectifier, is required for the fast repolarization of action potentials. In tonically firing auditory neurons, I(A), the transient outward rectifier, defines the discharge pattern. I(DS), a delayed rectifier-like current distinguished by its low threshold of activation, is found in phasically firing auditory and some developing vestibular neurons where it limits firing to one or a few spikes, and also may contribute to forming short-duration excitatory postsynaptic potential (EPSPs). Also, I(DS) sets the threshold for action potential generation rather high, which may prevent spontaneous discharge in phasically firing cells. During development, there is a gradual acquisition and loss of some potassium conductances, suggesting developmental regulation. As there are similarities in membrane properties of second-order auditory and vestibular neurons, investigations on firing pattern and its underlying mechanisms in one system should help to uncover fundamental properties of the other.

Action Potentials↗