Calcium-independent depolarization-activated potassium currents in superior colliculus-projecting rat visual cortical neurons

1995 ◽  
Vol 73 (6) ◽  
pp. 2163-2178 ◽  
Author(s):  
J. L. Albert ◽  
J. M. Nerbonne
Keyword(s):  
Superior Colliculus ◽  
Cortical Neurons ◽  
Outward Current ◽  
Delayed Rectifier ◽  
Voltage Dependent ◽  
K Current ◽  
Current Densities ◽  
Visual Cortical ◽  
K Currents

1. K+ conductances were characterized in isolated, identified superior colliculus-projecting (SCP) rat visual cortical neurons. SCP neurons were identified in vitro under epifluorescence illumination after in vivo retrograde labeling with rhodamine-labeled microspheres or "beads." For experiments, SCP neurons were isolated from the primary visual cortex of postnatal day 7 to 16 (P7-P16) Long Evans rat pups after bead injections into the ipsilateral superior colliculus at p5. 2. Recording conditions were optimized to allow the characterization of Ca2+ -independent K+ conductances. SCP cells that were largely devoid of processes were selected for recording, and experiments were completed 2-30 h after cell isolation. Ca2+ -independent, depolarization-activated K+ currents were routinely recorded during 200-ms voltage steps to potentials positive to -50 mV from a holding potential of -70 mV. 3. Peak outward current densities and the relative amplitudes of the peak and plateau outward currents evoked during 200-ms voltage steps varied among SCP cells. Although cells were isolated from animals at different ages (P7-P16) and maintained for varying times in vitro (2-30 h), no correlations were found between the variations in peak current densities or peak to plateau current ratios and the age of the animal from which the cell was isolated or the length of time the cell was maintained in vitro before recording. 4. Pharmacological experiments revealed the coexpression of three K+ current components in SCP cells that could be separated on the basis of differing sensitivities to the K+ channel blockers, 4-aminopyridine (4-AP) and tetraethylammonium (TEA). Varying the concentration of 4-AP, for example, facilitated the separation of two rapidly activating K+ currents similar to A (IA) and D(ID) type currents in other cells. ID in SCP neurons is blocked by micromolar concentrations of 4-AP, whereas micromolar concentrations of 4-AP are required to effect complete block of IA in these cells. The current component remaining in the presence of high concentrations (5-10 mM) of 4-AP is slowly activating outward K+ current, similar to delayed rectifier (IK) currents in other cells. IK in SCP neurons is blocked by micromolar concentrations of TEA. 5. Activation of IA, ID, and IK in SCP neurons is voltage dependent, although the three current components display distinct time- and voltage-dependent properties. For example, although both IA and ID begin to activate at approximately -50 mV, IA activates two to three times faster than ID. In addition, the threshold for activation of IK (-30 mV) is approximately 20 mV depolarized from that of IA (or ID), and the voltage dependence of IK activation is steeper than that of IA and ID.(ABSTRACT TRUNCATED AT 400 WORDS)

Choline chloride activates time-dependent and time-independent K+ currents in dog atrial myocytes

1994 ◽  
Vol 266 (1) ◽  
pp. C42-C51 ◽  
Author(s):  
B. Fermini ◽  
S. Nattel
Keyword(s):  
Choline Chloride ◽  
Outward Current ◽  
Time Dependent ◽  
Equilibrium Potential ◽  
Delayed Rectifier ◽  
Atrial Myocytes ◽  
Patch Clamp Technique ◽  
Voltage Dependent ◽  
K Current ◽  
K Currents

Using the whole cell configuration of the patch-clamp technique, we studied the effect of isotonic replacement of bath sodium chloride (NaCl) by choline chloride (ChCl) in dog atrial myocytes. Our results show that ChCl triggered 1) activation of a time-independent background current, characterized by a shift of the holding current in the outward direction at potentials positive to the K+ equilibrium potential (EK), and 2) activation of a time- and voltage-dependent outward current, following depolarizing voltage steps positive to EK. Because the choline-induced current obtained by depolarizing steps exhibited properties similar to the delayed rectifier K+ current (IK), we named it IKCh. The amplitude of IKCh was determined by extracellular ChCl concentration, and this current was generally undetectable in the absence of ChCl. IKCh was not activated by acetylcholine (0.001-1.0 mM) or carbachol (10 microM) and could not be recorded in the absence of ChCl or when external NaCl was replaced by sucrose or tetramethylammonium chloride. IKCh was inhibited by atropine (0.01-1.0 microM) but not by the M1 antagonist pirenzepine (up to 10 microM). This current was carried mainly by K+ and was inhibited by CsCl (120 mM, in the pipette) or barium (1 mM, in the bath). We conclude that in dog atrial myocytes, ChCl activates a background conductance comparable to ACh-dependent K+ current, together with a time-dependent K+ current showing properties similar to IK.

Na+, K+ and Ca2+ currents in identified leech neurones in culture

1989 ◽  
Vol 141 (1) ◽  
pp. 1-20
Author(s):  
R. R. Stewart ◽  
J. G. Nicholls ◽  
W. B. Adams
Keyword(s):  
Minor Component ◽  
Outward Current ◽  
Membrane Properties ◽  
Delayed Rectifier ◽  
Inactivation Kinetics ◽  
Channel Blockers ◽  
Sensory Neurones ◽  
K Current ◽  
The Individual ◽  
K Currents

1. Na+, K+ and Ca2+ currents have been measured by voltage-clamp in Retzius (R), anterior pagoda (AP) and sensory (pressure, touch and nociceptive) cells dissected from the central nervous system (CNS) of the leech. These cells maintain their distinctive membrane properties and action potential configurations in culture. Currents carried by the individual ions were analysed by the use of channel blockers and by their kinetics. Since the cells are isopotential they can be voltage-clamped effectively. 2. Depolarization, as expected, gave rise to an early inward Na+ current followed by a delayed outward K+ current. In Na+-free medium containing tetraethylammonium (TEA+), and in the presence of 4-aminopyridine (4-AP), inward Ca2+ currents were revealed that inactivated slowly and were blocked by Cd2+ and Mn2+. 3. Na+ and Ca2+ currents were similar in their characteristics in R. AP and sensory neurones. In contrast, K+ currents showed marked differences. Three principal K+ currents were identified. These differed in their time courses of activation and inactivation and in their responses to Ca2+ channel blockers. 4. K+ currents of the A-type (IA) activated and inactivated rapidly, were not affected by Ca2+ channel blockers and were eliminated by steady-state inactivation at holding potentials of −30 mV. A-type K+ currents were found in AP cells and as a minor component of the outward current in R cells. A Ca2+-activated K+ current (IC), that inactivated more slowly and was reduced by Ca2+ channel blockers, constituted the major outward current in R cells. The third K+ current resembled the delayed rectifier currents (IK1 and IK2) of squid axons with slow activation and inactivation kinetics. Such currents were found in R cells and in the sensory neurones (T, P and N). 5. The principal differences in membrane properties of identified leech neurones can be explained in terms of the numbers of Na+ channels and the distinctive kinetics of K+ channels in each type of cell.

scholarly journals A time- and voltage-dependent K+ current in single cardiac cells from bullfrog atrium.

1986 ◽  
Vol 88 (6) ◽  
pp. 777-798 ◽  
Author(s):  
J R Hume ◽  
W Giles ◽  
K Robinson ◽  
E F Shibata ◽  
R D Nathan ◽  
...  
Keyword(s):  
Time Course ◽  
Voltage Dependence ◽  
Outward Current ◽  
Cardiac Cells ◽  
Delayed Rectifier ◽  
Mechanical Dispersion ◽  
Atrial Cells ◽  
Voltage Dependent ◽  
K Current ◽  
Kinetics Of

Individual myocytes were isolated from bullfrog atrium by enzymatic and mechanical dispersion, and a one-microelectrode voltage clamp was used to record the slow outward K+ currents. In normal [K+]o (2.5 mM), the slow outward current tails reverse between -95 and -100 mV. This finding, and the observed 51-mV shift of Erev/10-fold change in [K+]o, strongly suggest that the "delayed rectifier" in bullfrog atrial cells is a K+ current. This current, IK, plays an important role in initiating repolarization, and it is distinct from the quasi-instantaneous, inwardly rectifying background current, IK. In atrial cells, IK does not exhibit inactivation, and very long depolarizing clamp steps (20 s) can be applied without producing extracellular K+ accumulation. The possibility of [K+]o accumulation contributing to these slow outward current changes was assessed by (a) comparing reversal potentials measured after short (2 s) and very long (15 s) activating prepulses, and (b) studying the kinetics of IK at various holding potentials and after systematically altering [K+]o. In the absence of [K+]o accumulation, the steady state activation curve (n infinity) and fully activated current-voltage (I-V) relation can be obtained directly. The threshold of the n infinity curve is near -50 mV, and it approaches a maximum at +20 mV; the half-activation point is approximately -16 mV. The fully activated I-V curve of IK is approximately linear in the range -40 to +30 mV. Semilog plots of the current tails show that each tail is a single-exponential function, which suggests that only one Hodgkin-Huxley conductance underlies this slow outward current. Quantitative analysis of the time course of onset of IK and of the corresponding envelope of tails demonstrate that the activation variable, n, must be raised to the second power to fit the sigmoid onset accurately. The voltage dependence of the kinetics of IK was studied by recording and curve-fitting activating and deactivating (tail) currents. The resulting 1/tau n curve is U-shaped and somewhat asymmetric; IK exhibits strong voltage dependence in the diastolic range of potentials. Changes in the [Ca2+]o in the superfusing Ringer's, and/or addition of La3+ to block the transmembrane Ca2+ current, show that the time course and magnitude of IK are not significantly modulated by transmembrane Ca2+ movements, i.e., by ICa. These experimentally measured voltage- and time-dependent descriptors of IK strongly suggest an important functional role for IK in atrial tissue: it initiates repolarization and can be an important determinant of rate-induced changes in action potential duration.

scholarly journals Voltage-dependent conductances in Limulus ventral photoreceptors.

1982 ◽  
Vol 79 (2) ◽  
pp. 187-209 ◽  
Author(s):  
J E Lisman ◽  
G L Fain ◽  
P M O'Day
Keyword(s):  
Outward Current ◽  
Delayed Rectifier ◽  
Molluscan Neurons ◽  
Inward Current ◽  
Transient Component ◽  
Outward Currents ◽  
Voltage Dependent ◽  
Inward Currents ◽  
K Current ◽  
A Current

The voltage-dependent conductances of Limulus ventral photoreceptors have been investigated using a voltage-clamp technique. Depolarization in the dark induces inward and outward currents. The inward current is reduced by removing Na+ or Ca2+ and is abolished by removing both ions. These results suggest that both Na+ and Ca2+ carry voltage-dependent inward current. Inward current is insensitive to tetrodotoxin but is blocked by external Ni2+. The outward current has a large transient component that is followed by a smaller maintained component. Intracellular tetraethylammonium preferentially reduces the maintained component, and extracellular 4-amino pyridine preferentially reduces the transient component. Neither component is strongly affected by removal of extracellular Ca2+ or by intracellular injection of EGTA. It is concluded that the photoreceptors contain at least three separate voltage-dependent conductances: 1) a conductance giving rise to inward currents; 2) a delayed rectifier giving rise to maintained outward K+ current; and 3) a rapidly inactivating K+ conductance similar to the A current of molluscan neurons.

Characterization of macroscopic outward currents of canine colonic myocytes

1989 ◽  
Vol 257 (3) ◽  
pp. C461-C469 ◽  
Author(s):  
W. C. Cole ◽  
K. M. Sanders
Keyword(s):  
Outward Current ◽  
Cell Voltage ◽  
Muscle Cells ◽  
Time Dependent ◽  
Delayed Rectifier ◽  
Delayed Rectifier Current ◽  
Outward Currents ◽  
Voltage Dependent ◽  
K Current ◽  
Time Courses

Outward currents of colonic smooth muscle cells were characterized by the whole cell voltage-clamp method. Four components of outward current were identified: a time-independent and three time-dependent components. The time-dependent current showed strong outward rectification positive to -25 mV and was blocked by tetraethylammonium. The time-dependent components were separated on the basis of their time courses, voltage dependence, and pharmacological sensitivities. They are as follows. 1) A Ca2+-activated K current sensitive to external Ca2+ and Ca2+ influx was blocked by ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid (0.1 X 10(-3) M) and nifedipine (1 X 10(-6) and was increased by elevated Ca2+ (8 X 10(-6) M) and BAY K 8644 (1 X 10(-6) M). 2) A "delayed rectifier" current was observed that decayed slowly with time and showed no voltage-dependent inactivation. 3) Spontaneous transient outward currents that were blocked by ryanodine (2 X 10(-6) M) were also recorded. The possible contributions of these currents to the electrical activity of colonic muscle cells in situ are discussed. Ca2+-activated K current may contribute a significant conductance to the repolarizing phase of electrical slow waves.

Somatostatin increases voltage-dependent potassium currents in rat somatotrophs

1990 ◽  
Vol 259 (6) ◽  
pp. C854-C861 ◽  
Author(s):  
C. Chen ◽  
J. Zhang ◽  
J. D. Vincent ◽  
J. M. Israel
Keyword(s):  
Growth Hormone ◽  
Cell Voltage ◽  
Inhibitory Effect ◽  
Delayed Rectifier ◽  
Hormone Release ◽  
Growth Hormone Release ◽  
Voltage Dependent ◽  
Inward Currents ◽  
K Current ◽  
K Currents

To study the modulatory effects of somatostatin on membrane K+ currents, whole cell voltage-clamp recordings were performed on identified rat somatotrophs in primary culture. In the presence of Co2+ (2 mM) and tetrodotoxin (1 microM) in the bath solution to block Ca2+ and Na+ inward currents, two types of voltage-activated K+ currents were identified on the basis of their kinetics and pharmacology. First, a delayed rectifier K+ current (IK) had a threshold of -20 mV, did not decay during voltage steps lasting 300 ms, and was markedly attenuated by extracellular application of tetraethylammonium (TEA, 10 mM). Second, a transient outward K+ current (IA) was activated at -40 mV (from a holding potential of -80 mV) and persisted despite the presence of TEA. This IA was blocked by 4-aminopyridine (2 mM). Somatostatin (10 nM) increased IK by 75% and IA by 45% without obvious effects on steady-state voltage dependency of activation or inactivation, and these effects were reversible. This increase in K+ currents may contribute in part to the inhibitory effect of somatostatin on growth hormone release.

A fast transient potassium current in thalamic relay neurons: kinetics of activation and inactivation

1991 ◽  
Vol 66 (4) ◽  
pp. 1304-1315 ◽  
Author(s):  
J. R. Huguenard ◽  
D. A. Coulter ◽  
D. A. Prince
Keyword(s):  
Steady State ◽  
Reversal Potential ◽  
Cell Voltage ◽  
Inactivation Kinetics ◽  
Voltage Dependent ◽  
Steady State Inactivation ◽  
K Current ◽  
K Currents ◽  
Relay Neurons

1. Whole-cell voltage-clamp techniques were used to record K+ currents in relay neurons (RNs) that had been acutely isolated from rat thalamic ventrobasal complex and maintained at 23 degrees C in vitro. Tetrodoxin (TTX; 0.5 microM) was used to block Na+ currents, and reduced extracellular levels of Ca2+ (1 mM) were used to minimize contributions from Ca2+ current (ICa). 2. In RNs, depolarizing commands activate K+ currents characterized by a substantial rapidly inactivating (time constant approximately 20 ms) component, the features of which correspond to those of the transient K+ current (IA) in other preparations, and by a smaller, more slowly activating K+ current, "IK". IA was reversibly blocked by 4-aminopyridine (4-AP, 5 mM), and the reversal potential varied with [K+]o as predicted by the Nernst equation. 3. IA was relatively insensitive to blockade by tetraethylammonium [TEA; 50%-inhibitory concentration (IC50) much much greater than 20 mM]; however, two components of IK were blocked with IC50S of 30 microM and 3 mM. Because 20 mM TEA blocked 90% of the sustained current while reducing IA by less than 10%, this concentration was routinely used in experiments in which IA was isolated and characterized. To further minimize contamination by other conductances, 4-AP was added to TEA-containing solutions and the 4-AP-sensitive current was obtained by subtraction. 4. Voltage-dependent steady-state inactivation of peak IA was described by a Boltzman function with a slope factor (k) of -6.5 and half-inactivation (V1/2) occurring at -75 mV. Activation of IA was characterized by a Boltzman curve with V1/2 = -35 mV and k = 10.8. 5. IA activation and inactivation kinetics were best fitted by the Hodgkin-Huxley m4h formalism. The rate of activation was voltage dependent, with tau m decreasing from 2.3 ms at -40 mV to 0.5 ms at +50 mV. Inactivation was relatively voltage independent and nonexponential. The rate of inactivation was described by two exponential decay processes with time constants (tau h1 and tau h2) of 20 and 60 ms. Both components were steady-state inactivated with similar voltage dependence. 6. Temperature increases within the range of 23-35 degrees C caused IA activation and inactivation rates to become faster, with temperature coefficient (Q10) values averaging 2.8. IA amplitude also increased as a function of temperature, albeit with a somewhat lower Q10 of 1.6. 7. Several voltage-dependent properties of IA closely resemble those of the transient inward Ca2+ current, IT. (ABSTRACT TRUNCATED AT 400 WORDS)

scholarly journals Physiological Roles of the Rapidly Activated Delayed Rectifier K+ Current in Adult Mouse Heart Primary Pacemaker Activity

2021 ◽  
Vol 22 (9) ◽  
pp. 4761
Author(s):  
Wei Hu ◽  
Robert B. Clark ◽  
Wayne R. Giles ◽  
Erwin Shibata ◽  
Henggui Zhang
Keyword(s):  
Adult Mouse ◽  
Delayed Rectifier ◽  
Pacemaker Activity ◽  
Mouse Heart ◽  
Voltage Dependent ◽  
Electrophysiological Studies ◽  
Ionic Mechanisms ◽  
K Current ◽  
Significant Expression

Robust, spontaneous pacemaker activity originating in the sinoatrial node (SAN) of the heart is essential for cardiovascular function. Anatomical, electrophysiological, and molecular methods as well as mathematical modeling approaches have quite thoroughly characterized the transmembrane fluxes of Na+, K+ and Ca2+ that produce SAN action potentials (AP) and ‘pacemaker depolarizations’ in a number of different in vitro adult mammalian heart preparations. Possible ionic mechanisms that are responsible for SAN primary pacemaker activity are described in terms of: (i) a Ca2+-regulated mechanism based on a requirement for phasic release of Ca2+ from intracellular stores and activation of an inward current-mediated by Na+/Ca2+ exchange; (ii) time- and voltage-dependent activation of Na+ or Ca2+ currents, as well as a cyclic nucleotide-activated current, If; and/or (iii) a combination of (i) and (ii). Electrophysiological studies of single spontaneously active SAN myocytes in both adult mouse and rabbit hearts consistently reveal significant expression of a rapidly activating time- and voltage-dependent K+ current, often denoted IKr, that is selectively expressed in the leading or primary pacemaker region of the adult mouse SAN. The main goal of the present study was to examine by combined experimental and simulation approaches the functional or physiological roles of this K+ current in the pacemaker activity. Our patch clamp data of mouse SAN myocytes on the effects of a pharmacological blocker, E4031, revealed that a rapidly activating K+ current is essential for action potential (AP) repolarization, and its deactivation during the pacemaker potential contributes a small but significant component to the pacemaker depolarization. Mathematical simulations using a murine SAN AP model confirm that well known biophysical properties of a delayed rectifier K+ current can contribute to its role in generating spontaneous myogenic activity.

Voltage-activated potassium currents of rabbit osteoclasts: effects of extracellular calcium

1994 ◽  
Vol 267 (4) ◽  
pp. C1103-C1111 ◽  
Author(s):  
L. G. Hammerland ◽  
A. S. Parihar ◽  
E. F. Nemeth ◽  
M. C. Sanguinetti
Keyword(s):  
Negative Charge ◽  
Voltage Dependence ◽  
Physiological Function ◽  
Inward Rectifier ◽  
Delayed Rectifier ◽  
Voltage Dependent ◽  
K Current ◽  
Kinetics Of ◽  
K Currents ◽  
Simple Surface

The effects of increased extracellular Ca2+ concentration ([Ca2+]e) were examined on a delayed-rectifier K+ current (IK) and an inward-rectifier K+ current (IK1) in rabbit osteoclasts. Elevation of [Ca2+]e from 1.8 to 18 mM shifted the half point for IK activation by +11.5 mV and the voltage dependence of inactivation by +9.7 mV and slowed the rate of IK activation and deactivation. These effects of elevated [Ca2+]e on IK are consistent with screening of cell surface negative charge. However, elevation of [Ca2+]e increased the voltage-dependent kinetics of IK inactivation at all potentials tested, inconsistent with that predicted by simple surface charge theory. This finding suggests an additional, regulatory role for [Ca2+]e in the gating of IK channels. Some osteoclasts had an IK1, which was decreased when [Ca2+]e was raised from 1.8 to 18 mM. The physiological function of both types of K+ currents remains to be determined, and it is not clear whether these currents are involved with the coupling of cytosolic [Ca2+] to [Ca2+]e.

scholarly journals A whole-cell and single-channel study of the voltage-dependent outward potassium current in avian hepatocytes.

1988 ◽  
Vol 91 (2) ◽  
pp. 255-274 ◽  
Author(s):  
C Marchetti ◽  
R T Premont ◽  
A M Brown
Keyword(s):  
Single Channel ◽  
Reversal Potential ◽  
Outward Current ◽  
Single Type ◽  
K Channel ◽  
Delayed Rectifier ◽  
Patch Clamp Technique ◽  
Voltage Dependent ◽  
Single Channel Currents ◽  
K Currents

Voltage-dependent membrane currents were studied in dissociated hepatocytes from chick, using the patch-clamp technique. All cells had voltage-dependent outward K+ currents; in 10% of the cells, a fast, transient, tetrodotoxin-sensitive Na+ current was identified. None of the cells had voltage-dependent inward Ca2+ currents. The K+ current activated at a membrane potential of about -10 mV, had a sigmoidal time course, and did not inactivate in 500 ms. The maximum outward conductance was 6.6 +/- 2.4 nS in 18 cells. The reversal potential, estimated from tail current measurements, shifted by 50 mV per 10-fold increase in the external K+ concentration. The current traces were fitted by n2 kinetics with voltage-dependent time constants. Omitting Ca2+ from the external bath or buffering the internal Ca2+ with EGTA did not alter the outward current, which shows that Ca2+-activated K+ currents were not present. 1-5 mM 4-aminopyridine, 0.5-2 mM BaCl2, and 0.1-1 mM CdCl2 reversibly inhibited the current. The block caused by Ba was voltage dependent. Single-channel currents were recorded in cell-attached and outside-out patches. The mean unitary conductance was 7 pS, and the channels displayed bursting kinetics. Thus, avian hepatocytes have a single type of K+ channel belonging to the delayed rectifier class of K+ channels.

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