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1 arybdotoxin-sensitive (BK) calcium-dependent potassium current.
2 fied potassium current and transient outward potassium current.
3 equired for generating the transient outward potassium current.
4  which leads to an increase in voltage-gated potassium current.
5 that is mediated by a slow calcium-activated potassium current.
6 hat are mediated by a slow calcium-activated potassium current.
7 ch dictated by a different calcium-dependent potassium current.
8  current and a decrease of transient outward potassium current.
9 cardiac rapidly activating delayed rectifier potassium current.
10 which was attributable to a barium-sensitive potassium current.
11 rols the outward/repolarizing slow rectifier potassium current.
12 vation of bulk calcium inhibits a persistent potassium current.
13 s of voltage-dependent and calcium-dependent potassium current.
14 s that underlie dendrotoxin-sensitive D-type potassium current.
15 xpressions and attenuated the peak of inward potassium current.
16 ontributions to the depolarization-activated potassium current.
17 voltage-dependent contribution to ACh-evoked potassium current.
18 -dependent changes in slow delayed rectifier potassium current.
19 ntrast, NRG1 had minor effects on whole-cell potassium currents.
20 nd the acquisition of mature inner hair cell potassium currents.
21  increased inactivation of voltage-activated potassium currents.
22 r6.2 (I(KATP)) and reducing inward rectifier potassium currents.
23 pe, delayed rectifier, and calcium-dependent potassium currents.
24 cing calcium currents and increasing outward potassium currents.
25 nel gating kinetics of the calcium dependent potassium currents.
26 on as wild-type channels but fail to conduct potassium currents.
27  the fast-inactivating and calcium-activated potassium currents.
28 nce, depolarisation block, and low-threshold potassium currents.
29  slowly rising and falling calcium-dependent potassium currents.
30                          DHPG also decreased potassium currents.
31 sion, increased degradation and smaller Kir3 potassium currents.
32 failed to alter holding or voltage-dependent potassium currents.
33 her mechanisms may also lead to reduction of potassium currents.
34 d by calcium-activated, cyclic AMP-sensitive potassium currents.
35 e) cause compensatory decreases in postspike potassium currents.
36 sociated with two distinct calcium-activated potassium currents.
37 bility by reducing BK-type calcium-activated potassium currents.
38 east in part, by decreased Kv7.2/3 (KCNQ2/3) potassium currents.
39 n of a G protein-coupled inwardly rectifying potassium current, (2) inhibition of a voltage-gated Ca(
40 ory processing and that changes in levels of potassium currents across the nuclei, by mechanisms such
41 rane potential hyperpolarized due in part to potassium current activation.
42 d docking simulations we show that the novel potassium current activator, NS5806, binds at a hydropho
43             M-current is a slowly activating potassium current, active at subthreshold potentials.
44                        The transient outward potassium current agonist NS5806 (5 muM) and the Ca(2+)-
45 rkably, daily antiphase cycles of sodium and potassium currents also drive mouse clock neuron rhythms
46 ting from reduction of the transient outward potassium current, alters properties of EC coupling.
47  associated with decreased transient outward potassium current and Kv4.2 and KChIP2 protein expressio
48  the Drosophila brain reveal that whole-cell potassium current and properties of single dSlo channels
49 ons express the fast delayed rectifier (FDR) potassium current and raise questions about the function
50 ation via normalization of transient outward potassium current and sarcoplasmic reticulum Ca(2+) cont
51 ion of a large conductance calcium-dependent potassium current and the opening of a transient outward
52 ns across models identified inward rectifier potassium current and the sodium-potassium pump as the t
53 ith blockade of ultrarapid delayed rectified potassium current and transient outward potassium curren
54 v4.2 is a major constituent of A-type (I(A)) potassium currents and a key regulator of neuronal membr
55 2.1 and SK, which underlie delayed rectifier potassium currents and afterhyperpolarization respective
56 are responsible for distinct types of native potassium currents and are associated with several human
57 alretinin cells (85%) exhibited large A-type potassium currents and delayed firing action potential d
58  cells that include inhibition of KIR and KV potassium currents and elevations of intracellular calci
59  used in cancer can prolong QT by inhibiting potassium currents and increasing late sodium current (I
60 toplasmic calcium activated Ca(2+) dependent potassium currents and led to neuronal apoptosis in KO h
61 heir stimulation inhibits M-type [Kv7, K(M)] potassium currents and N-type (Ca(V)2.2) calcium current
62 the functional repertoire of Kv3.1 and Kv3.2 potassium currents and suggest roles for these alpha sub
63 clofenac, dramatically enhanced KCNQ (K(v)7) potassium currents and suppressed L-type voltage-sensiti
64                 In na mutants, expression of potassium currents and the key neuropeptide PDF are elev
65 o fourfold interanimal variability for three potassium currents and their mRNA expression.
66 rent, inhibition of a slow calcium-activated potassium current, and activation of a calcium-dependent
67  current was outweighed by calcium-activated potassium current, and in current clamp, nimodipine usua
68 lcium entry and subsequent calcium-activated potassium current, and the hyperpolarizing shift in post
69 delayed firing discharge, large rapid A-type potassium currents, and central, radial or vertical cell
70 and small (SK) conductance calcium-activated potassium currents, and hyperpolarization-activated (I(H
71 rrents, depressed the slow delayed rectifier potassium currents, and increased the resting membrane p
72 elayed repolarization from downregulation of potassium currents, and multiple reentry circuits during
73                               POSH decreased potassium currents, and the inhibitory effect of POSH on
74 es in the leak, sodium and calcium-activated potassium currents are central to these two developmenta
75 ased in pathological situations where A-type potassium currents are decreased.
76                                       A-type potassium currents are important determinants of neurona
77 rom differential expression of voltage-gated potassium currents, as tufted cells exhibited faster act
78 dominant-negative reduction of the resulting potassium current at subthreshold membrane potentials.
79 rrent (I(M)), and may also underlie the slow potassium current at the node of Ranvier, I(Ks).
80 did not affect hERG/IKr or any other cardiac potassium current at therapeutic concentrations.
81 urve (2 voltage sensor mutations) decreasing potassium currents at the subthreshold level at which th
82         In addition to modulating sodium and potassium currents, beta subunits play nonconducting rol
83 ence of rapidly activating delayed rectifier potassium current blockade.
84 ence of rapidly activating delayed rectifier potassium current blockers (E-4031 and cisapride), incre
85          We observed large voltage-dependent potassium currents, but only a small chromanol sensitive
86 ly because of lack of inhibition of the I(A) potassium current by ERK.
87                                   Background potassium currents carried by the KCNK family of two-por
88 gets, including the I(Ks) (slowly activating potassium current) channel.
89 y (HEK) 293 cells produced a noninactivating potassium current characteristic of M current.
90 GS and GLAST expressions and enhanced inward potassium currents compared with those in the COH rats w
91      Taken together these data indicate that potassium currents constitute a basic determinant for C.
92  positive membrane potential, the ACh-evoked potassium current decayed exponentially over approximate
93               We observed reduced sodium and potassium current densities in ventricular myocytes, as
94                    Pergolide inhibited PASMC potassium current density, resulting in membrane depolar
95           The balance between two particular potassium currents dictates how heart cells respond to p
96  Individual neurons with different levels of potassium currents differ in their ability to follow spe
97 ings are consistent with the hypothesis that potassium current downregulation leads to abnormal repol
98 lock phase involve persistent suppression of potassium current, downstream of Per1 gene induction, in
99 esults from frequency-dependent reduction of potassium current during spike repolarization.
100                              Inactivation of potassium currents during maintained firing results in a
101 e M-current, a low-threshold noninactivating potassium current, during seizures.
102  the G protein-activated inwardly-rectifying potassium current evoked by receptor-saturating concentr
103 ting the duration of the AP, the BK-mediated potassium current exerts control over the frequency of A
104 ll-cell coupling lead to regional changes in potassium current expression, which in this case facilit
105                               Reduced inward potassium current following nerve ligation would increas
106                              Noninactivating potassium current formed by KCNQ2 (Kv7.2) and KCNQ3 (Kv7
107     They are responsible for background leak potassium currents found in many cell types.
108 patch-clamp techniques, recordings of either potassium current from rat posterior taste receptor cell
109 contact sites and has been shown to regulate potassium current gating kinetics as well as channel tra
110 non-inactivating low-threshold voltage-gated potassium current generated by the M-channel.
111 urons requires ultra-rapid delayed rectifier potassium currents generated by homomeric or heteromeric
112                                              Potassium currents generated by voltage-gated potassium
113 he magnitude of fast delayed rectifier (FDR) potassium currents has a diurnal rhythm that peaks durin
114 f-function mutations in the gene for outward potassium currents have been shown to underlie the conge
115 , we evaluated whether the transient outward potassium current I(A) is expressed in PVN-RVLM neurones
116  often caused by direct block of the cardiac potassium current I(Kr)/hERG, which is crucial for termi
117 ed most often by direct block of the cardiac potassium current I(Kr)/hERG.
118                             Apamin sensitive potassium current (I KAS), carried by the type 2 small c
119                                       A-type potassium current (I(A)) both activates and inactivates
120 med to address whether the transient outward potassium current (I(A)) in identified rostral ventrolat
121 hat DA could immediately alter the transient potassium current (I(A)) of identified neurons in the st
122 dine and 0.5 mM Ba2+, consistent with A-type potassium current (I(A)).
123 n the time course of acetylcholine-activated potassium current (I(K)(ACh)) activation and deactivatio
124 a(2+) current (I(CaL)) and delayed rectifier potassium current (I(K)) in guinea pig SAN pacemaker cel
125  (I(Na)) and 4AP-sensitive and TEA-resistant potassium current (I(K)).
126 a)) and to suppress a delayed rectifier-like potassium current (I(K)).
127 ynaptic integration: a low-voltage-activated potassium current (I(K-LVA)) and a hyperpolarization-act
128 n important role for the inwardly rectifying potassium current (I(K1)) in controlling the dynamics of
129 rrent mechanisms are the inwardly rectifying potassium current (I(K1)), which is important for mainte
130 ductance differences in the inward rectifier potassium current (I(K1)).
131 hannels mediate the cardiac inward rectifier potassium current (I(K1)).
132 ally depended on the expression of an A-type potassium current (I(KA)), which when active attenuated
133  recorded block by lopinavir of repolarising potassium current (I(Kr)) channels in neonatal mouse car
134 hrough the blocking of the delayed rectifier potassium current (I(Kr)).
135 es an increase of the slow delayed rectifier potassium current (I(Ks)).
136  cAMP-dependent increase in the slow outward potassium current (I(Ks)).
137                Kv1.5 mediates the ultrarapid potassium current (I(Kur)) that controls atrial action p
138 nnels contributing to the ultrarapid outward potassium current (I(Kur)).
139 pression would predict different patterns of potassium current (I(Kv)) regulation.
140 nvolving inhibition of the delayed rectifier potassium current (I(Kv)).
141  heterogeneous loss of the transient outward potassium current (I(to))-mediated epicardial action pot
142 sed the inward and delayed outward rectifier potassium currents (I IRK and I DRK), calcium (Ca2+) rel
143 neurons, the amplitude of rapid inactivating potassium currents (I(A)) was significantly increased at
144 ge-dependent activation of voltage-sensitive potassium currents (I(K)).
145 treatment with blockers of calcium-activated potassium currents (I(KCa)) reproduced this shift and bl
146          The amplitudes of delayed rectifier potassium currents (I(Kd)) in CA1 neurons were progressi
147 t a novel coupled system of sodium-activated potassium currents (I(KNa)) and persistent sodium curren
148 that contribute to cardiac transient outward potassium currents (I(to)).
149 sing cultured DRG neurons, that of the total potassium current, I(K), the K(Na) current is predominan
150                  the rapid delayed rectifier potassium current, I(Kr), which flows through the human
151 pid compensatory interaction among a pair of potassium currents, I(A) and I(KCa), that stabilizes bot
152 ltage-clamp experiments, 2-AG reduced A-type potassium current (IA) through a cannabinoid receptor-in
153                  GxTX-1E also reduced A-type potassium current (IA), but much more weakly.
154  by the opposing actions of the fast outward potassium current, IA , mediated by alpha subunits of th
155 lux (IC(50), 1.4 nM) and inwardly rectifying potassium currents (IC(50), 1 nM) in CHO cells stably ex
156 system underlying the ultra-rapid rectifying potassium current (Ik(ur)), a major repolarizing current
157 solated CB preparation and decreased outward potassium current (Ik) in CB glomus cells to levels simi
158 pendent, time-independent rectifying outward potassium current (IK).
159            In each neuron, voltage-dependent potassium currents (IK) were evaluated and, in represent
160 25 microM) also suppressed voltage-activated potassium currents (IK+) and calcium currents (ICa2+).
161 lum Ca2+ concentrations, inwardly rectifying potassium current (IK1) density, and gap junction conduc
162 mulations predict that the inward rectifying potassium current (IK1) is an essential determinant of r
163 ssium current (IKr) and the inward rectifier potassium current (IK1) were also downregulated (P<0.05)
164         Delayed excitation, caused by A-type potassium current (IKA), was observed in most of NTS neu
165 armacological tools, acetylcholine-regulated potassium current (IKACh) with patch clamp recording, me
166 paper unveils the critical role of the brake potassium current IKD in damage-triggered cold allodynia
167                      A low voltage-activated potassium current, IKL, is found in auditory neuron type
168 utational modeling, that a low-voltage-gated potassium current, IKLT, underlies the resonance.
169 he rapid components of the delayed rectifier potassium current (IKr) and the inward rectifier potassi
170     Drugs are screened for delayed rectifier potassium current (IKr) blockade to predict long QT synd
171 ition of the cardiac rapid delayed rectifier potassium current (IKr).
172  and KCNE1 protein coassembly forms the slow potassium current IKS that repolarizes the cardiac actio
173  KCNE1, Kv7.1 conducts the slowly activating potassium current IKs, which is one of the major current
174        Effects on the slow delayed rectifier potassium current (IKs) are less recognized.
175 ate the slowly activating, voltage-dependent potassium current (IKs) in the heart that controls the r
176                   The slow delayed rectifier potassium current (IKs) is a key repolarizing current du
177 tion, which increases slow-delayed rectifier potassium current (IKs).
178 l, IKr, and the adrenergic-sensitive cardiac potassium current, IKs, are two primary contributors to
179 potassium channel and its associated cardiac potassium current, IKur.
180 foundly altered protein function, inhibiting potassium current in a dose-dependent manner.
181 that SNX-482 dramatically reduced the A-type potassium current in acutely dissociated dopamine neuron
182   Dysfunction of the fast-inactivating Kv3.4 potassium current in dorsal root ganglion (DRG) neurons
183 ily underlie a major component of the A-type potassium current in mammalian central neurons.
184           Moreover, POSH still decreased the potassium current in oocytes injected with a ROMK1 mutan
185 nsitization of the mu-opioid receptor-evoked potassium current in rat locus ceruleus neurons.
186  (rs1805128), known to modulate an important potassium current in the heart, predicted diLQTS with an
187                          The largest outward potassium current in the soma of neocortical pyramidal n
188 tamine produced a dose-dependent increase in potassium currents in a subset of bipolar cells.
189    The present study compared the changes of potassium currents in acutely dissociated hippocampal ne
190                                Low-threshold potassium currents in deprived NM neurons were not signi
191 n resulted in lack of time-dependent outward potassium currents in guard cells, higher rates of water
192 n previously shown to modulate voltage-gated potassium currents in heterologous expression systems.
193 results indicated that the voltage dependent potassium currents in hippocampal neurons were different
194 ion potential waveforms, and reduced outward potassium currents in isolated cardiac myocytes.
195                                              Potassium currents in olfactory bulb mitral cells from K
196 ression of CD63 had no significant effect on potassium currents in oocytes injected with ROMK1; howev
197 strated MYOCD-induced, iberiotoxin-sensitive potassium currents in porcine coronary SMCs.
198 d by reductions in BK-type calcium-activated potassium currents in spontaneously firing neurons, is e
199 e data support two highly novel conclusions: potassium currents in taste receptor cells are significa
200  we investigated Kv3.1b immunoreactivity and potassium currents in the auditory brainstem sound local
201                                         Leak potassium currents in the nervous system are often carri
202                                 By enhancing potassium currents in the ON bipolar cells, histamine is
203 H at 5 microM increased the amplitude of the potassium currents in the ON bipolar cells.
204 el mechanism for regulation of voltage-gated potassium currents in the setting of cardiac pathology a
205 NTS: Kv2 channels underlie delayed-rectifier potassium currents in various neurons, although their ph
206      Kv2 channels underlie delayed-rectifier potassium currents in various neurons, although their ph
207 al evidence that the mutant protein disrupts potassium current inactivation, strongly supports KCND2
208        In voltage clamp mode, the sodium and potassium currents increased significantly at higher [Na
209 regulated Kcna2, reduced total voltage-gated potassium current, increased excitability in DRG neurons
210 neurons in the locus ceruleus to measure the potassium current induced by morphine.
211 ctions) does not affect the extent of M-type potassium current inhibition produced by either receptor
212 at, at the cellular level, delayed-rectifier potassium current is a main contributor of KECG correlat
213  evidence that opposite regulation of A-type potassium current is an important factor in this bidirec
214 er, a mutation that impairs Shaker-dependent potassium current, is an allele of sleepless.
215                        I(Ks), the slow heart potassium current, is carried by the I(Ks) potassium cha
216 bunit in somatodendritic subthreshold A-type potassium current (ISA) channels.
217 gnificant reduction of the transient outward potassium current (Ito) in EPI but not in endocardial (E
218                   The fast transient outward potassium current (Ito,f) plays a critical role in the e
219 revealed downregulation of transient outward potassium current (Ito; P<0.05).
220 tagonized by activators of the ATP-sensitive potassium current (K(ATP)).
221 rpolarization-activated, inwardly rectifying potassium current (K(IR)).
222 the supernormal phase results from a reduced potassium current Kdr as a result of accumulation of per
223 on onsets were regeneratively amplified by a potassium current (KIR) whose activation promoted furthe
224  genes (hERG), which encode two repolarizing potassium currents known as I(Ks) and I(Kr).
225                                      Thus, a potassium current, likely mediated through BK channels,
226 n in rat neurons depresses delayed rectifier potassium currents, limits the magnitude of the K+ curre
227 ctive" mutations affecting calcium-dependent potassium currents localized to the C-domain of CaM.
228 BA(A) current and an intrinsic membrane slow potassium current (M-current).
229 hrough G-protein coupled inwardly rectifying potassium currents mediated by delta and mu opioid recep
230 e rat hippocampal slices we show that D-type potassium current modulates the size of the ADP and the
231 y consistent reductions in voltage-activated potassium currents near the action potential threshold a
232 lective, as NS5A1a does not depress neuronal potassium currents nor inhibit Src phosphorylation of Kv
233 led that the isoflurane-activated background potassium current observed in cortical pyramidal neurons
234 ion was mediated by activation of an outward potassium current or blockade of a tonically active inwa
235 tes, the slowly activating delayed rectifier potassium current, or IKs, is believed to be a heteromul
236 e two calcium channels and acting on the two potassium currents, or with differences in channel gatin
237 ation of the MOR and reduced activation of a potassium current over the same time course.
238  CHO-K1 cells line produces highly selective potassium current, overexpression of R162W mutant Kir7.1
239                        In the evening, basal potassium currents peak to silence clock neurons.
240 tassium current, the acetylcholine activated potassium current, peak sodium current, and L-type calci
241 le (CG) cells and many other neurons, A-type potassium currents play an important role in regulating
242  the major cause of ischemic cell death, and potassium currents play important roles in regulating th
243                          Importantly, A-type potassium currents recorded in mesoaccumbal neurons disp
244 t reduction, but the contribution to overall potassium current reduction was almost always much small
245 KS) (slow component of the delayed rectifier potassium current) remained intact.
246 age dependence of acetylcholine (ACh)-evoked potassium currents reveal a more complex relationship be
247 pression of KCNQ1-S140G with KCNE1 generated potassium currents (S140G-IKs) that exhibited greater se
248 -calcium exchanger activity, reduced outward potassium currents, sarcoplasmic reticulum Ca2+ defects,
249 ese is an apamin-sensitive calcium-dependent potassium current (SK).
250 nvolving small conductance calcium-dependent potassium currents (SK).
251 n of the small conductance calcium-activated potassium current, SK.
252 idal neurones we studied the modulation of a potassium current (slow AHP current, I(sAHP)) known to b
253 nce of calcium current and calcium-activated potassium current such that their net influence shifted
254 ent is a slowly activating, non-inactivating potassium current that has been shown to be present in n
255 , there was a component of calcium-dependent potassium current that showed frequency-dependent reduct
256      Since Hodgkin and Huxley discovered the potassium current that underlies the falling phase of ac
257  These channels produce background leak type potassium currents that act to regulate resting membrane
258 licited increases of the inwardly rectifying potassium currents that could be blocked by the GABA(B)
259 tal cholinergic interneurons are sculpted by potassium currents that give rise to prominent afterhype
260 fier potassium current, the inward rectifier potassium current, the acetylcholine activated potassium
261 ent, the slowly activating delayed-rectifier potassium current, the inward rectifier potassium curren
262 ing the rapidly activating delayed-rectifier potassium current, the slowly activating delayed-rectifi
263                  Expression of one important potassium current, the transient outward current (I(to))
264 ny medications inadvertently block the KCNH2 potassium current, these novel findings seem to have cli
265      The ability of crotamine to inhibit the potassium current through K(V) channels unravels it as t
266                                              Potassium currents through SK channels demonstrate inwar
267  channel 3, where SP enhances M-channel-like potassium currents through the NK1 receptor in a G prote
268 fort, a molecular-level understanding of the potassium current underlying the slow afterhyperpolariza
269  Little is known about the voltage-dependent potassium currents underlying spike repolarization in mi
270 selectively coupled to the calcium-dependent potassium currents underlying the AHPs, thereby creating
271 molecular correlate of the transient outward potassium current up-regulated by Abeta peptide, conside
272 specifically enhances an inwardly rectifying potassium current via NPY-Y1 receptors.
273 naptic efficacy, inhibiting postsynaptic Kv3 potassium currents (via phosphorylation), reducing EPSCs
274                                 Reduction of potassium current was also seen with multimeric G85R SOD
275                                Although this potassium current was described two decades ago, the mec
276 dent reduction of overall spike-repolarizing potassium current was identified as Kv3 current by its s
277                                          The potassium current was inhibited by 4-AP and by Heteropod
278 ion of G protein-coupled inwardly rectifying potassium current was measured using whole-cell voltage-
279        The effect of cross-linked 300 kDa on potassium current was reduced by removing Na(+) from the
280 tivation kinetics of D(2) receptor-dependent potassium current was studied using outside-out patch re
281 ution of afferent neuronal voltage-dependent potassium currents was a prominent feature of urethral a
282 nd the effects of these analogues on outward potassium current were evaluated by using two electrode
283                     Whole-cell recordings of potassium currents were made from bipolar cells in slice
284                                    The major potassium currents were not different in LDLr(-/-) and A
285                                              Potassium currents were recorded using 2-microelectrode
286                                In 10 mM TEA, potassium currents were reduced in all the bipolar cells
287                         In contrast, outward potassium currents were significantly reduced by microin
288                                        Other potassium currents were spared, except to the extent tha
289 ntrast, depolarization-activated calcium and potassium currents were unaffected, thus supporting the
290 nts ("calcium sparks") and voltage-dependent potassium currents were unaffected.
291 his current matched that of the native Slack potassium current, which was identified using an siRNA a
292 with specific ionic currents, such as A-type potassium currents, which can linearize the frequency-in
293 ity may be limited by the presence of A-type potassium currents, which limit the effectiveness of the
294 nd sustained as well as rapidly inactivating potassium currents, which were sensitive to TEA and 4-AP
295 d of SK (small-conductance calcium-activated potassium) currents, which were essential for a wide lin
296  KCNQ channels might also contribute to this potassium current whose molecular identity is unknown.
297 tween sodium current and inwardly rectifying potassium current with increasing field strength.
298 ive rise to the M-current, a noninactivating potassium current with slow kinetics.
299 mulation, which regulate cardiac calcium and potassium currents with differential kinetics.
300 ffect of POSH on ROMK1 channels, we measured potassium currents with electrophysiological methods in

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