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1 l conductance and ion selectivity (i.e., the reversal potential).
2 ated channels rather than on a change in Cl- reversal potential.
3 esulted from a positive shift of the GABA(A) reversal potential.
4 lutions that unpredictably display a nonzero reversal potential.
5 IL-2 did not alter the reversal potential.
6 7.0 s, n= 18) were recorded, with a similar reversal potential.
7 also be recorded as a leftward shift in the reversal potential.
8 same ionic dependence, inhibitor profile and reversal potential.
9 to 10 mM, and this caused a +30 mV shift in reversal potential.
10 tage-independent, and IL-2 did not alter the reversal potential.
11 flow of I:(Ca) when V(m) exceeded the I:(Ca) reversal potential.
12 of neuronal depolarization above the GABA(A) reversal potential.
13 a transient collapse in the chloride (Cl(-)) reversal potential.
14 ) -selective and pass current above the K(+) reversal potential.
15 and a depolarization of the stimulus-evoked reversal potential.
16 exchange function and abnormal translocator reversal potential.
17 II boundary toward more hyperpolarized GABAR reversal potentials.
18 on GABA-mediated hyperpolarization and GABA reversal potentials.
19 oaded electrodes (predicted GABA(A) receptor reversal potential: 0 mV) at -15 mV revealed the unexpec
20 hloride pipettes (predicted GABA(A) receptor reversal potentials: 0 mV and -80 mV, respectively) dire
21 e in mean open time, unitary conductance, or reversal potential; (2) an increase in charge transfer i
22 body of Up state activity exhibited a steady reversal potential (-37 mV on average) for hundreds of m
23 s readily detected by DeltaFd beyond the ICa reversal potential (+65 to +100 mV) and was not abolishe
24 The current-voltage relationships and the reversal potential (about +10 mV) of the Na3VO4-, pp60c-
25 all drop in input resistance and an apparent reversal potential above spike threshold, facilitating i
26 sms (shifted gamma-aminobutyric acid [GABA]A reversal potential, altered synaptic transmission), ther
27 nduced by odorants, including onset latency, reversal potential and adaptation to repeated stimulatio
29 unted for by changes to the GABA(A) receptor reversal potential and demonstrates an important differe
30 cause dramatic depolarization of the GABA(A) reversal potential and dominating bicarbonate currents t
31 cellular chloride concentration and chloride reversal potential and how these are affected by changes
32 verload, revealed through a depolarized GABA reversal potential and increased expression of the chlor
33 d by IT led to hyperpolarizing shifts in the reversal potential and large outward currents that were
36 inward currents; the currents had a similar reversal potential and slope conductance to their sponta
37 n amplitude between E14 and E18, whereas Cl- reversal potential and synaptic conductances remained re
38 hat are characterized by a leftward shift in reversal potential and the emergence of large outward cu
40 y down-state events reversed at the chloride reversal potential and were blocked by GABA(A) antagonis
41 racterized by significantly more depolarized reversal potentials and concomitant increases in excitat
43 PNP calculations reproduce also experimental reversal potentials and permeability rations in asymmetr
44 ys, for instance, by dictating the GABAergic reversal potential, and thereby influencing neuronal exc
45 ntial ( approximately 8 mV) to GABA receptor reversal potential ( approximately -81 mV), and dampened
46 e relationship between -80 and +60 mV with a reversal potential around 0 mV, a mean open time of 2.6
47 al nonselective cation current of ChR-2 with reversal potential around zero in both mouse OHCs and HE
49 ore is also confirmed by measurements of the reversal potential at oppositely directed salt gradients
50 endritic compartments indicate that the GABA reversal potential at the distal dendrite is more hyperp
51 and sAMPAsEPSCs were outward rectified with reversal potentials at -12.2 mV and -10.8 mV, and that o
52 s was concentration independent, and for the reversal potential-based approaches were of comparable m
53 decrease in input resistance and an apparent reversal potential below spike threshold; consequently,
54 s, either an increase in conductance, with a reversal potential between -58 and +10 mV, or a parallel
55 rent was associated with a positive shift in reversal potential but no change in the kinetics or volt
56 ar charges has little effect on the chloride reversal potential, but greatly affects the effective in
57 eplacement of external Cl- by I- shifted the reversal potential by about -30 mV and lengthened the lo
58 ctification of the ionic current and shifted reversal potential by approximately +10 mV, indicating i
59 The stoichiometry was calculated from the reversal potential by measuring the current-voltage rela
60 oichiometry of kNBC1 was calculated from its reversal potential by measuring the current-voltage rela
61 stretch-activated channels' conductances and reversal potentials, can result in blocking action poten
62 membrane conductance, and this current had a reversal potential close to the K(+) equilibrium potenti
64 rizing or hyperpolarizing voltage ramps, had reversal potentials close to 0 mV, exhibited substantial
66 (+) (130 mM) revealed an inward current with reversal potential consistent with the Na(+)/Ca(2+) exch
67 d the current amplitude and left-shifted the reversal potential, consistent with a nonselective catio
68 ow a biphasic increase/decrease in Cm with a reversal potential corresponding to the voltage at peak
72 utward rectification is proposed whereby the reversal potential determines ion occupancy, and thus, c
74 re high in TRN neurons, resulting in a Cl(-) reversal potential (E(Cl)) significantly depolarized fro
75 Ps, driven by an extremely negative chloride reversal potential (E(Cl)), combined with a large hyperp
76 neocortical neurons, in order to compare the reversal potential (E(GABA)) and relative density of GAB
77 Here we present novel evidence that the GABA reversal potential (E(GABA)) of PVN presympathetic neuro
80 es, activated whole-cell currents that had a reversal potential (E(r)) of about +50 mV in 1.5 mM exte
82 holding potential (V(h) ) far from NBCe1-A's reversal potential (E(rev) ) for prolonged periods - fou
83 carbonate cotransporter kNBC1 determines the reversal potential (E(rev)) and thus the net direction o
89 onic current associated with this g(m) had a reversal potential (E(rev)) value of -87 +/- 1.1 mV (n=
90 ed age-related alternations in its kinetics, reversal potentials (E(Gly)) and sensitivity to antagoni
92 ional modeling, a depolarizing shift in GABA reversal potential (EGABA) and increased intrinsic excit
93 nsequent depolarization of the neuronal GABA reversal potential (EGABA) selectively impairs cortical
94 ted patch recordings, we found that the GABA reversal potential (EGABA) was -73.6 +/- 1.2 mV when ind
95 tsynaptic cells, BDNF induced a shift in the reversal potential (EIPSC) toward more positive levels,
96 ions, there was a spontaneous current with a reversal potential (Er) that was altered by replacement
98 ure by measuring the amplitudes and apparent reversal potentials (Erevs) of inhibitory responses evok
99 to K(+), as judged by the 51-55 mV shifts in reversal potential following a 10-fold change in [K(+)](
104 r was calculated in experiments in which the reversal potential for Cl- (ECl) was measured from the G
105 ronal K+/Cl- cotransporter KCC2 to shift the reversal potential for Cl- and thus alters the effective
106 induce persistent changes in neuronal E(Cl) (reversal potential for Cl-) did not alter vmax or Km of
108 orated patch recordings demonstrate that the reversal potential for GABA is more depolarized in mutan
109 e resting membrane potential relative to the reversal potential for GABA(A) receptors, the hyperpolar
110 mature in both DS models, with a depolarized reversal potential for GABA(A)-evoked currents compared
111 Seizures induce excitatory shifts in the reversal potential for GABA(A)-receptor-mediated respons
112 chloride homeostasis mechanisms that set the reversal potential for GABA(A)Rs, or by a change in the
115 CO3(-) measurements from the damselfish, the reversal potential for GABAA (EGABA) was calculated, ill
118 ivation also induced a negative shift of the reversal potential for ionic currents suggesting that in
119 ulate neurons, this effect reversed near the reversal potential for K+, suggesting that it is mediate
121 tage-clamp hyperpolarization negative to the reversal potential for NBCe failed, however, to terminat
122 odulation of KCC2 function will regulate the reversal potential for synaptic GABAergic inputs, thus s
127 sformation was accompanied by a shift of the reversal potential from that of chloride toward that of
128 than 15-fold under physiological conditions, reversal potential further decreased by another approxim
129 orated patch-clamp techniques to measure Cl- reversal potential, GABAergic synaptic responses, and vo
130 PAR GluA2 content and others in the chloride reversal potential, human stem-cell-derived neurons repr
133 al for Cl- (ECl) was measured from the GABAA reversal potential in low-HCO3- media during Cl- loading
136 discernable effect on the Cl(-) current, the reversal potential in the presence or absence of Cl(-)(o
138 kedly different rectification properties and reversal potentials in coronary compared to mesenteric a
143 e in mean open time, unitary conductance, or reversal potential, indicating an increase in n and/or P
144 GABA with currents which have unusually high reversal potentials, indicating that GABA may be excitat
145 ard citrate current had a markedly different reversal potential, ionic characteristics, inhibitor pro
146 by the fact that inward Ca2+ flux at the ICa reversal potential is exactly balanced by outward Cs+ cu
148 y under certain conditions in which the GABA reversal potential is shifted positive due to intracellu
149 of the resting potential and the inhibitory reversal potentials, is regulated together with extracel
150 parameters, including maximal conductances, reversal potentials, kinetics of ionic currents, measure
151 dence, strong inward rectification, positive reversal potential, limited cesium permeability, and sen
153 using fractional Ca(2+) currents (P(f)) and reversal potential measurements over a wide voltage and
158 uisqualate-induced current was linear with a reversal potential near 0 mV suggesting involvement of n
162 5 microM) or cadmium (100 microM), and had a reversal potential near E(Cl), indicating that they were
163 e I(RC)-V(Cone) relations are linear, with a reversal potential near the chloride reversal potential
164 e potassium (K(ATP)) channels since it had a reversal potential near the equilibrium potential for K(
165 tions of 5-HT, is inwardly rectifying with a reversal potential near the equilibrium potential for K+
166 sociated with a decreased conductance with a reversal potential near the K(+) equilibrium potential.
167 0.10 +/- 0.03 pA pF(-1) (rabbit, n= 9), with reversal potentials near -100 mV, consistent with N= 2.
168 ion, since neither NMDA current magnitude or reversal potential, nor the levels of NR1-NR2A-D subunit
169 smic N-terminal domain (Nt) of NBCn1-B had a reversal potential of -156.3 mV (compared with a membran
170 nward at membrane potentials negative to its reversal potential of -30 mV, in 10 of 24 cells tested,
171 vating in the diastolic potential range with reversal potential of -37.5+/-1.0 mV, confirming the exp
172 ship was slightly inwardly rectifying with a reversal potential of -52 +/- 2 mV, and the P(K)/P(Na) r
173 s a slow membrane hyperpolarization toward a reversal potential of -73 mV through a relatively small
174 P) conductance was 14.0 +/- 1.5 nS and had a reversal potential of -91.4 +/- 0.9 mV that shifted by 5
177 l conductance, maximum open probability, and reversal potential of AMPA receptors and did not find an
178 amate-gated anion conductance in cones has a reversal potential of approximately -30 mV compared with
180 P2X receptors was 12.3 as estimated from the reversal potential of ATP-induced current measured at di
181 amplifier, is accompanied by a shift of the reversal potential of BAS-CA1 postsynaptic potentials, a
182 versed at approximately -20 mV, close to the reversal potential of chloride, but treatment with dithi
183 pH 5/pH 8 gradient across the membrane, the reversal potential of colicin A is -21 mV, rather than 0
184 A inward/outward currents decreased, and the reversal potential of composite NMDA currents recorded i
189 rization in 40% of neurons at P0-P2, but the reversal potential of GABA-evoked currents (E(GABA)) was
190 of hippocampal neurons led to a shift in the reversal potential of GABA-induced Cl- currents (E(Cl))
191 ter KCC2, as confirmed by the changes in the reversal potential of GABA-induced currents and the rest
192 tracellular Cl- levels, which determines the reversal potential of GABAAR-mediated currents and is in
195 erologous expression system to show that the reversal potential of GAT-1 under physiologically releva
196 tion and induces a depolarizing shift in the reversal potential of glycine-mediated currents (E(glyci
199 hyperkalemia-mediated depolarization of the reversal potential of I(K1) (E(K1)) would reduce excitab
200 d patch clamp and there was no change in the reversal potential of IKr in the presence of isoprenalin
201 d substitutions that significantly shift the reversal potential of improved ChloC (iChloC) to the rev
202 , membrane potential, pH, secretion, and the reversal potential of inhibitory glycine and GABA(A) rec
203 2A receptors to serotonin hyperpolarizes the reversal potential of inhibitory postsynaptic potentials
206 e cell resting potentials estimated from the reversal potential of K+ currents through a cell-attache
208 e amplitude, kinetics, slope conductance and reversal potential of synaptic inputs in a dendritic dis
212 a time- and frequency-dependent shift in the reversal potential of the composite postsynaptic current
214 at this function can be achieved only if the reversal potential of the cotransporter is negative to t
216 rent are Na+ and Cl- dependent; however, the reversal potential of the induced current suggests a Na+
219 5 mm instead of 5 mm Cl- failed to shift the reversal potential of the inward current, indicating tha
225 gradients, lowered pH(o) largely shifts the reversal potential of TWIK-1, TASK-1, and TASK-3 K(+) ch
228 r Cl(-) concentration was estimated from the reversal potential of whole-cell currents evoked by loca
231 lative Ca(2+) permeability measured from the reversal potentials of ATP-gated currents was unaffected
233 at a holding potential intermediate for the reversal potentials of GABA(A) and P2X receptors, little
237 ion independent when derived from changes in reversal potentials on going from a Na(+) reference solu
238 when P(Ca)/P(Na) was derived from changes in reversal potentials on going from a Na(+) reference solu
239 zed gamma-Aminobutyric acid receptor (GABAR) reversal potential or co-activation of alpha-amino-3-hyd
241 r, there are no data available on either the reversal potential or the HCO3-:Na+ stoichiometry of pNB
242 hair cells were depolarized near the Ca(2+) reversal potential or their hair bundles were exposed to
244 nd outside the cell greatly affect the Cl(-) reversal potential, particularly when osmolar transmembr
245 nine, and currents showed a 58.5 mV shift in reversal potential per 10-fold change in [Cl-], consiste
246 The method is insensitive to changes in the reversal potential, pipette capacitance, or widely varyi
247 n perforated-patch recording revealed a GABA reversal potential positive to both the resting membrane
251 pass both K(+) and Na(+) and conduct above a reversal potential reflecting the mixed permeability of
253 , as resting membrane potential and the IPSC reversal potential remained within a few millivolts (1-4
254 Ca2+ influx through NMDARs as determined by reversal potential shift analysis and by a combination o
255 ar calcium to determine the magnitude of the reversal potential shift in the two conditions as well a
257 mV; the response was further reduced and the reversal potential shifted to -90 mV in a low-Na+, high-
258 was substituted with glutamate or I(-), the reversal potential shifted to more positive or more nega
259 d inward rectification and calcium-dependent reversal potential shifts decreased by 80%, and 50%, res
263 ent had a reversal potential close to the K+ reversal potential suggesting that TRH inhibits resting
264 daily changes in K(+) currents and the GABA reversal potential, suggesting a role in modifying membr
265 high correlation between up- and down-state reversal potential suggests that despite these drastic c
268 tward-rectifying total leak conductance with reversal potential that was depolarized by approximately
269 substantial positive shifts in the GABAergic reversal potential that were proportional to the charge
271 either the membrane resistance or the Na(+) reversal potential, the conductance and the permeability
272 sociated with KORC (analysis of tail current reversal potentials), there is no correlation between Ca
273 nt and spatial spread of changes in the GABA reversal potential thereby altering homosynaptic as well
274 evoked GABA-A IPSPs and hyperpolarizes their reversal potential through a postsynaptic change in Cl(-
277 bicarbonate exposure produced a shift in the reversal potential to more negative potentials, consiste
278 attenuated Ca2+ permeability measured using reversal potentials under biionic conditions and fractio
280 g Na(+) with K(+) caused a leftward shift in reversal potential (V(Rev)) that correlated with the cor
281 idin-perforated-patch method and found their reversal potential (V(rev)) to be depolarized relative t
282 ated strongly with the positive shift of the reversal potential (V(rev)) upon switching to a sodium-f
284 ctivation significantly without changing its reversal potential, voltage dependence of activation, or
285 currents had a unitary conductance of 23 pS, reversal potential (Vr) of +10 mV and a low open probabi
287 gave a positive (depolarizing) shift in the reversal potential (Vrev, equivalent to the membrane pot
290 uced current was inwardly rectified, and the reversal potential was dependent on external potassium c
292 occurred regardless of whether the chloride reversal potential was hyperpolarizing (ECl-=-70 mV) or
293 ard current at potentials positive to the K+ reversal potential was observed through Kir3.1/Kir3.4, b
298 r K+ was replaced with Cs+, IPO tail current reversal potentials were dependent upon the extracellula
300 influx by depolarization to above the I(Ca) reversal potential, with high intracellular Ca(2)(+) buf