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1 ng variation can be applied to models of any excitable cell.
2 e quantification of calcium responses in non-excitable cells.
3 al, thereby enabling electrical signaling in excitable cells.
4 ng subthreshold oscillations in electrically excitable cells.
5 tion of discrete downstream responses in non-excitable cells.
6 ls, transporters, and signaling molecules in excitable cells.
7 on potentials during electrical signaling in excitable cells.
8 ls which leads to physiological signaling in excitable cells.
9 between VGSC activity and gene expression in excitable cells.
10 iological voltages and calcium levels in non-excitable cells.
11 re not physiological conditions for most non-excitable cells.
12 gated Ca(2+) channels controls activities of excitable cells.
13 er membrane-associated proteins found within excitable cells.
14 ion and conduction of electrical impulses in excitable cells.
15 nist-induced cytosolic Ca(2+) signals in non-excitable cells.
16 nels widely employed for photostimulation of excitable cells.
17 s the main pathway for Ca(2+) extrusion from excitable cells.
18 tif conferring membrane targeting in primary excitable cells.
19 n of other ion channels in neurons and other excitable cells.
20 in a functional context, in neurons or other excitable cells.
21 elation to SOC channels in excitable and non-excitable cells.
22  initiate and propagate action potentials in excitable cells.
23 in cellular Ca2+ to fundamental responses in excitable cells.
24 n-B targets ion channels and transporters in excitable cells.
25 of action potential firing frequency in many excitable cells.
26 ibitory effects of many neurotransmitters on excitable cells.
27  Ca(2+) channels including Ca(v)1.3 in other excitable cells.
28 ce shapes the complex electrical response of excitable cells.
29 e primary mechanism for mCa(2+) extrusion in excitable cells.
30 ys a critical role in Ca2+ signalling in non-excitable cells.
31 stimulation approaches to optical control of excitable cells.
32  Calcium Entry (SOCE) is well studied in non-excitable cells.
33 nnels to the function and differentiation of excitable cells.
34 tion and propagation of action potentials in excitable cells.
35 intenance of specialized membrane domains in excitable cells.
36 ium channels (Cav) mediate calcium influx in excitable cells.
37 K+ leak (K2P) pores that control activity of excitable cells.
38 ting electrical impulses in nerves and other excitable cells.
39 about how this process might be modulated in excitable cells.
40 overed role in electrical synchronization of excitable cells.
41 rrents and TRPM8-mediated calcium signals in excitable cells.
42 t least two complementary modes of action on excitable cells.
43 r the electrophysiological behaviour of many excitable cells.
44  a role for control of membrane potential of excitable cells.
45 way responsible for diverse functions in non-excitable cells.
46  channels) are involved in repolarization of excitable cells.
47 signal transduction elements in electrically excitable cells.
48 ng in signaling in taste receptors and other excitable cells.
49 cation current (Ih) is widely distributed in excitable cells.
50 ant determinants of firing frequency in many excitable cells.
51 rucial for the normal electrical activity of excitable cells.
52 ar communication in astrocytes and other non-excitable cells.
53 d to encode SOCCs responsible for CCE in non-excitable cells.
54 l signal transduction in nearby electrically excitable cells.
55  and frequency of action-potential firing in excitable cells.
56 nels play important functional roles in many excitable cells.
57 orses of spike generation and propagation in excitable cells.
58 ical forces regulate membrane traffic in non-excitable cells.
59 how Ca2+ channels regulate the physiology of excitable cells.
60 axiK channel expression in non-excitable and excitable cells.
61 l players in many physiological processes in excitable cells.
62 a diverse array of cellular functions within excitable cells.
63 e electrical signalling in neurons and other excitable cells.
64  entry and downstream signal transduction in excitable cells.
65  cellular function in both excitable and non-excitable cells.
66 ly act as a fluorescent activity reporter in excitable cells.
67 cally important events in the development of excitable cells.
68 facilitate voltage-sensitive Ca(2+) entry in excitable cells.
69 nderstanding of the role of Kv11 currents in excitable cells.
70 xpression characteristics of Kv1 channels in excitable cells.
71 membrane potential in both excitable and non-excitable cells.
72 ion channels have been clearly identified in excitable cells.
73 hich follows the stimulation of a variety of excitable cells.
74 e-dependent Ca2+ currents, characteristic of excitable cells.
75 tic changes and the electrical properties of excitable cells.
76 distinct functions in both excitable and non-excitable cells.
77 ell and also in a cable model with a ring of excitable cells.
78 e input/output relationships of electrically excitable cells.
79 tions in both electrically excitable and non-excitable cells.
80  and may be a general signaling mechanism in excitable cells.
81 rsal mode of signalling in excitable and non-excitable cells.
82 oles in shaping the electrical properties of excitable cells.
83  understood to mean the junction between two excitable cells.
84 eterogeneity of voltage-gated K+ channels in excitable cells.
85 nnels often overlaps in neurons and in other excitable cells.
86 eatly enhances their functional diversity in excitable cells.
87 of action potentials is commonly observed in excitable cells.
88 als in nerve, muscle, and other electrically excitable cells.
89 um (K(+)) channel desirable for silencing of excitable cells.
90  for optogenetic stimulation of electrically excitable cells.
91 ght control of resting membrane potential in excitable cells.
92 s a novel regulator of cell processes in non-excitable cells.
93 sodium channels (Navs) play crucial roles in excitable cells.
94  critical for proper electrical signaling in excitable cells.
95 rize the voltage dynamics of large groups of excitable cells.
96 tion and propagation of action potentials in excitable cells.
97 Nav) channels propagate action potentials in excitable cells.
98 annel activity to gene expression changes in excitable cells.
99 trigger or modify action potentials (APs) in excitable cells.
100 maintenance of resting membrane potential in excitable cells.
101 ials is important to understand electrically-excitable cells.
102 iming mechanisms across different systems of excitable cells.
103 rol the upstroke of the action potentials in excitable cells.
104 on and propagation of electrical impulses in excitable cells.
105 protein underlying the membrane potential in excitable cells.
106 lectrical signals to biological responses in excitable cells.
107 cal for chemical and electrical signaling in excitable cells.
108 els are crucial for electrical signalling in excitable cells.
109 propagates action potentials in electrically excitable cells.
110 action potentials in nerve, muscle and other excitable cells.
111 t in the amplification of Ca(2+) influx into excitable cells.
112 hibitory effect of many neurotransmitters on excitable cells.
113 o quickly recycle vesicle proteins in highly excitable cells.
114 se intracellular Ca(2+) concentration in non-excitable cells.
115 tial for initiating action potentials within excitable cells.
116  of fundamental activities in other kinds of excitable cells.
117              In cardiac myocytes, as in most excitable cells, action potential propagation depends es
118  mechanism through which calcium influx into excitable cells activates gene expression.
119 l cellular process particularly important in excitable cell activities such as hearing.
120  applications in analyzing the regulation of excitable cell activity in genetically tractable organis
121                                       In non-excitable cells, agonist-induced depletion of intracellu
122  maintain high input resistance in these non-excitable cells also requires the K(+) channel subunits
123                    Our results indicate that excitable cells and animal behavior can provide modulato
124 ) channels initiate electrical signalling in excitable cells and are the molecular targets for drugs
125                          The extent to which excitable cells and behavior modulate animal development
126 annels (Kv) are responsible for repolarizing excitable cells and can be heavily glycosylated.
127 concentration dynamics in a general class of excitable cells and cell assemblies of concentric cylind
128 teins in biology, regulating the activity of excitable cells and changing in diseases.
129 data previously reported for SK3 channels in excitable cells and hepatocytes.
130 the predominant Ca(2+) influx pathway in non-excitable cells and is activated in response to depletio
131                        In humans, ICG labels excitable cells and is routinely visualized transdermall
132 t as the negative resistance of electrically excitable cells and of tunnel diodes can be embedded in
133 (BK-type) channels, abundantly distribute in excitable cells and often localize to the proximity of v
134 se results demonstrate that Merkel cells are excitable cells and suggest that they release neurotrans
135 e for understanding electrical signalling in excitable cells and the actions of drugs used for pain,
136 contribute to the subthreshold properties of excitable cells and thereby influence behaviors such as
137 urthermore, we demonstrate that biosynthetic excitable cells and tissues can repair large conduction
138 after large electric shocks are delivered to excitable cells and tissues.
139 nnels are fundamental signaling molecules in excitable cells, and are molecular targets for local ane
140 ns, genes that function in multiple types of excitable cells, and genes in the signaling pathway of t
141 esting membrane voltage in many electrically excitable cells, and heritable mutations cause periodic
142 requenin) are expressed at highest levels in excitable cells, and some of them regulate desensitizati
143  vascular smooth muscle tissue, electrically excitable cells, and some tumors.
144 rofound impact on the electrical behavior of excitable cells, and the regulation of this property cou
145 the upstroke of the action potential in most excitable cells, and their fast inactivation is essentia
146 ping the input-output profiles of individual excitable cells, and therefore the activity of neuronal
147 l muscle with Ca(2+) entry mechanisms in non-excitable cells are also reviewed.
148                                 Electrically excitable cells are important in the normal functioning
149 ds used to assess the electrical activity of excitable cells are often limited by their poor spatial
150      Agonist-activated Ca(2+) signals in non-excitable cells are profoundly influenced by calcium ent
151 ost of hair cells, as well as those of other excitable cells, are still immature.
152 ral patterns of resting potentials among non-excitable cells as instructive cues in embryogenesis, re
153 nd their relation to the normal functions of excitable cells as well as pathophysiology.
154 Ca2+ stores and mediate Ca2+ influx into non-excitable cells at resting membrane potential.
155 hannels are fundamental to the physiology of excitable cells because they underlie the generation and
156    These results indicate that regulation of excitable cell behavior by neurotransmitter-mediated mod
157 m channels (K(Na)), suggested to function in excitable cells both during physiological conditions and
158 ium-release-activated current (ICRAC) in non-excitable cells but at present there is little informati
159 ts in the generation of action potentials in excitable cells, but despite numerous structure-function
160  a variety of functions in neurons and other excitable cells, but excessive calcium influx through th
161     LEMS antibodies inhibit Ca2+ currents in excitable cells, but it is not known whether there are a
162 NCX) is a critical calcium efflux pathway in excitable cells, but little is known regarding its auton
163 els is essential for electrical signaling in excitable cells, but the structural basis for voltage se
164  suppression of high-frequency discharges of excitable cells by local anesthetics (LA) is largely det
165  ion flux and generate electrical signals in excitable cells by opening and closing pore gates.
166                                  In many non-excitable cells Ca2+ influx is mainly controlled by the
167 ltage-regulated Ca2+ channels whereas in non-excitable cells Ca2+ influx is mediated by store-operate
168                                  In most non-excitable cells, calcium influx is signaled by depletion
169 er increase or decrease in calcium influx in excitable cells can be associated with BD.
170  model to simulate calcium transients in non-excitable cells (consisting of a plasma membrane Ca2+ pu
171  ClC proteins regulate membrane potential of excitable cells, contribute to epithelial transport, and
172    Collectively LOTUS-V extends the scope of excitable cell control and simultaneous voltage phenotyp
173          Data and simulations suggested that excitable cells could use differences in K(+) channel gl
174 ctrophysiology beyond canonical electrically excitable cells could yield exciting new findings.
175 for activation of CICR by Ca2+ influx in non-excitable cells, demonstrate a previously unrecognized r
176 sfunction in these pathways results in human excitable cell disease.
177          Potassium (K(+)) exits electrically excitable cells during normal and pathophysiological act
178 nd light-sensitive ion currents operating in excitable cells, e.g. cardiomyocytes or neurons.
179  expressed in electrically excitable and non-excitable cells, either as alpha-subunit (BKalpha) tetra
180                                              Excitable cells express a variety of ion channels that a
181                                         Many excitable cells express L-type Ca(2+) channels (LTCCs),
182 en used in vertebrate systems to investigate excitable cell firing and calcium transients, but both t
183 hannels, CaV, regulate Ca(2+) homeostasis in excitable cells following plasma membrane depolarization
184 e activation of channelrhodopsin 2 (ChR2) in excitable cells for the first time to our knowledge.
185                          In electrically non-excitable cells, for example epithelial cells, this is a
186      Whether nonexcitable cells may modulate excitable cell function or even contribute to AP conduct
187 s an important but potentially toxic role in excitable cell function.
188 ssing questions central to understanding how excitable cells function.
189                                 Electrically excitable cells harness voltage-coupled calcium influx t
190           The G protein-coupled receptors in excitable cells have prominent roles in controlling Ca2+
191 nt of intracellular Ca(2+) signaling in many excitable cells; however, the role of this mechanism in
192 tration of localized chemical stimulation of excitable cells illustrates the potential of this techno
193 istently, cell-specific ablation of dopamine-excitable cells in dorsal, but not ventral, striatum inh
194 versely, optogenetic stimulation of dopamine-excitable cells in dorsal, but not ventral, striatum sub
195 gnals can be used to control the function of excitable cells in intact tissues or organisms.
196 nnels mediate synaptic communication between excitable cells in mammals.
197 ODs) by reshaping the electric discharges of excitable cells in the periphery.
198 urrounding myocytes, suggesting that the non-excitable cells in the scar closely follow myocyte actio
199 hannel function and SOCE in a variety of non-excitable cells including lymphocytes and other immune c
200 pes continue to express IP3R channels but in excitable cells including skeletal and cardiac muscles t
201 igand-gated cation channels, present on many excitable cells including vas deferens smooth muscle cel
202 niques to follow the activation state of non-excitable cells, including lymphocytes.
203  the rising phase of the action potential in excitable cells, including neurons and skeletal and card
204              KATPs are found in a variety of excitable cells, including neurons of the central nervou
205 to determine the mechanism through which non-excitable cells influence the spontaneous activity of mu
206                              For example, in excitable cells inwardly rectifying potassium (GIRK) cha
207                                           In excitable cells, ion channels are frequently challenged
208 signaling by homomeric P2XRs expressed in an excitable cell is subtype-specific, which provides an ef
209                           Calcium entry into excitable cells is an important physiological signal, su
210 is unique to neurons or also occurs in other excitable cells is currently unknown.
211       Receptor-enhanced entry of Ca2+ in non-excitable cells is generally ascribed to a capacitative
212 d physiological function of such currents in excitable cells is not known.
213  that cortactin-mediated actin remodeling in excitable cells is not only important for cell structure
214                                Exocytosis in excitable cells is strongly coupled to Ca2+ entry throug
215 cally regulates the flow of sodium ions into excitable cells, is a common functional consequence of i
216 neration of Ca2+i signals, especially in non-excitable cells, is store-operated Ca2+ entry (SOCE).
217 erences can limit the translational value of excitable cells isolated from model organisms.
218                                      In many excitable cells, KATP channels respond to intracellular
219  CaV1 function and suggests a means by which excitable cells may dynamically tune CaV activity.
220 ponse to voltage changes across electrically excitable cell membranes.
221 d may play a fundamental role in controlling excitable cell metabolic regulation.
222 to modulate the plasma membrane potential of excitable cells, mitochondria have thus far eluded optog
223 ts suggest that electrically integrated, non-excitable cells modulate the excitability of cardiac pac
224 differences between cardiomyocytes and other excitable cells modulate vulnerability to conduction fai
225                          To signal properly, excitable cells must establish and maintain the correct
226                                          The excitable cells of Dictyostelium discoideum show traveli
227 trol the upstroke of the action potential in excitable cells of nerve and muscle tissue, making them
228 t drives action potential generation in many excitable cells of the brain, heart, and nervous system.
229 t signaling pathways control the activity of excitable cells of the nervous system and heart, and are
230 tosolic free Ca2+ concentration ([Ca2+]i) in excitable cells often acts as a negative feedback signal
231                                           In excitable cells, oscillations in intracellular free calc
232                       In addition, unlike in excitable cells, our data suggest a minimal physiologica
233 t voltage-gated Ca(2+) entry, which typifies excitable cells, overwhelms the effect of any capacitati
234 questration mechanisms to various aspects of excitable cell physiology are incompletely understood.
235 fic plasma membrane domains is necessary for excitable cell physiology.
236                      These data suggest that excitable cells possess a store-operated Ca2+ influx mec
237                                           In excitable cells, receptor-induced Ca(2+) release from in
238 sequences of such activity in the setting of excitable cells remains the central focus of much of the
239 iggering CICR, and indicate that CICR in non-excitable cells resembles CICR in cardiac myocytes with
240    Alterations in K(v)7-mediated currents in excitable cells result in several diseased conditions.
241                 Opening of Na(+) channels in excitable cells results in influx of Na(+) and cellular
242 d synaptic patterning, as well as aspects of excitable cell signal transduction and neuromodulation.
243                                           In excitable cells, small-conductance Ca2+-activated potass
244 ecules subserving transmembrane signaling of excitable cells; special emphasis is placed here on prot
245 ole Ca2+ entry mechanism in a variety of non-excitable cells, store-operated calcium (SOC) influx is
246                                       In non-excitable cells stromal interaction molecule 1 (STIM1) i
247               They also are expressed in non-excitable cells such as macrophages and neoplastic cells
248 um channels initiate electrical signaling in excitable cells such as muscle and neurons.
249  Ca2+ channels, previously known to exist in excitable cells such as neurons and muscle cells, are sh
250 high frequency oscillating magnetic field on excitable cells such as neurons are well established.
251 an important role in electrical signaling of excitable cells such as neurons, cardiac myocytes, and v
252 nd viability impairment in aggregate-exposed excitable cells such as peripheral neurons and cardiomyo
253 utamate-gated chloride channels in essential excitable cells such as those of the pharynx.
254 eau bursting is typical of many electrically excitable cells, such as endocrine cells that secrete ho
255                                 Electrically excitable cells, such as neurons, exhibit tremendous div
256 aracterization of several other types of non-excitable cells, such as the microglia (brain macrophage
257 oduce and analyse a simple model for two non-excitable cells that are dynamically coupled by a gap ju
258 erkel cells are genetically programmed to be excitable cells that may participate in touch reception,
259 itions by all TC neurones and other types of excitable cells that possess an IT 'window' component wi
260                            Corticotrophs are excitable cells that receive input from two hypothalamic
261                            Corticotrophs are excitable cells that receive input from two hypothalamic
262               In the case of ion channels in excitable cells, the dynamics of signaling to the nucleu
263                                       In non-excitable cells, the initial Ca2+ release is typically f
264                                  As in other excitable cells, the ion channels of sensory receptors p
265                                           In excitable cells, the main mediators of sodium conductanc
266                                       In non-excitable cells, the major Ca2+ entry pathway is the sto
267                                  In many non-excitable cells, the predominant mode of agonist-activat
268 hannels are important in the heart and other excitable cells, there are virtually no specific drugs f
269                                           In excitable cells these channels are composed of the ion-f
270 rmed in subsequent years and for students of excitable cells, they dominate our teaching and research
271                                       In non-excitable cells, thiol-oxidizing agents have been shown
272 nnels fine-tunes the electrical signaling in excitable cells through an internal timing mechanism tha
273 current inhibition that is widely present in excitable cells through modulation of ion channels by sp
274 ulation of K(+) channel inactivation enables excitable cells to adjust action potential firing.
275 ium channels (ICa,V) links depolarization of excitable cells to critical cellular processes, such as
276 ycosylation of ion channels could be used by excitable cells to modify cell signaling.
277 brane potential and regulate the response of excitable cells to various stimuli.
278 + signalling in the rat megakaryocyte, a non-excitable cell type in which membrane potential can mark
279 as investigated in rat megakaryocytes, a non-excitable cell type recently shown to exhibit depolarisa
280 lular stores in the rat megakaryocyte, a non-excitable cell type.
281  local Ca(2+) ion signalling in a variety of excitable cell types.
282 v) channels at sites of function in multiple excitable cell types.
283 ying transient outward K(+) currents in many excitable cell types.
284 ribute to the afterhyperpolarization in many excitable cell types.
285 eld of agonist-activated Ca(2+) entry in non-excitable cells underwent a revolution some 5 years ago
286                                              Excitable cells use ion channels to tailor their biophys
287 dulating the firing patterns of electrically-excitable cells using surface plasmon resonance phenomen
288 es significant thermally mediated effects on excitable cells via basic thermodynamic mechanisms that
289                                           In excitable cells, voltage-gated calcium channels (Cav) ar
290                                           In excitable cells, voltage-gated calcium influx provides a
291                                           In excitable cells, voltage-gated sodium (Na(V)) channels a
292      Indeed, when the ratio of intrinsically excitable cells was increased or decreased, the number o
293 erent from those expressed in other types of excitable cells, we compared the properties of the hNE s
294  the restricted expression of scn1ba mRNA in excitable cells, we detected scn1bb transcripts and prot
295 ant role in propagating action potentials in excitable cells, we have identified a novel role in rege
296 channels (SK channels) have been reported in excitable cells, where they aid in integrating changes i
297 how these enzymes are regulated by Ca(2+) in excitable cells, where they predominate.
298 cs (LAs) block voltage-gated Na+ channels in excitable cells, whereas batrachotoxin (BTX) keeps these
299                     Ventricular myocytes are excitable cells whose voltage threshold for action poten
300 ctivate different regions of ChR2-sensitized excitable cells with high spatial resolution.

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