ライフサイエンスコーパス: pacemaking

1 s worth considering as a new form of cardiac pacemaking.

2 decipher the multigenic control of circadian pacemaking.

3 ogy are poorly defined for the generation of pacemaking.

4 also restores the precision of Purkinje cell pacemaking.

5 these processes interferes with SCN cellular pacemaking.

6 sues, revealing its global role in circadian pacemaking.

7 ent generators and their potential for alpha pacemaking.

8 results in small net inward currents during pacemaking.

9 er the range (10-50 mV/s) typical of natural pacemaking.

10 ) flies suggest that CRY is involved in core pacemaking.

11 induces a reversion to the juvenile form of pacemaking.

12 re in more detail the contribution of NCX to pacemaking.

13 nmasked, causing transient suppression of SN pacemaking.

14 ), pancreatic insulin secretion, and cardiac pacemaking.

15 icked the effects of D2 receptor agonists on pacemaking.

16 ed to a reduction in Na+ currents underlying pacemaking.

17 pave a way for further treatment of cardiac pacemaking.

18 robust, spontaneous, tetrodotoxin-sensitive pacemaking.

19 ls suggesting that it is important in normal pacemaking.

20 rizing current capable of modulating regular pacemaking.

21 neurons is quite different than for cardiac pacemaking.

22 a repolarizing current capable of modulating pacemaking.

23 tterning events that are critical for proper pacemaking.

24 the initiation of de novo oscillation or in pacemaking.

25 ance increased gain but had little effect on pacemaking.

26 ubset of LMCs, are responsible for mouse cLV pacemaking.

27 modulation of spine Ca(2+) signaling during pacemaking.

28 R-mediated Ca(2+) cycling that regulates SAN pacemaking.

29 VGCC isoform in the regulation of lymphatic pacemaking.

30 s an important role in sinoatrial node (SAN) pacemaking.

31 ersistent" sodium current important for such pacemaking.

32 ptoms reminiscent of severe human disease of pacemaking.

33 suggesting that the membrane clock underpins pacemaking.

34 nt generators and assess their potential for pacemaking.

35 In cell-attached recordings of spontaneous pacemaking, 10 mM 4-AP slowed rather than speeded firing

36 The molecular underpinnings of its pacemaking abilities are debated.

37 in the IK1/If parameter space for generating pacemaking action potentials in different states was pro

38 the ability and stability of bio-engineered pacemaking action potentials.

39 de-gated (HCN) channels(1) are essential for pacemaking activity and neural signalling(2,3).

40 A moderate increase of If promoted pacemaking activity but excessive increase of If resulte

41 responsible for VMs to generate spontaneous pacemaking activity by regulating IK1 and If density wer

42 Pacemaking activity in adult substantia nigra (SN) dopam

43 r cell types and their possible relevance to pacemaking activity in cells of the DRN.

44 studies show that, in normal conditions, the pacemaking activity in DA neurons is inhibited by the TR

45 omputational modeling to examine the role of pacemaking activity in lymph transport.

46 ation-activated current (Ih) and its role in pacemaking activity in rat hippocampal stratum oriens-al

47 ucleotide-gated (HCN) channels contribute to pacemaking activity in specialized neurons and cardiac m

48 l fibrillation is often triggered by ectopic pacemaking activity in the myocardium sleeves of the pul

49 xposure to nicotine doubles the frequency of pacemaking activity in these neurons.

50 to measure the effect of the NCX current on pacemaking activity in vivo, ex vivo, and in isolated SA

51 udies in Caenorhabditis elegans suggest that pacemaking activity may be controlled in part by microRN

52 The pacemaking activity of specialized tissues in the heart

53 These neurons respond with a pause in their pacemaking activity, enabling synaptic integration with

54 , many neurons in the motor system also show pacemaking activity, often rapid, including cerebellar P

55 ch inhibition by simultaneously reducing the pacemaking activity.

56 a feasible modality to regulate the cardiac pacemaking activity.

57 Many neurons in the mammalian brain show pacemaking activity: rhythmic generation of action poten

58 and cardiac Nav1.5 isoforms are involved in pacemaking, although the cardiac Nav1.5 isoform alone is

59 iled atrial action potential model result in pacemaking and a sinus node-like action potential.

60 matical model of mouse sinoatrial nodal cell pacemaking and an autonomic clamping protocol, to dissec

61 arge transfer through L-type channels during pacemaking and bursting.

62 The cardiac pacemaking and conduction system sets and maintains the

63 iac myocytes and specifically in the cardiac pacemaking and conduction system.

64 may be preferentially associated with early pacemaking and conduction tissue development.

65 in 2, which has an important role in cardiac pacemaking and conduction, due in part to its cyclic AMP

66 de a basis for tissue engineering of cardiac pacemaking and conductive cells.

67 eat is dependent on a specialized network of pacemaking and conductive cells.

68 s critical for distinguishing mechanisms for pacemaking and coordination of sequential population act

69 For the SAN to show pacemaking and drive atrial muscle, theoretically, there

70 play between IK1 and If in generating stable pacemaking and dysrhythmias was evaluated.

71 stained Cav2.3 availability during simulated pacemaking and enhanced Ca(2+)-currents during bursts.

72 The cellular and molecular determinants of pacemaking and fast spiking in GPe neurons are not fully

73 tic mouse model plays a critical role in SAN pacemaking and HRV.

74 ssure is the dominant regulator of lymphatic pacemaking and pumping, with pulsatile NO having only mi

75 Viral delivery of HCN2 subunits restored pacemaking and reduced burst spiking in GPe neurons.

76 for the automaticity of action potentials in pacemaking and rhythmic electrical circuits in the human

77 Na as well as TTX-sensitive iNa, slowed both pacemaking and SA node conduction.

78 ility, we found that 100 nM 2-AG accelerated pacemaking and steepened the frequency-current relations

79 medullary raphe neurons, which exhibit slow pacemaking and strong spiking adaptation.

80 In these Nav1.6 null neurons, pacemaking and the capacity for fast spiking were impair

81 ge-gated calcium channels are well suited to pacemaking and to supporting calcium flux near the resti

82 n substantia nigra (SN) dopamine (DA) neuron pacemaking and vulnerability to Parkinson's disease.

83 TTX had broader, smaller spikes than normal pacemaking and was stopped by removal of external calciu

84 ether BMAL1 ubiquitination affects circadian pacemaking and what ubiquitin ligase(s) is involved.

85 A major consequence of this is that pacemaking and, even more so, bursting are associated wi

86 ct center and drive atrial muscle as well as pacemaking) and the aim was to study expression in both

87 t by regulating coronary blood flow, cardiac pacemaking, and contractility.

88 tude oscillation, initiation of rhythmicity, pacemaking, and determination of phase.

89 tude oscillation, initiation of rhythmicity, pacemaking, and phase are differentially regulated: astr

90 elayed gastric emptying, impaired electrical pacemaking, and reduced motor neurotransmission.

91 rhythms to the intercellular control of SCN pacemaking are poorly understood.

92 s of impulse generation, that is, defects in pacemaking, are often life-threatening.

93 l setting, and can provide new insights into pacemaking, arrhythmogenesis and suppression or cardiove

94 SCN firing rate is fundamental to circadian pacemaking as both an input to and output of the molecul

95 voltage-clamp experiments, using records of pacemaking as command voltage, cobalt-sensitive current

96 y determinants of the regularity and rate of pacemaking as well as striatal resetting of this activit

97 ce caused a significant reduction in ICC and pacemaking at distances up to 5 cm from the anastomosis

98 e that Ih is an important contributor to the pacemaking behavior of the intact heart.

99 In SNc DANs, NALCN is not critical for pacemaking but inhibition of NALCN makes cells more sens

100 e essential for proper sinoatrial node (SAN) pacemaking, but the influence of intracellular Ca(2+) on

101 blockade of NALCN in medial VTA DANs slowed pacemaking by 49.08%.

102 d the role of subthreshold sodium current in pacemaking by performing voltage-clamp experiments using

103 activity in vivo deviated from single-spike pacemaking by phasic increases in firing rate via two qu

104 ation current (I(h)), and calcium current to pacemaking by using the cell's own firing as a voltage c

105 Biological pacemaking can be achieved by modulating ionic currents

106 iratory rhythms is the role of the intrinsic pacemaking capabilities that some respiratory neurons ex

107 By contrast, pacemaking capability is broadly distributed in the earl

108 We conclude that there are specialised pacemaking cells in the rabbit urethra that may be respo

109 er culture allowed for the identification of pacemaking cells using the multielectrode array platform

110 itivity to Cav1.3 variants during SN DA-like pacemaking compared with Cav1.2 during aSM-like activity

111 The cellular circuit pacemaking components that generate these critical emerg

112 l matrix, we found that calcium entry during pacemaking created a basal mitochondrial oxidant stress.

113 pe calcium channels during normal autonomous pacemaking created an oxidant stress that was specific t

114 Pacemaking current is carried by the Na+-Ca2+ exchanger,

115 c nucleotide-gated (HCN) channels generate a pacemaking current, I(h), which regulates neuronal excit

116 ric oxide exerts a facilitatory influence on pacemaking currents in the sino-atrial node.

117 e show a form of bidirectional plasticity of pacemaking currents induced by chronic heavy drinking wi

118 voltage-clamp experiments using a cell's own pacemaking cycle as voltage command.

119 us APs; however, its precise role during the pacemaking cycle remains unresolved.

120 ensitive sodium current flows throughout the pacemaking cycle, even at voltages as negative as -70 mV

121 on channels may also contribute to the ionic pacemaking cycle.

122 CN) channels regulate neuronal excitability, pacemaking, dendritic integration, and homeostatic plast

123 To determine whether neuronal pacemaking depends on active glucose metabolism, we swit

124 he rate of spontaneous depolarization during pacemaking, did evoke subthreshold outward currents.

125 nnels by dihydropyridines re-establishes the pacemaking driven by sodium and HCN channels found in ju

126 tivity after pauses and positively regulated pacemaking during slow heart rate in a numerical model o

127 The reduced models capture normal pacemaking dynamics with a small complement of ionic cur

128 Pacemaking dysfunction (PD) may result in heart rhythm d

129 For example, the pacemaking electrical signal is known to originate in th

130 rigin of periodicity consists of specialized pacemaking elements that synchronize and drive the rest

131 These results show that the pacemaking "engine" from I(NaP) is an inherent property

132 brane protein 16A) contributes to intestinal pacemaking, fluid secretion, cellular excitability, and

133 d with its excitability predominantly define pacemaking frequency and AP shape, such that large varia

134 , as neither action potential properties nor pacemaking frequency is correlated with AIS morphology.

135 Surprisingly, we found that AP shape and pacemaking frequency were independent of AIS geometry.

136 ir influence on neuronal output (spontaneous pacemaking frequency, action potential [AP] shape).

137 Nimodipine produced a slowing of pacemaking frequency.

138 o the suprachiasmatic nucleus, regulation of pacemaking function by PIP(2) in the IGL may influence s

139 nduce Hcn4 expression and suggest a temporal pacemaking function for the DMP during early cardiogenes

140 Shox2 in the regulation of SAN formation and pacemaking function in addition to several other organs.

141 demonstrate a fully developed SAN and normal pacemaking function in Shox2(KI/KI) mice.

142 Shox2 dose appears to be critical for normal pacemaking function.

143 xhibits region-specific sexual dimorphism in pacemaking gene sets.

144 ragranular generator acting as primary local pacemaking generator.

145 ragranular generator acting as primary local pacemaking generator.

146 4C and deep layers containing primary local pacemaking generators, suggesting the involvement of the

147 d funding, as physiological understanding of pacemaking gives hope to being better able to treat clin

148 Biological pacemaking has been performed with viral vectors, human

149 ronal signaling, muscle contraction, cardiac pacemaking, hormone secretion and cell proliferation.

150 A synchronized heart beat is controlled by pacemaking impulses conducted through Purkinje fibers.

151 c heart beat is coordinated by conduction of pacemaking impulses through the cardiac conduction syste

152 f CHZ successfully restored the precision of pacemaking in a dose-dependent manner.

153 ese properties of Ca(v)1.3 affect sinoatrial pacemaking in a mathematical model.

154 y the influence of IP3 signalling on cardiac pacemaking in a system where periodic intracellular Ca(2

155 sufficiently powerful to maintain circadian pacemaking in arrhythmic Cry-null SCN, deficient in esse

156 Detaching SN unmasked ectopic pacemaking in AVRs and pacemaker action potentials were

157 f TTX, which block TTX-sensitive iNa, slowed pacemaking in both intact SA node preparations and isola

158 e of these mutations is loss of precision of pacemaking in cerebellar Purkinje cells.

159 Inhibition of NALCN reduced pacemaking in DANs projecting to medial nucleus accumben

160 ntity of calcium channels that contribute to pacemaking in DCN neurons of juvenile rats.

161 We analyzed ionic currents that regulate pacemaking in dopaminergic neurons of the mouse ventral

162 We analyzed the ionic currents that drive pacemaking in dopaminergic VTA neurons, studied in mouse

163 The loss of the precision of pacemaking in EA2 is the consequence of reduced activati

164 ,5-trisphosphate receptors (IP3 Rs) modulate pacemaking in embryonic heart, but their role in adult s

165 ls are important for signal transduction and pacemaking in eukaryotes.

166 Electrical pacemaking in gastrointestinal muscles is generated by s

167 Previous studies suggest that pacemaking in ICC is dependent upon metabolic activity 1

168 perpolarizing stimuli.SIGNIFICANCE STATEMENT Pacemaking in midbrain dopaminergic neurons (DAN) relies

169 in the control of cellular excitability and pacemaking in neuronal, cardiac, and sensory cells.

170 that NALCN plays a prominent role in driving pacemaking in projection-defined VTA DAN subpopulations.

171 e hypothesis that the precision of intrinsic pacemaking in Purkinje cells is essential for motor coor

172 estores the severely diminished precision of pacemaking in Purkinje cells of EA2 mutant mice by prolo

173 interneuronal signals responsible for robust pacemaking in SCN cells and circuits, we have developed

174 restore cellular synchrony and amplitude of pacemaking in SCN circuits lacking vasoactive intestinal

175 ehavior in vivo alongside cellular molecular pacemaking in SCN slices in vitro demonstrated that such

176 In contrast to VTA DANs, however, pacemaking in SNc DANs was unaffected by inhibition of N

177 By contrast, pacemaking in SNc neurons does not rely on NALCN.

178 mitochondria is a prerequisite of electrical pacemaking in the gastrointestinal tract.

179 s with mutant circadian periods we show that pacemaking in the host SCN is specified by the genotype

180 SK channels have demonstrable effects on SAN pacemaking in the mouse.

181 To investigate the contribution of NCX to pacemaking in the SAN, we performed optical voltage mapp

182 determines cell- and circuit-level circadian pacemaking in the SCN.

183 cently been shown to play important roles in pacemaking in the sino-atrial node.

184 Circadian pacemaking in the suprachiasmatic nucleus (SCN) revolves

185 rstanding of the ionic mechanisms underlying pacemaking in these neurons is rapidly evolving, yieldin

186 activity nor does disruption of the SR alter pacemaking in these primary pacemaker cells.

187 Pacemaking in tissues was studied by intracellular elect

188 N makes substantial contributions to driving pacemaking in VTA DAN subpopulations.

189 suggesting that NALCN is a primary driver of pacemaking in VTA DANs.

190 extracellular calcium concentration speeded pacemaking in wildtype but not NALCN conditional knockou

191 eostatic responses to ASOX (e.g., stressless pacemaking) in DMV neurons.

192 conceptual framework for the role of I(f) in pacemaking, in which it operates at a very small fractio

193 Cardiac pacemaking initiated by the sinus node is attributable t

194 c role for electrical remodelling of the key pacemaking ion channel HCN4 in this process.

195 RATIONALE: Downregulation of the pacemaking ion channel, HCN4 (hyperpolarization-activate

196 ation of pacemaker cardiomyocytes expressing pacemaking ion channels (HCN1, HCN4, CACNA1D) and transc

197 approach to show that the binding of cGMP to pacemaking ion channels is weakened by a slower internal

198 ire spontaneously because of the activity of pacemaking ion channels.

199 Pacemaking is a property that this type of retinal amacr

200 The irregular pacemaking is caused by reduced activation of calcium-ac

201 ith their own firing patterns, we found that pacemaking is driven by two kinds of subthreshold sodium

202 Cardiac pacemaking is governed by specialized cardiomyocytes loc

203 mutant mice, the precision of Purkinje cell pacemaking is lost such that there is a significant degr

204 This 'engine' of pacemaking is present in almost all neurons and must be

205 an clock, but in vivo evidence for intrinsic pacemaking is still lacking.

206 er, carry no CREs, and how CRY-dependent SCN pacemaking is synchronized remains unclear.

207 ut their role in adult sinoatrial node (SAN) pacemaking is uncertain.

208 ium channel, a key mediator of Purkinje cell pacemaking, is improperly spliced in RbFox2 and Rbfox1 m

209 on, which could affect their contribution to pacemaking, is unknown.

210 Although not necessary for pacemaking, L-type channels helped support pacemaking wh

211 nt neurons, separate elements of the central pacemaking machinery regulate pdf or its product in nove

212 escription of the anatomical site of uterine pacemaking, may be disappointed.

213 The pacemaking mechanism in VTA neurons differs from that in

214 These findings demonstrate that the pacemaking mechanism of cholinergic MHb neurons controls

215 2+) channels (VGCCs) were implicated in this pacemaking mechanism, based on the effects of the repute

216 tes spiking frequency and contributes to the pacemaking mechanism.

217 ns in the substantia nigra pars compacta use pacemaking mechanisms common to neurons not affected in

218 Circadian (~24 hour) pacemaking mechanisms exist within single cells.

219 e seeking a conclusive account of myometrial pacemaking mechanisms, or indeed a definitive descriptio

220 ynamics enables us to identify oscillatory ('pacemaking') mechanisms at the cellular, tissue and syst

221 th a twofold acceleration of stable in vitro pacemaking, mediated by Kv4.3 potassium channel downregu

222 important for the stable rhythmic firing of pacemaking neurons and could significantly affect synapt

223 avior by synchronizing a small population of pacemaking neurons and maintaining rhythmicity in a larg

224 In fact, the relevant pacemaking neurons are themselves circadian photorecepti

225 all neurons and must be held in check in non-pacemaking neurons by sufficiently large competing outwa

226 Although the spontaneous rhythmic firing of pacemaking neurons is phenomenologically similar to card

227 ated mouse tuberomammillary nucleus neurons, pacemaking neurons with large I(A) currents in which sub

228 y of terminals emanating from PDF-containing pacemaking neurons, indicating a functional connection b

229 ior are controlled by a circuit of circadian pacemaking neurons.

230 Pacemaking occurred in all NRVM-Cx43 HEK pairs with cell

231 , calcium current plays only a minor role in pacemaking of dissociated SCN neurons, although it can d

232 TTX-sensitive sodium current in driving the pacemaking of many central neurons has been proposed, bu

233 oltage-dependent calcium channels in driving pacemaking of midbrain dopamine neurons and suggest that

234 Slow pacemaking of neurons releasing modulatory transmitters

235 ast two ion conductances are involved in the pacemaking of the circadian rhythms.

236 m pump dysfunction that alters the intrinsic pacemaking of these neurons, resulting in erratic burst

237 This selective enhancement of "stressful pacemaking" of DA SN neurons in vivo defines a functiona

238 Cardiac pacemaking offers a unique opportunity for direct gene t

239 underlie the dependence of gastrointestinal pacemaking on oxidative metabolism.

240 nd peripheral regions (center is adapted for pacemaking only, whereas periphery is adapted to protect

241 During SN DA-like pacemaking, only Cav1.3 variants conducted Ca(2+) curren

242 n understanding of the underlying biology of pacemaking opens up new prospects for better alternative

243 he issue of how a metabolite remote from the pacemaking origin of the oscillation may nevertheless co

244 We discover that an independent RhoA pacemaking oscillator controls this instability, generat

245 The role of T-type Ca(2+) channels in pacemaking outside the sinus node is unknown.

246 Applying pacemaking parameters in this modeling framework effecti

247 has been suggested to play a role in cardiac pacemaking, particularly in association with Ca2+ releas

248 During the later phase of pacemaking (positive to -60 mV), TTX-sensitive sodium cu

249 els reflected the multichannel nature of the pacemaking process.

250 increase of If resulted in a slowdown in the pacemaking rate and even an unstable pacemaking state.

251 s with exogenous buffer had little effect on pacemaking rate.

252 the cardiac maximal diastolic potentials and pacemaking rates recorded in cell pairs, whereas reprodu

253 he substantia nigra pars compacta (SNc), the pacemaking relies more on Ca(2+) channels and that the d

254 of L-type Ca(2+) channels during autonomous pacemaking renders SNc DA neurons susceptible to mitocho

255 channels to drive their maintained, rhythmic pacemaking renders them vulnerable to stressors thought

256 ue using wild-type (WT) "graft" SCN to drive pacemaking (reported by PER2::LUCIFERASE bioluminescence

257 ourth, simulation of cholinergic interneuron pacemaking revealed that a modest increase in the entry

258 SCN pacemaking revolves around feedback loops in which expre

259 d it is not known which ones actually play a pacemaking role in vivo.

260 r cells also have a SR-dependence of cardiac pacemaking since the rate of beating of guinea-pig SA no

261 Before isoproterenol, the earliest pacemaking site occurred in the inferior SAN, and LDCAE

262 y far the dominant mechanism determining the pacemaking site of lymphatic collectors, and challenge e

263 micromol/L) increased sinus rate and shifted pacemaking site to superior SAN, concomitant with the ap

264 t that in human myometrium there is no fixed pacemaking site, but rather mobile, initiation sites pro

265 e and space was determined by specifying the pacemaking sites and parameters obtained from experiment

266 ers T-type channels a capacity to serve as a pacemaking sodium current in the primitive heart and bra

267 Slow inactivation of the pacemaking sodium currents promotes a constant frequency

268 in the pacemaking rate and even an unstable pacemaking state.

269 To help fill this gap, pacemaking substantia nigra dopaminergic neurons were st

270 clear and cytoplasmic processes in circadian pacemaking, such that the pacemakers of some species mig

271 ck is an integral component of the circadian pacemaking system.

272 entify cardiac structures that are potential pacemaking targets with low optical excitation threshold

273 gal motoneurons acquire a stressless form of pacemaking that diminishes mitochondrial and cytosolic o

274 During normal pacemaking, the early phase of spontaneous depolarizatio

275 ation of an ion channel that is essential in pacemaking, the hyperpolarization and cyclic nucleotide-

276 ons is phenomenologically similar to cardiac pacemaking, the underlying ionic mechanism in most neuro

277 ronal physiology, specifically Purkinje cell pacemaking, through their shared control of sodium chann

278 rs to be a common mechanism in many types of pacemaking tissue since the rate reducing effects of rya

279 h more abundant SK channels in the atria and pacemaking tissues compared with the ventricles.

280 two components of sodium current during the pacemaking trajectory using action potential clamp.

281 ors and signalling pathways known to control pacemaking, transcripts from genes identified by GWAS as

282 dritic Ca2+ oscillations but left autonomous pacemaking unchanged.

283 The robustness of pacemaking underscores its biological importance and pro

284 g stable and robust pacemaker cells from non-pacemaking VMs by the interplay of IK1 and If, which may

285 as not reversed, suggesting that the loss of pacemaking was a consequence, rather than a cause, of ke

286 Normal pacemaking was also consistently silenced by replacement

287 Pacemaking was also slowed by the P/Q-channel blocker om

288 transient striatal GABAergic input to reset pacemaking was dependent on dendritic HCN2/HCN1 channels

289 Damage to ICC and pacemaking was greatly attenuated in the absence of NO d

290 Pacemaking was not inhibited by blocking hyperpolarizati

291 Pacemaking was potentiated by isoproterenol and abolishe

292 Lastly, activating spines during pacemaking, we observed an unexpected enhancement of spi

293 ICC networks and pacemaking were protected in iNOS(-/-) mice.

294 Cell doses >700,000 are sufficient for pacemaking when administered to left ventricular myocard

295 r pacemaking, L-type channels helped support pacemaking when challenged with cationic channel blocker

296 ence was critical to fast spiking but not to pacemaking, which appeared to be dependent on the positi

297 was a progressive decline in autonomous GPe pacemaking, which normally serves to desynchronize activ

298 At a cellular level, cardiac pacemaking, which sets the rate and rhythm of the heartb

299 synapses on the sinoatrial node (SAN) impact pacemaking, while synapses on contractile cells alter co

300 ellular heterogeneity in synchronization and pacemaking within the healthy and diseased SAN.