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1 also restores the precision of Purkinje cell pacemaking.
2 these processes interferes with SCN cellular pacemaking.
3 sues, revealing its global role in circadian pacemaking.
4 ent generators and their potential for alpha pacemaking.
5  results in small net inward currents during pacemaking.
6 er the range (10-50 mV/s) typical of natural pacemaking.
7 ) flies suggest that CRY is involved in core pacemaking.
8  induces a reversion to the juvenile form of pacemaking.
9 re in more detail the contribution of NCX to pacemaking.
10 ), pancreatic insulin secretion, and cardiac pacemaking.
11 icked the effects of D2 receptor agonists on pacemaking.
12 ed to a reduction in Na+ currents underlying pacemaking.
13  robust, spontaneous, tetrodotoxin-sensitive pacemaking.
14 rizing current capable of modulating regular pacemaking.
15 ls suggesting that it is important in normal pacemaking.
16  modulation of spine Ca(2+) signaling during pacemaking.
17 R-mediated Ca(2+) cycling that regulates SAN pacemaking.
18 s an important role in sinoatrial node (SAN) pacemaking.
19 ersistent" sodium current important for such pacemaking.
20 ptoms reminiscent of severe human disease of pacemaking.
21 a repolarizing current capable of modulating pacemaking.
22 nt generators and assess their potential for pacemaking.
23 decipher the multigenic control of circadian pacemaking.
24 ogy are poorly defined for the generation of pacemaking.
25   In cell-attached recordings of spontaneous pacemaking, 10 mM 4-AP slowed rather than speeded firing
26                                              Pacemaking activity in adult substantia nigra (SN) dopam
27 r cell types and their possible relevance to pacemaking activity in cells of the DRN.
28 studies show that, in normal conditions, the pacemaking activity in DA neurons is inhibited by the TR
29 ation-activated current (Ih) and its role in pacemaking activity in rat hippocampal stratum oriens-al
30 ucleotide-gated (HCN) channels contribute to pacemaking activity in specialized neurons and cardiac m
31 l fibrillation is often triggered by ectopic pacemaking activity in the myocardium sleeves of the pul
32 xposure to nicotine doubles the frequency of pacemaking activity in these neurons.
33  to measure the effect of the NCX current on pacemaking activity in vivo, ex vivo, and in isolated SA
34 udies in Caenorhabditis elegans suggest that pacemaking activity may be controlled in part by microRN
35                                          The pacemaking activity of specialized tissues in the heart
36  These neurons respond with a pause in their pacemaking activity, enabling synaptic integration with
37 ch inhibition by simultaneously reducing the pacemaking activity.
38  a feasible modality to regulate the cardiac pacemaking activity.
39  and cardiac Nav1.5 isoforms are involved in pacemaking, although the cardiac Nav1.5 isoform alone is
40 arge transfer through L-type channels during pacemaking and bursting.
41                                  The cardiac pacemaking and conduction system sets and maintains the
42 iac myocytes and specifically in the cardiac pacemaking and conduction system.
43  may be preferentially associated with early pacemaking and conduction tissue development.
44 de a basis for tissue engineering of cardiac pacemaking and conductive cells.
45 eat is dependent on a specialized network of pacemaking and conductive cells.
46 s critical for distinguishing mechanisms for pacemaking and coordination of sequential population act
47                          For the SAN to show pacemaking and drive atrial muscle, theoretically, there
48   The cellular and molecular determinants of pacemaking and fast spiking in GPe neurons are not fully
49     Viral delivery of HCN2 subunits restored pacemaking and reduced burst spiking in GPe neurons.
50 Na as well as TTX-sensitive iNa, slowed both pacemaking and SA node conduction.
51 ility, we found that 100 nM 2-AG accelerated pacemaking and steepened the frequency-current relations
52  medullary raphe neurons, which exhibit slow pacemaking and strong spiking adaptation.
53                In these Nav1.6 null neurons, pacemaking and the capacity for fast spiking were impair
54 ge-gated calcium channels are well suited to pacemaking and to supporting calcium flux near the resti
55 n substantia nigra (SN) dopamine (DA) neuron pacemaking and vulnerability to Parkinson's disease.
56  TTX had broader, smaller spikes than normal pacemaking and was stopped by removal of external calciu
57 ether BMAL1 ubiquitination affects circadian pacemaking and what ubiquitin ligase(s) is involved.
58          A major consequence of this is that pacemaking and, even more so, bursting are associated wi
59 ct center and drive atrial muscle as well as pacemaking) and the aim was to study expression in both
60 t by regulating coronary blood flow, cardiac pacemaking, and contractility.
61 elayed gastric emptying, impaired electrical pacemaking, and reduced motor neurotransmission.
62  rhythms to the intercellular control of SCN pacemaking are poorly understood.
63 s of impulse generation, that is, defects in pacemaking, are often life-threatening.
64 l setting, and can provide new insights into pacemaking, arrhythmogenesis and suppression or cardiove
65  SCN firing rate is fundamental to circadian pacemaking as both an input to and output of the molecul
66  voltage-clamp experiments, using records of pacemaking as command voltage, cobalt-sensitive current
67 y determinants of the regularity and rate of pacemaking as well as striatal resetting of this activit
68 ce caused a significant reduction in ICC and pacemaking at distances up to 5 cm from the anastomosis
69 e that Ih is an important contributor to the pacemaking behavior of the intact heart.
70 e essential for proper sinoatrial node (SAN) pacemaking, but the influence of intracellular Ca(2+) on
71 d the role of subthreshold sodium current in pacemaking by performing voltage-clamp experiments using
72 ation current (I(h)), and calcium current to pacemaking by using the cell's own firing as a voltage c
73                                   Biological pacemaking can be achieved by modulating ionic currents
74       We conclude that there are specialised pacemaking cells in the rabbit urethra that may be respo
75 er culture allowed for the identification of pacemaking cells using the multielectrode array platform
76 itivity to Cav1.3 variants during SN DA-like pacemaking compared with Cav1.2 during aSM-like activity
77 l matrix, we found that calcium entry during pacemaking created a basal mitochondrial oxidant stress.
78 pe calcium channels during normal autonomous pacemaking created an oxidant stress that was specific t
79                                              Pacemaking current is carried by the Na+-Ca2+ exchanger,
80 c nucleotide-gated (HCN) channels generate a pacemaking current, I(h), which regulates neuronal excit
81 ric oxide exerts a facilitatory influence on pacemaking currents in the sino-atrial node.
82 e show a form of bidirectional plasticity of pacemaking currents induced by chronic heavy drinking wi
83 voltage-clamp experiments using a cell's own pacemaking cycle as voltage command.
84 ensitive sodium current flows throughout the pacemaking cycle, even at voltages as negative as -70 mV
85 CN) channels regulate neuronal excitability, pacemaking, dendritic integration, and homeostatic plast
86                To determine whether neuronal pacemaking depends on active glucose metabolism, we swit
87 he rate of spontaneous depolarization during pacemaking, did evoke subthreshold outward currents.
88 nnels by dihydropyridines re-establishes the pacemaking driven by sodium and HCN channels found in ju
89 tivity after pauses and positively regulated pacemaking during slow heart rate in a numerical model o
90            The reduced models capture normal pacemaking dynamics with a small complement of ionic cur
91                             For example, the pacemaking electrical signal is known to originate in th
92 rigin of periodicity consists of specialized pacemaking elements that synchronize and drive the rest
93                  These results show that the pacemaking "engine" from I(NaP) is an inherent property
94             Nimodipine produced a slowing of pacemaking frequency.
95 o the suprachiasmatic nucleus, regulation of pacemaking function by PIP(2) in the IGL may influence s
96 nduce Hcn4 expression and suggest a temporal pacemaking function for the DMP during early cardiogenes
97 Shox2 in the regulation of SAN formation and pacemaking function in addition to several other organs.
98 demonstrate a fully developed SAN and normal pacemaking function in Shox2(KI/KI) mice.
99 Shox2 dose appears to be critical for normal pacemaking function.
100 ragranular generator acting as primary local pacemaking generator.
101 ragranular generator acting as primary local pacemaking generator.
102  4C and deep layers containing primary local pacemaking generators, suggesting the involvement of the
103                                   Biological pacemaking has been performed with viral vectors, human
104 ronal signaling, muscle contraction, cardiac pacemaking, hormone secretion and cell proliferation.
105   A synchronized heart beat is controlled by pacemaking impulses conducted through Purkinje fibers.
106 c heart beat is coordinated by conduction of pacemaking impulses through the cardiac conduction syste
107 f CHZ successfully restored the precision of pacemaking in a dose-dependent manner.
108 ese properties of Ca(v)1.3 affect sinoatrial pacemaking in a mathematical model.
109 y the influence of IP3 signalling on cardiac pacemaking in a system where periodic intracellular Ca(2
110  sufficiently powerful to maintain circadian pacemaking in arrhythmic Cry-null SCN, deficient in esse
111 f TTX, which block TTX-sensitive iNa, slowed pacemaking in both intact SA node preparations and isola
112 e of these mutations is loss of precision of pacemaking in cerebellar Purkinje cells.
113 ntity of calcium channels that contribute to pacemaking in DCN neurons of juvenile rats.
114     We analyzed ionic currents that regulate pacemaking in dopaminergic neurons of the mouse ventral
115    We analyzed the ionic currents that drive pacemaking in dopaminergic VTA neurons, studied in mouse
116                 The loss of the precision of pacemaking in EA2 is the consequence of reduced activati
117 ,5-trisphosphate receptors (IP3 Rs) modulate pacemaking in embryonic heart, but their role in adult s
118 ls are important for signal transduction and pacemaking in eukaryotes.
119                Previous studies suggest that pacemaking in ICC is dependent upon metabolic activity 1
120 e hypothesis that the precision of intrinsic pacemaking in Purkinje cells is essential for motor coor
121 estores the severely diminished precision of pacemaking in Purkinje cells of EA2 mutant mice by prolo
122 interneuronal signals responsible for robust pacemaking in SCN cells and circuits, we have developed
123  restore cellular synchrony and amplitude of pacemaking in SCN circuits lacking vasoactive intestinal
124 ehavior in vivo alongside cellular molecular pacemaking in SCN slices in vitro demonstrated that such
125 mitochondria is a prerequisite of electrical pacemaking in the gastrointestinal tract.
126 s with mutant circadian periods we show that pacemaking in the host SCN is specified by the genotype
127 SK channels have demonstrable effects on SAN pacemaking in the mouse.
128    To investigate the contribution of NCX to pacemaking in the SAN, we performed optical voltage mapp
129 determines cell- and circuit-level circadian pacemaking in the SCN.
130 cently been shown to play important roles in pacemaking in the sino-atrial node.
131                                    Circadian pacemaking in the suprachiasmatic nucleus (SCN) revolves
132 rstanding of the ionic mechanisms underlying pacemaking in these neurons is rapidly evolving, yieldin
133 activity nor does disruption of the SR alter pacemaking in these primary pacemaker cells.
134                                              Pacemaking in tissues was studied by intracellular elect
135 eostatic responses to ASOX (e.g., stressless pacemaking) in DMV neurons.
136                                      Cardiac pacemaking initiated by the sinus node is attributable t
137             RATIONALE: Downregulation of the pacemaking ion channel, HCN4 (hyperpolarization-activate
138 approach to show that the binding of cGMP to pacemaking ion channels is weakened by a slower internal
139 ire spontaneously because of the activity of pacemaking ion channels.
140                                              Pacemaking is a property that this type of retinal amacr
141                                The irregular pacemaking is caused by reduced activation of calcium-ac
142 ith their own firing patterns, we found that pacemaking is driven by two kinds of subthreshold sodium
143                                      Cardiac pacemaking is governed by specialized cardiomyocytes loc
144  mutant mice, the precision of Purkinje cell pacemaking is lost such that there is a significant degr
145 an clock, but in vivo evidence for intrinsic pacemaking is still lacking.
146 er, carry no CREs, and how CRY-dependent SCN pacemaking is synchronized remains unclear.
147 ut their role in adult sinoatrial node (SAN) pacemaking is uncertain.
148 ium channel, a key mediator of Purkinje cell pacemaking, is improperly spliced in RbFox2 and Rbfox1 m
149 on, which could affect their contribution to pacemaking, is unknown.
150                   Although not necessary for pacemaking, L-type channels helped support pacemaking wh
151 nt neurons, separate elements of the central pacemaking machinery regulate pdf or its product in nove
152                                          The pacemaking mechanism in VTA neurons differs from that in
153          These findings demonstrate that the pacemaking mechanism of cholinergic MHb neurons controls
154 tes spiking frequency and contributes to the pacemaking mechanism.
155 ns in the substantia nigra pars compacta use pacemaking mechanisms common to neurons not affected in
156                         Circadian (~24 hour) pacemaking mechanisms exist within single cells.
157  important for the stable rhythmic firing of pacemaking neurons and could significantly affect synapt
158 avior by synchronizing a small population of pacemaking neurons and maintaining rhythmicity in a larg
159                        In fact, the relevant pacemaking neurons are themselves circadian photorecepti
160 ated mouse tuberomammillary nucleus neurons, pacemaking neurons with large I(A) currents in which sub
161 y of terminals emanating from PDF-containing pacemaking neurons, indicating a functional connection b
162 ior are controlled by a circuit of circadian pacemaking neurons.
163                                              Pacemaking occurred in all NRVM-Cx43 HEK pairs with cell
164 , calcium current plays only a minor role in pacemaking of dissociated SCN neurons, although it can d
165  TTX-sensitive sodium current in driving the pacemaking of many central neurons has been proposed, bu
166 oltage-dependent calcium channels in driving pacemaking of midbrain dopamine neurons and suggest that
167 ast two ion conductances are involved in the pacemaking of the circadian rhythms.
168 m pump dysfunction that alters the intrinsic pacemaking of these neurons, resulting in erratic burst
169     This selective enhancement of "stressful pacemaking" of DA SN neurons in vivo defines a functiona
170                                      Cardiac pacemaking offers a unique opportunity for direct gene t
171  underlie the dependence of gastrointestinal pacemaking on oxidative metabolism.
172 nd peripheral regions (center is adapted for pacemaking only, whereas periphery is adapted to protect
173                            During SN DA-like pacemaking, only Cav1.3 variants conducted Ca(2+) curren
174 n understanding of the underlying biology of pacemaking opens up new prospects for better alternative
175 he issue of how a metabolite remote from the pacemaking origin of the oscillation may nevertheless co
176         We discover that an independent RhoA pacemaking oscillator controls this instability, generat
177        The role of T-type Ca(2+) channels in pacemaking outside the sinus node is unknown.
178 has been suggested to play a role in cardiac pacemaking, particularly in association with Ca2+ releas
179                    During the later phase of pacemaking (positive to -60 mV), TTX-sensitive sodium cu
180 els reflected the multichannel nature of the pacemaking process.
181 s with exogenous buffer had little effect on pacemaking rate.
182 the cardiac maximal diastolic potentials and pacemaking rates recorded in cell pairs, whereas reprodu
183 he substantia nigra pars compacta (SNc), the pacemaking relies more on Ca(2+) channels and that the d
184  of L-type Ca(2+) channels during autonomous pacemaking renders SNc DA neurons susceptible to mitocho
185 channels to drive their maintained, rhythmic pacemaking renders them vulnerable to stressors thought
186 ue using wild-type (WT) "graft" SCN to drive pacemaking (reported by PER2::LUCIFERASE bioluminescence
187 ourth, simulation of cholinergic interneuron pacemaking revealed that a modest increase in the entry
188                                          SCN pacemaking revolves around feedback loops in which expre
189 d it is not known which ones actually play a pacemaking role in vivo.
190 r cells also have a SR-dependence of cardiac pacemaking since the rate of beating of guinea-pig SA no
191           Before isoproterenol, the earliest pacemaking site occurred in the inferior SAN, and LDCAE
192 micromol/L) increased sinus rate and shifted pacemaking site to superior SAN, concomitant with the ap
193 ers T-type channels a capacity to serve as a pacemaking sodium current in the primitive heart and bra
194                     Slow inactivation of the pacemaking sodium currents promotes a constant frequency
195 clear and cytoplasmic processes in circadian pacemaking, such that the pacemakers of some species mig
196 ck is an integral component of the circadian pacemaking system.
197 entify cardiac structures that are potential pacemaking targets with low optical excitation threshold
198 gal motoneurons acquire a stressless form of pacemaking that diminishes mitochondrial and cytosolic o
199                                During normal pacemaking, the early phase of spontaneous depolarizatio
200 ation of an ion channel that is essential in pacemaking, the hyperpolarization and cyclic nucleotide-
201 ronal physiology, specifically Purkinje cell pacemaking, through their shared control of sodium chann
202 rs to be a common mechanism in many types of pacemaking tissue since the rate reducing effects of rya
203 h more abundant SK channels in the atria and pacemaking tissues compared with the ventricles.
204  two components of sodium current during the pacemaking trajectory using action potential clamp.
205 dritic Ca2+ oscillations but left autonomous pacemaking unchanged.
206                            The robustness of pacemaking underscores its biological importance and pro
207 as not reversed, suggesting that the loss of pacemaking was a consequence, rather than a cause, of ke
208                                       Normal pacemaking was also consistently silenced by replacement
209                                              Pacemaking was also slowed by the P/Q-channel blocker om
210  transient striatal GABAergic input to reset pacemaking was dependent on dendritic HCN2/HCN1 channels
211                            Damage to ICC and pacemaking was greatly attenuated in the absence of NO d
212                                              Pacemaking was not inhibited by blocking hyperpolarizati
213             Lastly, activating spines during pacemaking, we observed an unexpected enhancement of spi
214                             ICC networks and pacemaking were protected in iNOS(-/-) mice.
215       Cell doses >700,000 are sufficient for pacemaking when administered to left ventricular myocard
216 r pacemaking, L-type channels helped support pacemaking when challenged with cationic channel blocker
217 ence was critical to fast spiking but not to pacemaking, which appeared to be dependent on the positi
218  was a progressive decline in autonomous GPe pacemaking, which normally serves to desynchronize activ
219                 At a cellular level, cardiac pacemaking, which sets the rate and rhythm of the heartb

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