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1 maining adaptation process is independent of calcium entry.
2  appear to depend explicitly on the route of calcium entry.
3 esicles (SVs) that are distal to the site of calcium entry.
4 binding of annexins to membranes at sites of calcium entry.
5 nto signalosomes, resulting in BCR-activated calcium entry.
6 type channels contribute modestly to overall calcium entry.
7 to investigate the mechanism of PACAP-evoked calcium entry.
8 ediated signaling or store depletion-induced calcium entry.
9 4 mM) was added to suppress channel-mediated calcium entry.
10 to synchronous EPSC amplitude, activity, and calcium entry.
11 otide-dependent pathways coupled to neuronal calcium entry.
12 rform other roles unrelated to voltage-gated calcium entry.
13 l Ca(2+), also referred to as store-operated calcium entry.
14 zation of T cells using KCl does not lead to calcium entry.
15 coupled to intracellular calcium release and calcium entry.
16  to contribute to action potential-dependent calcium entry.
17 n including decreased chemotaxis and reduced calcium entry.
18 rane calcium influx channels or capacitative calcium entry.
19 anilloid receptor 1 triggered store operated calcium entry.
20  showing the critical role of TRPM2-mediated calcium entry.
21 to membrane depolarization and voltage-gated calcium entry.
22 olved in agonist-stimulated and capacitative calcium entry.
23 ings and processes including mitogenesis and calcium entry.
24 tivates STIM1/Orai1-dependent store-operated calcium entry.
25 ts deficiency had no effect on TCR-initiated calcium entry.
26 release is associated with CaV and not TRPV1 calcium entry.
27 acute loss of Orai1-dependent store-operated calcium entry.
28 stitute the core machinery of store-operated calcium entry.
29  STIM2) are key modulators of store-operated calcium entry.
30 tore depletion, KSR2 is required for optimal calcium entry.
31 (1) subunit important for excitation-coupled calcium entry?
32 ator (ORAI) pathway controls store-dependent calcium entry, a major mechanism of physiological calciu
33 s as a negative regulator of agonist-induced calcium entry (ACE) that suppresses surface accumulation
34                         In eukaryotic cells, calcium entry across the cell surface activates nuclear
35 ular calcium stores activates store-operated calcium entry across the plasma membrane in many cells.
36 sting that the oscillations were mediated by calcium entry across the plasma membrane in response to
37                                              Calcium entry activated by ablation of both JP45-CASQ1 a
38                        During store-operated calcium entry activation, calcium depletion from the end
39 nnels make comparable contributions to total calcium entry after an action potential.
40 ted calcium channels (VGCCs) allow for rapid calcium entry and are expressed during early neural stag
41 y affecting the electrical driving force for calcium entry and calcium channel gating.
42 o pH 6.4 caused inhibition of Orai1-mediated calcium entry and conferred capability for PDGF to evoke
43 NA and proteins and abrogated store-operated calcium entry and I(CRAC) in VSMC; control shRNA was tar
44 sigargin was used to activate store-operated calcium entry and increase cytosolic calcium in endothel
45 r siRNA silencing of P2X(7) receptors blocks calcium entry and inhibits T-cell activation.
46 erpotentials, which often follow APs, affect calcium entry and neurotransmitter release.
47 alcium channels (Cav) are the major route of calcium entry and regulate multiple functions such as co
48 s reveal a more complex relationship between calcium entry and release from stores.
49 findings demonstrate the close apposition of calcium entry and release sites and the dynamics of such
50 Ps), particularly the falling phase, affects calcium entry and small changes in calcium influx can pr
51 per (Slo3) are core regulators of sperm tail calcium entry and sperm hyperactivated motility.
52  In particular, reduced spike height reduces calcium entry and subsequent calcium-activated potassium
53 Tonic synapses are specialized for sustained calcium entry and transmitter release, allowing them to
54 1 substantially reduced thapsigargin-induced calcium entry, and more modestly diminished the frequenc
55 idual oligomers larger than trimers inducing calcium entry as they cross the cell membrane, a result
56 is a rare genetic disorder of store-operated calcium entry, associated with a complex syndrome includ
57       Moreover, we show that WAVE2 regulates calcium entry at a point distal to PLCgamma1 activation
58 ed to interact at common sites downstream of calcium entry at amphibian motor nerve endings.
59                     During irregular firing, calcium entry at both timescales can be detected, sugges
60 e to polyamine-mediated rectification, favor calcium entry at hyperpolarized potentials.
61 nstrate that cholinergic excitation promotes calcium entry at subthreshold membrane potentials to rap
62                     This mechanism regulates calcium entry at the end of APs and therefore stabilizes
63 redict human genes involved in mitochondrial calcium entry based on clues from comparative physiology
64 s well as display robust apoptosis following calcium entry blockade.
65 well as display far less apoptosis following calcium entry blockade.
66 ular calcium or inhibition of store-operated calcium entry blocked DIR, but the L-type calcium channe
67 d STIM2 punctum formation and enhanced basal calcium entry but decreased sarco/endoplasmic reticulum
68 MEM20 (POST), does not affect store-operated calcium entry but does reduce plasma membrane Ca(2+) pum
69 llular calcium or inhibition of capacitative calcium entry by 2-APB prevented ciglitazone-induced EGF
70 -1, -2, and -3 enhanced thapsigargin-induced calcium entry by 50-150% in cells stably overexpressing
71                   Blocking voltage-dependent calcium entry by cadmium or replacement of external calc
72                Pharmacological inhibitors of calcium entry, calmodulin activation, and CaMKII activit
73 lates proliferation by inducing capacitative calcium entry (CCE).
74 ed receptor expression was due to attenuated calcium entry, cells were incubated with the calcium che
75 as recently been shown to exhibit myocardial calcium entry channel blocking activity, substantially h
76            Interestingly, the store-operated calcium entry channel inhibitor (SK&F96365) also reduced
77 sing a mouse model in which the gene for the calcium entry channel protein, Orai1, has been deleted.
78 n in stores, and Orai-1, the calcium-induced calcium entry channel, are colocalized with SP, in the s
79 nt receptor potential vanilloid 4 (Trpv4), a calcium-entry channel, is expressed in normal cholangioc
80 ntrolling cell function, can be generated by calcium entry channels activated by plasma membrane depo
81      Our data suggest that activation of P2X calcium entry channels may have profound therapeutic ben
82 ithelial P2X(4) receptors serve as ATP-gated calcium entry channels that induce a sustained increase
83 lcium stores to plasma membrane capacitative calcium entry channels.
84 culum calcium release-induced store-operated calcium entry contributes to intracellular calcium incre
85 f the filtration coefficient, in a dose- and calcium-entry dependent manner.
86                               Store-operated calcium entry depicts the movement of extracellular Ca2+
87 ons in the L-type calcium channel that abort calcium entry do not produce this phenotype.
88 reas streptomycin antagonized TRPM8-mediated calcium entry, downregulated UCP-1 expression, and mitig
89 ient as CaV2.2 N-type channels at supporting calcium entry during action potential-like stimuli.
90 nd not STIM2 that is exclusively involved in calcium entry during calcium oscillations.
91 te an AHNAK1-dependent mechanism controlling calcium entry during CTL effector function.
92 ads to a complete loss of excitation-coupled calcium entry during KCl depolarization and a more rapid
93 d to the mitochondrial matrix, we found that calcium entry during pacemaking created a basal mitochon
94 ed CPK32 activates CNGC18, further promoting calcium entry during the elevation phase of Ca(2+) oscil
95         The comparison of excitation-coupled calcium entry (ECCE) between FDB fibers from WT, JP45KO,
96 sms of action is to block excitation-coupled calcium entry (ECCE) in both adult mouse flexor digitoru
97 mational coupling, termed excitation-coupled calcium entry (ECCE) is triggered by the alpha(1s)-DHPR
98 ypothesize that under conditions of enhanced calcium entry, elevation of intracellular calcium will r
99 ize, indicating that a separate mechanism of calcium entry exists, corresponding to cell loss at the
100            In hippocampal pyramidal neurons, calcium entry following an action potential burst result
101 tsynaptic spiking alone and that it requires calcium entry following synaptic NMDA receptor activatio
102 microns away from the wound, allowing direct calcium entry from extracellular fluid into damaged cell
103 craniosensory fibers release glutamate using calcium entry from two sources: CaVs and TRPV1.
104    After chemical blockade of Orai1-mediated calcium entry, however, PDGF caused redistribution.
105 esults indicate that the P2Y6/store-operated calcium entry/IL-8 axis is involved in MSU crystal-induc
106 (s) involved in regulation of store operated calcium entry in Darier's disease (DD) is not known.
107 c Cav-1, we show that Cav-1 is essential for calcium entry in endothelial cells and governs the local
108 mbrane potential but abolishes mitochondrial calcium entry in intact and permeabilized cells, and att
109 nnels, thereby inhibiting glucose-stimulated calcium entry in isolated mouse pancreatic beta cells.
110      CaT1 also contributes to store-operated calcium entry in Jurkat T-lymphocytes and prostate cance
111 annel opening, providing a new mechanism for calcium entry in lymphocytes.
112 lcium-selective cation channels that mediate calcium entry in many different cell types.
113 RAC) channels constitutes a primary route of calcium entry in most cells.
114 wanted cross-talk between pathways, sites of calcium entry in neurons are localized to specific membr
115 of the proteasome is dependent upon external calcium entry in part through N-methyl-D-aspartate recep
116 in HEK293 cells and exhibited TRPC3-mediated calcium entry in response to agonist activation.
117 pen with fast kinetics and carry substantial calcium entry in response to individual action potential
118 this study, we show that RBCs exhibit robust calcium entry in response to mechanical stretch and that
119                                              Calcium entry in response to store depletion with thapsi
120                        Thus, activity-evoked calcium entry in sensory neurons may provide differentia
121 d non-functional Orai1 R91W attenuated basal calcium entry in shTRPC2 cells.
122 ASQ1 (CASQ, calsequestrin) and JP45-CASQ2 on calcium entry in slow twitch muscles.
123 n STIM1 completely abolishing store-operated calcium entry in T cells.
124 nificant deficits in BCR triggering-mediated calcium entry in the cytosol, which correlates with impa
125 it caused calcium release and Orai1-mediated calcium entry in the same time period.
126                  Thus, Cav-1 is required for calcium entry in vascular endothelial cells and perhaps
127 a(2+) channels (LTCC) are the main route for calcium entry in vascular smooth muscle cells (VSMC).
128 t effect on endogenous, thapsigargin-induced calcium entry in wild-type cells (HEK-293, COS1), in HEK
129 erning why other known routes of significant calcium entry, in particular, VGCCs, are not similarly t
130 and DeltaE9 cells showed larger capacitative calcium entry indicating a direct effect on Ca2+ influx
131 es not affect the time course of presynaptic calcium entry, indicating that the reduced Ca(influx) re
132 nous TRPC1 or TRPC4 inhibited store-operated calcium entry, indicating they are part of the native SO
133          Activation of alternative routes of calcium entry induced neuronal death in proportion to th
134  influx, which was blocked by store-operated calcium entry inhibitors.
135 ch recently were suggested to play a role in calcium entry into CD4(+) T cells.
136 lutamate modulation of H(+) flux arises from calcium entry into cells with subsequent activation of t
137            Various cellular signals initiate calcium entry into cells, and there is evidence that lip
138 dies described here show that HBx stimulates calcium entry into cells, resulting in an increased plat
139 ve hypothesized that digitoxin might mediate calcium entry into cells.
140 , cell growth, and phospholipase C-dependent calcium entry into cells.
141                                     Although calcium entry into endothelial cells is critical for los
142                                              Calcium entry into excitable cells is an important physi
143 report here that digitoxin molecules mediate calcium entry into intact cells.
144  annexins and calcium, resulting in enhanced calcium entry into MV.
145                                              Calcium entry into myocytes drives contraction of the em
146 epolarization but not after 1 hr and require calcium entry into neurons.
147 ved as one of the most important players for calcium entry into presynaptic endings responsible for t
148 pecifically, we show that CpG/SR-B1 triggers calcium entry into primary B lymphocytes via phospholipa
149 uration CS responses in Purkinje cells, more calcium entry into Purkinje cells, larger synaptic depre
150               Synchronous release is tied to calcium entry into synaptic boutons via P/Q type calcium
151   Here we have shown an additional route for calcium entry into T cells-through the low-voltage-activ
152 y, these alterations were found to be due to calcium entry into the mitochondria, because the swellin
153 hondrial calcium uniporter (MCU) facilitates calcium entry into the mitochondrial matrix to stimulate
154          Calcium flux through store-operated calcium entry is a central regulator of intracellular ca
155             Calcium overload due to enhanced calcium entry is a mechanism for spontaneous calcium rel
156     A unique mechanism called store-operated calcium entry is activated when ER calcium is depleted,
157              In support of this, presynaptic calcium entry is affected by afterpotentials after stand
158                               The pathologic calcium entry is dependent on the sodium overload, which
159 t that, under normal conditions, the role of calcium entry is to sustain [Ca(2+)](i) oscillations.
160 hat pairing IP3 with climbing fiber-mediated calcium entry leads to a large calcium release transient
161 e show that the activation of Orai1-mediated calcium entry leads to enhancing focal adhesion turnover
162 f extracellular calcium through capacitative calcium entry may be an unrecognized component that prov
163 activity-dependent regulation of presynaptic calcium entry may contribute to homeostatic regulation o
164                                              Calcium entry may function to trigger Ca(2+) release via
165        We identified a novel plasma membrane calcium entry mechanism that extends the range of rod ph
166 led that caspase-3 activation, extracellular calcium entry, mitochondrial membrane permeability, and
167 ly demonstrated that neuronal store-operated calcium entry (nSOC) in hippocampal neurons is regulated
168 barrage firing, suggesting that the required calcium entry occurs in other cells.
169                             In immune cells, calcium entry occurs through store-operated Ca(2+) relea
170 mGluR-dependent plasticity is independent of calcium entry or calcium dynamics.
171 ivated by depolarization (excitation-coupled calcium entry or ECCE).
172 hat requires store depletion (store-operated calcium entry or SOCE) and a second that is independent
173                    In addition to regulating calcium entry, our data suggest that eicosanoid-activate
174 cium channel CaV1.3 constitutes an important calcium entry pathway implicated in the regulation of sp
175 s through the store-operated or capacitative calcium entry pathway.
176 STIM1 activation and did not activate the PM calcium entry pathway.
177 ol-stimulated, or carbachol (CCh)-stimulated calcium entry pathways in HEK-293 cells.
178 al level in the regulation of store-operated calcium entry pathways.
179 on conductance (I(CAN)) that is activated by calcium entry predominantly through L-type calcium chann
180  as a predominant mediator of store-operated calcium entry, proliferation, and cytokine production in
181                                Downstream of calcium entry, RCH conditions significantly increased th
182 in naive CD8(+) T cells, and is critical for calcium entry required for their proper function during
183 posed to form nonselective receptor-operated calcium entry (ROCE) cation channels that are activated
184              We investigated the location of calcium entry sites and synaptic ribbons in the type-Mb
185 d Ca2+ (I(crac)) channels and store-operated calcium entry (SOC) channels.
186 e in cell proliferation rate, store-operated calcium entry (SOCE) amplitude, cationic channel TRPC6,
187                               Store-operated calcium entry (SOCE) and TRPC protein expression were in
188 gnaling pathways initiated by store-operated calcium entry (SOCE) are known to regulate neutrophil ac
189  the present study, we report store-operated calcium entry (SOCE) as a novel target of TRPM7 kinase a
190  Our previous studies implied store-operated calcium entry (SOCE) as the major pathway for this Ca(2+
191                               Store-operated calcium entry (SOCE) by calcium release activated calciu
192 ers ER morphology and affects store-operated calcium entry (SOCE) by decreasing STIM1 puncta formatio
193 sed to form Ca(2+)-selective, store-operated calcium entry (SOCE) channels that are activated by stor
194 allowed a novel "permissive" store-operative calcium entry (SOCE) following the initial platelet-acti
195  model wherein STIM1-mediated store-operated calcium entry (SOCE) governs the Ca(2+) signaling requir
196 ing intracellular calcium and store-operated calcium entry (SOCE) in fast- and slow-twitch muscle fib
197 rine neutrophils show loss of store-operated calcium entry (SOCE) in response to both soluble ligands
198 nnel subunit that facilitates store operated calcium entry (SOCE) in T cells and is necessary for for
199                               Store-operated calcium entry (SOCE) is a fundamental mechanism of calci
200                               Store-operated calcium entry (SOCE) is a key evolutionarily conserved p
201                               Store-operated calcium entry (SOCE) is a major Ca(2+) signaling pathway
202                               Store-operated calcium entry (SOCE) is a ubiquitous mechanism that is m
203                               Store-operated calcium entry (SOCE) is an important Ca(2+) entry pathwa
204                               Store-operated calcium entry (SOCE) is involved in various cellular fun
205                               Store-operated calcium entry (SOCE) is required for polymorphonuclear n
206                               Store-operated calcium entry (SOCE) is the mechanism by which extracell
207                               Store-operated calcium entry (SOCE) is the predominant Ca(2+) entry mec
208                               Store operated calcium entry (SOCE) is thought to primarily regulate ca
209 Transcriptional regulation by Store-operated Calcium Entry (SOCE) is well studied in non-excitable ce
210                 By inhibiting store-operated calcium entry (SOCE) or voltage-gated Ca(2+) channels (V
211                           The store-operated calcium entry (SOCE) pathway is an important route for g
212 ent advances in understanding store-operated calcium entry (SOCE) regulation, the fundamental questio
213 etion of ER calcium activates store-operated calcium entry (SOCE) through activation of the ER calciu
214 e of [Ca(2+)]cyt elevation is store-operated calcium entry (SOCE) through plasmalemmal calcium channe
215 ogical studies suggested that store-operated calcium entry (SOCE), a calcium refilling mechanism resp
216 ntrations in GC cells through store-operated calcium entry (SOCE), and then mediated Ca(2+)-dependent
217 ological characteristics with store-operated calcium entry (SOCE), is required to maintain baseline [
218 ed Ca(2+) signaling, known as store-operated calcium entry (SOCE), occurs downstream of immunorecepto
219 amatically inhibited (52-68%) store-operated calcium entry (SOCE), whereas suppression of TRPC4 or TR
220 ochondrial calcium uptake and store-operated calcium entry (SOCE).
221 elated with the occurrence of store-operated calcium entry (SOCE).
222  by calcium store release and store-operated calcium entry (SOCE).
223 tion-contraction coupling and store-operated calcium entry (SOCE).
224 lcium influx pathway known as store-operated calcium entry (SOCE).
225 sensor protein that initiates store-operated calcium entry (SOCE).
226      This mechanism is called store-operated calcium entry (SOCE).
227  been considered as a part of store-operated calcium entry (SOCE).
228  melastatin 7 (TRPM7) reduces store-operated calcium entry (SOCE).
229  the subsequent activation of store-operated calcium entry (SOCE).
230 tified two main components of store-operated calcium entry (SOCE): the endoplasmic reticulum-localize
231 , and indicate that inhibitors of ADPR-gated calcium entry, such as 8Br-ADPR, have the potential to b
232  that exocytosis was more loosely coupled to calcium entry than in fast synapses.
233 olecular mechanism underlying store-operated calcium entry that replenishes ER stores in mouse Muller
234 tions augmented colbalt influx, a marker for calcium entry that selectively occurs through calcium pe
235 ous pacemakers with broad spikes, leading to calcium entry that was weakly buffered.
236 rimary pathway for so-called "store-operated calcium entry" - the cellular entry of calcium induced b
237                 Under conditions of enhanced calcium entry, the rate of calcium uptake was faster com
238                                              Calcium entry through a plasma membrane defect leads to
239  by conduction to adjacent SMCs where phasic calcium entry through CavL sums to produce tone.
240                                        Local calcium entry through CRAC channels activates expression
241 nductances generated by firing revealed that calcium entry through ICAT controls the emergence of the
242 ent with physiological findings showing that calcium entry through L-type calcium channels in pyramid
243  channels causes membrane depolarization and calcium entry through L-type calcium channels.
244 vious work has shown that activity-dependent calcium entry through L-type channels elevates perinucle
245                           Activity-dependent calcium entry through L-type channels increased mitochon
246  drugs approved for human use can antagonize calcium entry through L-type channels, these results poi
247                                              Calcium entry through postsynaptic NMDA-Rs and subsequen
248 on at the neuromuscular junction, suggesting calcium entry through presynaptic N-type calcium channel
249            In addition, the model shows that calcium entry through store-operated calcium channels is
250                 The inhibition is not due to calcium entry through store-operated channels but rather
251 in the sarcoplasmic reticulum, by subsequent calcium entry through store-operated channels, and by in
252 the ductus arteriosus at birth is related to calcium entry through store-operated channels, encoded b
253                          Tight regulation of calcium entry through the L-type calcium channel CaV1.2
254           We previously showed in vitro that calcium entry through Trpc1 ion channels regulates myobl
255 re-operated channels but rather results from calcium entry through TRPC7 channels themselves.
256 ion of the TRPM2 pore mutant E960D, in which calcium entry through TRPM2 is abolished, also resulted
257 reases in glutamate release, suggesting that calcium entry through TRPV1 channels may trigger glutama
258 action-potential duration, which would limit calcium entry through voltage-dependent calcium channels
259                                              Calcium entry through voltage-gated calcium channels has
260 alian motor nerve endings by reducing Ca(2+) calcium entry through voltage-gated calcium channels or,
261                               High levels of calcium entry through voltage-gated channels also impair
262 ls is critical for calcium oscillations, but calcium entry through voltage-gated channels has much le
263 ine is associated with a reduction in Ca(2+) calcium entry through voltage-gated P/Q Ca(2+) channels
264 ntaining receptors on syntaxin-1 opening and calcium entry to enhance probability of vesicle fusion.
265  of neurotransmitters and drugs that inhibit calcium entry, transmitter release and nociception throu
266 xygenation status resulting in extracellular calcium entry, uncouples RGS9-2 from R7BP, triggering it
267  were hyperproliferative and showed enhanced calcium entry upon T cell receptor stimulation.
268 ents, as a tool to investigate mechanisms of calcium entry upon wounding.
269 lly-uncoupled canine wedge model of enhanced calcium entry, using I(Ks) blockade with beta-adrenergic
270  maintain [Ca(2+)]i at extremely low levels; calcium entry usually occurs briefly, and within seconds
271 excitable cells are profoundly influenced by calcium entry via both store-operated and store-independ
272  to ER-plasma membrane junctions, leading to calcium entry via Ca(2+) release-activated Ca(2+) (CRAC)
273 ion was sensitive to apamin, phase-locked to calcium entry via Cav2.2 channels, and necessary for pre
274      These data suggest that during hypoxia, calcium entry via CRAC channels leads to AMPK activation
275 s expressing C4958S- or C4961S-RyR1 triggers calcium entry via ECCE that resembles that for wild-type
276 ients induced by tetanic stimulation rely on calcium entry via La(3+)- and nifedipine-sensitive calci
277                   These results suggest that calcium entry via Orai1 is the predominant SOCE that coo
278 ement of T cell receptors (TCRs) followed by calcium entry via store-operated calcium channels.
279 s well as thapsigargin, a known activator of calcium entry via store-operated channels, all increased
280 angiotensin to induce pericytes to contract, calcium entry via VDCCs serves to enhance the contractil
281 ansmission depends critically on presynaptic calcium entry via voltage-gated calcium (Ca(V)) channels
282 how that burst-induced depression depends on calcium entry via voltage-gated channels, is blocked by
283                               Store-operated calcium entry was also reduced in peripheral blood monon
284                            When capacitative calcium entry was blocked with Gd3+, 2-APB caused an inc
285         In TRPC1-KD cells, receptor-operated calcium entry was decreased.
286                                        Basal calcium entry was enhanced in shTRPC2 cells, whereas the
287                                     Finally, calcium entry was found to be dependent upon generation
288                               Store-operated calcium entry was indistinguishable between the two cell
289                                  The path of calcium entry was investigated.
290                                              Calcium entry was significantly reduced when Orai1 funct
291 selective blockers indicated that the lethal calcium entry was via reverse operation of a sodium-calc
292  UTP dose-dependent increase in capacitative calcium entry when calcium was added to the extracellula
293 es calcium-dependent inactivation and limits calcium entry, whereas CaBP1 blocks calcium-dependent in
294  affecting the cytoskeleton near the site of calcium entry, whereas calcium-dependent dendritic growt
295 ude, and shape of the AP falling phase alter calcium entry, which can affect neurotransmitter release
296             Here we show that TRPV6 mediates calcium entry, which is highly increased in PCa due to t
297                                              Calcium entry, which is initially facilitated by transie
298 rs through a process known as store-operated calcium entry, which is initiated by calcium sensor prot
299 asmic reticulum (ER) induced large sustained calcium entry, which was blocked by SOC inhibitors, but
300  subunits, and observe the diffusive wave of calcium entry within the dendritic spine that follows ch

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