ライフサイエンスコーパス: calcium release

1 tic calcium release mediated by enhanced RyR calcium release.

2 es to phospholipase C-mediated intracellular calcium release.

3 lation and enhanced 5-HT2A receptor-mediated calcium release.

4 f IP3 at concentrations sufficient to induce calcium release.

5 bout the mechanism coupling NAADP binding to calcium release.

6 ontent and its more pronounced decline after calcium release.

7 (3)RII levels and therefore pro-hypertrophic calcium release.

8 ryanodine receptor by way of calcium-induced calcium release.

9 ion of PLCgamma1 and increased intracellular calcium release.

10 sitol 1,4,5-trisphosphate receptor-dependent calcium release.

11 ation, or by ionomycin-induced intracellular calcium release.

12 ven in the presence of direct stimulators of calcium release.

13 release profile and the rate of spontaneous calcium release.

14 ex is required specifically for Fas-mediated calcium release.

15 estospongin C, an inhibitor of IP3R-mediated calcium release.

16 signaling, blocked T-cell receptor-mediated calcium release.

17 hanced M3R-mediated augmentation of GSIS and calcium release.

18 acidic organelles to mediate NAADP-dependent calcium release.

19 with mutant htt and normalized intracellular calcium release.

20 as an agonist with regard to US28-stimulated calcium release.

21 large concentrations of IP3 are required for calcium release.

22 tokine-mediated suppression of functional ER calcium release.

23 is mediated by ryanodine receptor-dependent calcium release.

24 -RyRs increases the incidence of spontaneous calcium release.

25 loma cells accompanied by apoptosis-inducing calcium release.

26 found that the H2R induces Galphaq-mediated calcium release.

27 s released by the process of calcium-induced calcium release.

28 but no effect on intracellular RyR2-mediated calcium release.

29 ge changes and then triggering intracellular calcium release.

30 n, which in turn results in another abnormal calcium release.

31 to the nucleus specifically after lysosomal calcium release.

32 ,4,5-trisphosphate-dependent intra-acrosomal calcium release.

33 n of TMTC1 or TMTC2 increased the stimulated calcium released.

34 endothelial NO synthase is activated 1), via calcium release, 2), via phosphorylation reactions, and

35 nship between abnormal TATS and asynchronous calcium release, a major determinant of cardiac contract

36 Store-operated calcium entry (SOCE) by calcium release activated calcium (CRAC) channels consti

37 ed to wild-type cells as a result of reduced calcium release activated calcium currents, and independ

38 interaction molecule 1) clustering and CRAC (calcium release activated calcium) channel activation.

39 forms a highly calcium-selective pore of the calcium release activated channel, and alpha-SNAP is nec

40 es and then inhibits SOCE and the underlying calcium release-activated Ca2+ current (I CRAC).

41 roposed as core components of store-operated calcium release-activated calcium (CRAC) and store-opera

42 membrane protein Orai forms the pore of the calcium release-activated calcium (CRAC) channel and gen

43 Remarkably, BTP2, a small-molecule calcium release-activated calcium (CRAC) channel blocker

44 ORAI1 is the pore-forming subunit of the calcium release-activated calcium (CRAC) channel, a stor

45 rystal structure of Orai, the pore unit of a calcium release-activated calcium (CRAC) channel, is use

46 require long-lasting calcium influx through calcium release-activated calcium (CRAC) channels and th

47 ia activates AMPK by ROS-mediated opening of calcium release-activated calcium (CRAC) channels.

48 illatory to a sustained elevated pattern via calcium release-activated calcium (CRAC)-mediated capaci

49 traps Orai1 in the PM through binding of its calcium release-activated calcium activation domain.

50 The two key components of the store-operated calcium release-activated calcium channel are the Ca(2+)

51 However, it is unlikely that the calcium release-activated calcium channel is the sole me

52 hich are known to be essential components of calcium release-activated calcium channel, allows entry

53 ignal mediator, ORAI1, a pore subunit of the calcium release-activated calcium channel, was identifie

54 In addition to calcium release-activated calcium channel/ORAI calcium c

55 Store-operated Ca2+ entry through calcium release-activated calcium channels is the chief

56 vation of engineered chemokine receptors and calcium release-activated calcium channels.

57 tromal interaction molecule (STIM) 1 and the calcium release-activated calcium modulator (ORAI) 1-med

58 The stromal interaction molecule (STIM)-ORAI calcium release-activated calcium modulator (ORAI) pathw

59 phocytes express not only cell membrane ORAI calcium release-activated calcium modulator 1 but also v

60 nts, such as stromal interaction molecule 1, calcium release-activated calcium modulator 1, and trans

61 CRAC (Calcium Release-Activated Calcium) channels represent th

62 hly Ca(2+)-selective channels known as CRAC (calcium release-activated calcium) channels.

63 ew studies have recorded STIM2-induced CRAC (calcium release-activated calcium) currents.

64 y LFA-1 facilitates the cooperation with the calcium release-activated channel Orai1 in directing loc

65 ained by Ca(2+) entry through store-operated calcium-release-activated calcium (CRAC) channels.

66 Additionally, the calcium release allows the N-lobe to rotate relative to

67 Disruption of intracellular calcium release also prevented DIR.

68 nation of specially developed cell lines and calcium release analysis hardware, has created a new and

69 e- or inositol 1,4,5-trisphosphate-dependent calcium release and abolished when both lysosomal and en

70 lacement of CGB decreases InsP(3)R-dependent calcium release and alters normal signaling patterns.

71 ulations based on a model of calcium-induced calcium release and cell-to-cell diffusion through gap j

72 ent T cells exhibited severe defects in both calcium release and dephosphorylation of nuclear factor

73 s provide insight into regulation of cardiac calcium release and how alterations to this process may

74 tment of HSG cells resulted in intracellular calcium release and induction of endocytosis at levels s

75 ct independently of beta-catenin to modulate calcium release and influence cell polarity.

76 This model uses the calcium-induced calcium release and inositol cross-coupling mechanisms c

77 g that H(2)O(2) accumulation is dependent on calcium release and Krebs cycle activity.

78 race that can drive temporal order-dependent calcium release and LTD induction in Purkinje cells and

79 mutation decreases sensitivity to activated calcium release and myoplasmic calcium levels, subsequen

80 indicating that NO synthesis is dependent on calcium release and occurs in organelles.

81 evoke redistribution, even though it caused calcium release and Orai1-mediated calcium entry in the

82 n cysteine residues on intralumenal loops of calcium release and reuptake channels have been implicat

83 ake channels have been implicated in altered calcium release and reuptake.

84 fects and acting to promote effects, such as calcium release and stress signaling, via intracellular

85 ering membrane depolarization, intracellular calcium release, and actomyosin contraction.

86 t duration, increased incidence of diastolic calcium release, and ectopic contractility.

87 ent cytosolic and mitochondrial pH decrease, calcium release, and phosphorylation of stress signaling

88 Calcium release at 2, 3, and 12 h was inhibited by 2-(4-

89 eractions between synaptically and ER-evoked calcium release at glutamatergic synapses in young AD tr

90 tive enhancement of bradykinin (BDK)-induced calcium release, because of a decrease in BDK ED50 value

91 The grafts exhibit contractile and calcium release behavior, characteristic of functional m

92 e reduction of ryanodine receptor 1 mediated calcium release but, since knocking out genes in animal

93 7,8-diol (SKF83959), found no stimulation of calcium release, but it did find a broad range of cross-

94 osed role of calsequestrin in termination of calcium release by conformationally inducing closure of

95 abeled calmodulin can be used to demonstrate calcium release by flash photolysis.

96 The molecular basis for calcium release by NAADP, however, is not clear and subj

97 idue within a putative pore region abrogated calcium release by NAADP.

98 lts, polymer treatment reduced the amount of calcium released by 27% to 30% in comparison with the un

99 We demonstrated that mitochondrial calcium released by voltage-dependent anion channel 1 (V

100 F-TrkA-dependent signaling events, including calcium release, calcineurin activation and phosphorylat

101 alcium levels upon addition to cell culture, calcium release can be determined in these cell lines up

102 in the SR lumen after depolarization-induced calcium release cause the dissociation of JP45 from CASQ

103 e mammalian ryanodine receptor intracellular calcium release channel (RyR) with high (fM) potency and

104 er-S-nitrosylation of the ryanodine receptor calcium release channel (RyR1) in skeletal muscle disrup

105 um channel directly activates opening of the calcium release channel (RyR1) in the sarcoplasmic retic

106 Ca2+ leak via the cardiac ryanodine receptor/calcium release channel (RyR2) is thought to play a role

107 le, including the cardiac ryanodine receptor/calcium release channel (RyR2) required for muscle contr

108 The type 2 ryanodine receptor/calcium release channel (RyR2), required for excitation-

109 r (ITPR3) is the most abundant intracellular calcium release channel in cholangiocytes.

110 risphosphate receptor (ITPR2), the principle calcium release channel in hepatocytes.

111 The skeletal muscle calcium release channel RyR1 is activated by Ca(2+)-free

112 yanodine receptor (RyR), a large endoplasmic calcium release channel.

113 he skeletal muscle ryanodine receptor (RyR1) calcium release channel.

114 of the major cardiac sarcoplasmic reticulum calcium release channel/ryanodine receptor (RyR2), at Se

115 antial reduction in the expression levels of calcium release channels (ryanodine receptors, RyR2) in

116 f calcium cycling that luminal gating of the calcium release channels (RyRs) mediated by the luminal

117 d as a regulator of Ryanodine receptor (RyR) calcium release channels by serving as a SR luminal sens

118 receptors (RyRs), a family of intracellular calcium release channels essential for many cellular pro

119 d as a novel family of endolysosome-targeted calcium release channels gated by nicotinic acid adenine

120 ble progress has been made in characterizing calcium release channels in the nuclear membrane, very l

121 rons by stabilizing ryanodine receptor (RyR) calcium release channels in the open configuration, whic

122 ceptors (RyRs) form a class of intracellular calcium release channels in various excitable tissues an

123 Intracellular calcium release channels like ryanodine receptors (RyRs)

124 Ryanodine receptors (RyRs) form calcium release channels located in the membranes of the

125 Ryanodine receptors (Ryrs) are a family of calcium release channels on intracellular stores.

126 Ryanodine receptor (RyR) calcium release channels showed lower sensitivity to caf

127 ine receptor types 1 (RyR1) and 2 (RyR2) are calcium release channels that are highly enriched in ske

128 P2XRs regulate vacuole activity by acting as calcium release channels, activated by translocation of

129 protein that stabilizes the closed state of calcium release channels, i.e. the ryanodine receptors.

130 Ryanodine receptors (RyR) are calcium release channels, playing a major role in the re

131 el, and the intracellular ryanodine receptor calcium release channels.

132 e receptors are homotetrameric intracellular calcium release channels.

133 th ryanodine receptors (RyR) that form major calcium release channels.

134 and functions (phagocytosis, degranulation, calcium release, chemotaxis, and reactive oxygen species

135 essed for receptor function, using assays of calcium release, chemotaxis, receptor endocytosis, and l

136 ellular calcium, implicating calcium-induced calcium release (CICR) as the novel source of the Ca(i)(

137 e regulation of regenerative calcium-induced calcium release (CICR) during Ca(2+) spark evolution rem

138 ains, suggesting an aberrant calcium-induced calcium release (CICR) effect within spines and dendrite

139 ggesting that LMO4 regulates calcium-induced calcium release (CICR) in central neurons.

140 Stable calcium-induced calcium release (CICR) is critical for maintaining norma

141 y calcium influx or requires calcium-induced calcium release (CICR) is not yet known.

142 minished by the inhibitor of calcium-induced calcium release (CICR), dantrolene.

143 k-Y130E were deficient in antigen-stimulated calcium release, degranulation, and production of some c

144 cific for either MAPK/ERK phosphorylation or calcium release demonstrated that the two pathways conve

145 The effect of N-CGB on calcium release depended upon endogenous levels of cellu

146 nd on a beat-to-beat basis and mitochondrial calcium release depends on mNCE activity and mitochondri

147 Biochemically, we show that Spry3 represses calcium release downstream of BDNF signalling.

148 Blockade of lysosomal calcium release due to lysosomal lipid accumulation has

149 Moreover, reduction of mitochondrial calcium release, either by shRNA-mediated VDAC1 silencin

150 amic copper redistributions are dependent on calcium release, establishing a link between mobile copp

151 ayed Ca(2+) transients, frequent spontaneous calcium release events and increased susceptibility to p

152 me course of the sarcoplasmic reticulum (SR) calcium release flux underlying Delta[Ca2+].

153 Increasing HP causes calcium release from a ryanodine-sensitive cytoplasmic s

154 that sphingosine is a positive regulator of calcium release from acidic stores and that understandin

155 er hypothesis for NAADP action proposes that calcium release from acidic stores subsequently acts to

156 ne Dinucleotide Phosphate (NAADP) stimulates calcium release from acidic stores such as lysosomes and

157 ged Sph leads to a significant and transient calcium release from acidic stores that is independent o

158 provide further evidence that NAADP mediates calcium release from acidic stores through activation of

159 ium storage, 1,25(OH)(2)D not only increases calcium release from bone, but also inhibits calcium inc

160 inositol 1,4,5-trisphosphate (IP3)-dependent calcium release from endoplasmic reticulum by inducing d

161 lation activates ryanodine receptor-mediated calcium release from endoplasmic reticulum stores, leadi

162 showed that the potentiation of RyR-mediated calcium release from internal stores by caffeine was abs

163 ibition of voltage-gated calcium channels or calcium release from internal stores reduces regenerativ

164 ists include a significant contribution from calcium release from internal stores.

165 sphate (NAADP) is a messenger that regulates calcium release from intracellular acidic stores.

166 Cholinergic inhibitory responses depend on calcium release from intracellular calcium stores, and r

167 o block or enhance CICR to determine whether calcium release from intracellular stores affected actio

168 Interestingly, BMP-2 induced calcium release from intracellular stores and increased

169 ular communication through gap junctions and calcium release from intracellular stores as mediators o

170 lso produces vasomotor responses by inducing calcium release from intracellular stores through its pr

171 protein coupled receptors (GPCRs) that cause calcium release from intracellular stores while other st

172 ) activates signaling cascades, resulting in calcium release from intracellular stores, ERK1/2 activa

173 ults demonstrate that, in addition to gating calcium release from intracellular stores, mAChR activat

174 ibition of N- or P/Q-type VDCCs, or block of calcium release from intracellular stores.

175 e to an effect on calcium influx rather than calcium release from intracellular stores.

176 ospholipase C gamma(1), critical signals for calcium release from intracellular stores.

177 cium channels and ryanodine receptor-induced calcium release from intracellular stores.

178 ificantly, a specific inhibitor of apoptotic calcium release from IP3R strongly blocked lymphocyte ap

179 a cells by SW620 colon cancer cells requires calcium release from IP3R.

180 1a-mediated inositol phosphate formation and calcium release from mouse neurons in a PKC-dependent ma

181 erved function of AIP proteins is to inhibit calcium release from ryanodine receptors.

182 Abnormal calcium release from sarcoplasmic reticulum (SR) is cons

183 aled a unique receptor-mediated mechanism of calcium release from SGs that involves SG store-operated

184 ening on SG membranes as a potential mode of calcium release from SGs that may serve to raise local c

185 r, whereas increased axon outgrowth involves calcium release from stores through IP3 receptors as wel

186 Here we show that calcium release from the axonal endoplasmic reticulum (E

187 helial hyperplasia via apoptosis mediated by calcium release from the endoplasmic reticulum (ER), but

188 Induction of calcium release from the endoplasmic reticulum also lead

189 yR2-R4496C mutant HEK-293 cell line in which calcium release from the endoplasmic reticulum through t

190 We find here that localized calcium release from the endoplasmic reticulum via ryano

191 ed CD36 function in FA uptake and FA-induced calcium release from the endoplasmic reticulum, supporti

192 caused an increase in the InsP(3)-dependent calcium release from the endoplasmic reticulum.

193 as indicated by reduced RyR agonist-induced calcium release from the ER and RyR-mediated synaptic re

194 n induces endoplasmic reticulum (ER) stress, calcium release from the ER and subsequent uptake of cal

195 m overload in SOD1G93A astrocytes and excess calcium release from the ER during ATP stimulation.

196 d that purinergic stimulation induces excess calcium release from the ER stores in SOD1G93A astrocyte

197 FasL stimulation and found that LFG inhibits calcium release from the ER, a process that correlates w

198 Once liberated, ACh acts to trigger calcium release from the internal store in endothelial c

199 o serve as a countercurrent mechanism during calcium release from the nuclear envelope.

200 macromolecular complex devoted to control of calcium release from the sarcoplasmic reticulum.

201 m acidic stores subsequently acts to enhance calcium release from the SR.

202 oponin complex, CK-2017357 slows the rate of calcium release from troponin C and sensitizes muscle to

203 ner mechanistically dependent upon apoptotic calcium release from voltage-gated calcium channels.

204 Luminal calcium released from secretory organelles has been sugg

205 either TMTC1 or TMTC2 caused a reduction of calcium released from the ER following stimulation, wher

206 The ectopic calcium released from these receptors induces pro-hypert

207 tudy we examined the causal role of abnormal calcium releases from the sarcoplasmic reticulum in prod

208 > 10(-4) mol/g of dust, the amount of P (and calcium) released has a direct proportionality to the am

209 proaches, we demonstrated that IP(3)-induced calcium release (IICR) initiated the hypertrophy-associa

210 IP3-induced calcium release (IICR) is increased during ER stress, an

211 cium homeostasis, (ii) endoplasmic reticulum-calcium release, (iii) activation of the oxidative stres

212 ring inhibition of UTP-induced intracellular calcium release in 1321N1 astrocytoma cells stably trans

213 al slices, we show that increased RyR-evoked calcium release in 3xTg-AD mice "normalizes" an altered

214 s this question, sarcoplasmic reticulum (SR) calcium release in a mouse strain with a naturally occur

215 s for C/EPB homologous protein (CHOP) and ER calcium release in apoptosis, we hypothesized that apopt

216 imaging of zebrafish embryos shows defective calcium release in bin1 morphants, linking the presence

217 lt in exaggerated endoplasmic reticulum (ER) calcium release in cellular and animal models of Alzheim

218 Refractoriness of calcium release in heart cells is altered in several dis

219 Calcium release in HF myocytes was restricted to regions

220 ty of SDF1-ELP, as measured by intracellular calcium release in HL60 cells was dose dependent, and al

221 sHA 14-1 induced ER calcium release in human leukemic cells within 1 min, fo

222 We examined refractoriness of calcium release in mouse ventricular myocytes and invest

223 blocked the increased incidence of diastolic calcium release in mutant cells.

224 t amplitude variation in G-protein-activated calcium release in RAW264.7 macrophages is generally ext

225 tract, and fail to undergo calcium-dependent calcium release in response to electrical stimulation or

226 y capacity, protein kinase C expression, and calcium release in response to PMA and CF pathogens.

227 lve for the equilibrium open probability for calcium release in the model.

228 Calcium transient duration and diastolic calcium release in the mutant myocytes were tetrodotoxin

229 cADPR also controls intracellular calcium release in the protozoan parasite T. gondii; how

230 s study, we examined whether dysregulated ER calcium release in young 3xTg-AD neurons alters synaptic

231 inity binding of PSC-RANTES, analog-mediated calcium release (in desensitization assays), and analog-

232 We further show that endoplasmic reticulum calcium release-induced store-operated calcium entry con

233 In addition, ER calcium release induces elevated ATP release from SOD1G9

234 We found that refractoriness of calcium release is abbreviated by stimulation of the 'fi

235 ely one-third of the observed variability in calcium release is receptor-specific.

236 vated chloride conductances by intracellular calcium release is the key factor underlying spontaneous

237 emonstrated that ATP dependent intracellular calcium release leads to an increase of nearly 100% in o

238 Specifically, abnormal calcium release leads to electrical activation, which in

239 potent calcium messenger, is able to trigger calcium release, likely through two-pore channels (TPCs)

240 ffects that are dependent upon the apoptotic calcium release machinery.

241 T temperature by sensitizing the TRH-PLC-IP3-calcium release mechanism.

242 supported by a ROS-assisted calcium-induced calcium-release mechanism intimately involving ROS produ

243 a Ca(2+) diffusion-dominated calcium-induced calcium-release mechanism is insufficient to explain the

244 uated their ability to inhibit intracellular calcium release mediated by angiotensin II receptor type

245 the augmented synaptically evoked dendritic calcium release mediated by enhanced RyR calcium release

246 Calcium release mediated by IP3Rs influences many signal

247 dramatically affect calcium homeostasis and calcium release mediated through the ryanodine receptor

248 ternal organelles, specialized intracellular calcium release membranes, come into close apposition wi

249 s to form dyads within which calcium-induced-calcium-release occurs.

250 BAPTA chelation, and recruits intracellular calcium release on its way to activation of phosphatase

251 Inhibition of intracellular calcium release or protein kinase C delta, both of which

252 he results were corroborated by analyses for calcium release or uptake, tartrate-resistant acid phosp

253 hen both lysosomal and endoplasmic reticulum calcium release pathways were blocked.

254 content and sarcoplasmic reticulum-mediated calcium release, preserving cardiomyocyte contraction af

255 f calcium is inherent in the calcium-induced calcium release process.

256 the effect of changing CSQ expression on the calcium release profile and the rate of spontaneous calc

257 at CAPN3 knockout muscles exhibit attenuated calcium release, reduced calmodulin kinase (CaMKII) sign

258 o indicate that enhanced mGluR signaling and calcium release regulated by InsP(3)R as underlying caus

259 This photo-induced Sph-driven calcium release requires the two-pore channel 1 (TPC1) r

260 ma 2 (AIM2), which led to higher cytoplasmic calcium release responsible for calpain activation under

261 Calcium influx after ER calcium release resulted in phosphorylation of cPLA(2) a

262 Lastly, we show that ER calcium release resulting from barrier perturbation trig

263 cause triggered activity because spontaneous calcium release (SCR) activates sufficient Ca-sensitive

264 the atria from mice predisposed to abnormal calcium releases secondary to the absence of calsequestr

265 feedforward cycle between the increased RyR calcium release seen in presymptomatic AD mice and aberr

266 of luminal ATP translocation and ATP-evoked calcium release share common pharmacology, suggesting th

267 uous signaling system, translating a digital calcium release signal into calcium influx that can sign

268 ts ability to inhibit store-overload-induced calcium release (SOICR) through the RyR2 channel.

269 Cmpt mice exhibited a faster decline in calcium release, suggesting a compromised ability to ref

270 rate and increases the critical SR level for calcium release termination.

271 In this report, we demonstrate that calcium releases the C2 domain-mediated auto-inhibition

272 e directly suppresses sarcoplasmic reticulum calcium release-the cellular mechanism responsible for t

273 e small molecule triptolide induces cellular calcium release through a polycystin-2-dependent pathway

274 ium activity during axophilic migration, and calcium release through IP3 receptors was found to stimu

275 Herein we report that proper lysosomal calcium release through the calcium channel TRPML1 is re

276 s, uptake by mitochondria, and mitochondrial calcium release through the Na/Ca exchanger.

277 acutely couples changes in pO(2) to altered calcium release through the ryanodine receptor-Ca(2+)-re

278 InsP(3)-mediated calcium release through the type 2 inositol 1,4,5-trisph

279 Consistent with these observations we found calcium release to be significantly reduced in fibers fr

280 HSV triggers intracellular calcium release to promote viral entry.

281 s and were proposed to mediate endolysosomal calcium release triggered by the second messenger, nicot

282 fects of IVIg on several parameters, such as calcium release, tyrosine phosphorylation, BCR aggregati

283 calculation, we derive a minimal model of a calcium release unit which includes CSQ dependence.

284 um dynamics has revealed that the elementary calcium release units of the SR can become refractory in

285 bility to link microscopic properties of the calcium release units to whole cell behavior makes this

286 ) patients and demonstrate a greatly reduced calcium release upon Sph uncaging.

287 owth behaviors is due to Coronin-1-dependent calcium release via PLC-gamma1 signaling, which releases

288 ured from females, significantly potentiated calcium release via ryanodine receptors induced by caffe

289 s Akt phosphorylation, inhibited HSV-induced calcium release, viral entry, and plaque formation follo

290 Like BDK, vasopressin- and ATP-induced calcium release was enhanced with the same pattern in ce

291 neurons expressing actin-GFP or Lifeact-RFP, calcium release was found to stimulate leading process a

292 Although the voltage dependence of SR calcium release was not statistically different between

293 sis that ATP acts as a diffusible trigger of calcium release waves, local ejection of ATP triggered P

294 duration stimulus or a diastolic spontaneous calcium release, we observed that the stimulus needed wa

295 imilar kinetics and stronger intensity of ER calcium release were induced by the sarcoendoplasmic ret

296 litude and fractional sarcoplasmic reticulum calcium release were larger and action potential and QTc

297 is reversed upon normalization of RyR-evoked calcium release with chronic dantrolene treatment.

298 sted selectively inhibited histamine-induced calcium release with the best being chlorprothixene (IC(

299 y inhibiting inositol trisphosphate-mediated calcium release with Xestospongin C (XeC).

300 increase in ryanodine receptor (RyR)-evoked calcium release within synapse-dense regions of CA1 pyra