ライフサイエンスコーパス: stellate

1 kinin caused more extensive necrosis in both stellate and acinar cells than TLC-S alone.

2 We found that both stellate and basket cells engaged in synchronized waves

3 Molecular layer interneurons (MLIs, stellate and basket cells) of the cerebellar cortex are

4 sure appears to conserve the distribution of stellate and pyramidal cells, periodic arrangement of ca

5 eine adversely affected viability of hepatic stellate and sinusoidal endothelial cells, which was rev

6 We explored the heterogeneity of mouse stellate and thoracic ganglia and found an unexpected va

7 into two distinct cell types, pyramidal and stellate, based on morphology, immunoreactivity, and fun

8 For cerebellar granule cell to stellate cell (grc-->SC) synapses, AAV1 also led to arti

9 he role of inflammatory mediators in hepatic stellate cell (HSC) activation and HSC survival during f

10 receptors (LXRs) are determinants of hepatic stellate cell (HSC) activation and liver fibrosis.

11 yrosine kinases, which contribute to hepatic stellate cell (HSC) activation and liver fibrosis.

12 Hepatic stellate cell (HSC) activation and transforming growth f

13 Hepatic stellate cell (HSC) activation on liver injury facilitat

14 ncreased after pIVCL concurrent with hepatic stellate cell (HSC) activation.

15 merase chain reaction for markers of hepatic stellate cell (HSC) activation.

16 extracellular matrix components and hepatic stellate cell (HSC) activation.

17 ould partly account for reduction of hepatic stellate cell (HSC) activation.

18 nd the molecular mediators of EMT in hepatic stellate cell (HSC) and human liver cancer cells (HepG2)

19 on, LPC biliary differentiation, and hepatic stellate cell (HSC) chemotaxis.

20 beta-4 (TB4) involved in regulating hepatic stellate cell (HSC) functions remain unclear.

21 Hepatic stellate cell (HSC) transdifferentiation from a quiescen

22 f extracellular matrix components by hepatic stellate cell (HSC)-derived myofibroblasts.

23 n (qRT-PCR) and western blotting and hepatic stellate cell (HSC)-MF contractility by gel contraction

24 Yet by recording from axons of cerebellar stellate cell (SC) interneurons, we show that AP width v

25 y liver disease activity scores, and hepatic stellate cell activation (alpha-smooth muscle actin) com

26 ic alphaSMA expression, a marker for hepatic stellate cell activation (r = -0.31, P < 0.02).

27 enefitted liver fibrosis via altered hepatic stellate cell activation and extracellular matrix remode

28 cided with alterations in markers of hepatic stellate cell activation and extracellular matrix remode

29 Estrogens inhibit stellate cell activation and fibrogenesis.

30 fibrosis, but is also permissive for hepatic stellate cell activation and fibrosis.

31 he activity of the PAR2 pepducin on cultured stellate cell activation and hepatocyte reactive oxygen

32 he dKO mice had similar levels of markers of stellate cell activation and matrix remodeling as Ppara(

33 usoidal endothelial cell capillarization and stellate cell activation demonstrates allograft injury i

34 C1QTNF2 expression is reduced during hepatic stellate cell activation in culture and in a mouse model

35 Vitamin A loss is accompanied by stellate cell activation in hepatic tissue.

36 osis and suppressed expression of markers of stellate cell activation in livers of mice fed a diet ri

37 Finally, MSDC-0602 directly reduced hepatic stellate cell activation in vitro, and MSDC-0602 treatme

38 ent or hepatocyte MPC2 deletion also limited stellate cell activation indirectly by affecting secreti

39 Stellate cell activation leads to hepatic fibrosis; furt

40 FR reduced hepatic stellate cell activation markers (transforming growth fa

41 LOX inhibition attenuated hepatic stellate cell activation markers and promoted F4/80-posi

42 rentiation into polarized MPhis that mediate stellate cell activation via TGF-beta.

43 Hepatic stellate cell activation was detected by immunofluoresce

44 r sinusoidal endothelial cell activation and stellate cell activation was increased in patients with

45 tion of hepatic progenitor cell response and stellate cell activation, and normalization of liver enz

46 duced liver fibrosis associated with hepatic stellate cell activation, hepatitis, and liver injury.

47 r injury; or reduce expression of markers of stellate cell activation, liver inflammation, and injury

48 l protein adducts accompanied by evidence of stellate cell activation, matrix remodeling, and fibrosi

49 iated with hepatic progenitor cell features, stellate cell activation, NOTCH signaling, and an aggres

50 iferation, senescence, fibrosis, and hepatic stellate cell activation, which were reduced in Hdc(-/-)

51 substrate stiffening resulted in attenuated stellate cell activation, with reduced YAP/TAZ nuclear s

52 vated monocytes/macrophages promoted hepatic stellate cell activation.

53 amine the relationship between retinoids and stellate cell activation.

54 activity and membrane insertion in wild-type stellate cell activation.

55 ve, LD-associated protein that helps mediate stellate cell activation.

56 tivation, prothrombin activation and hepatic stellate cell activation.

57 models of monocyte/macrophage and/or hepatic stellate cell activation.

58 Furthermore, during licking, stellate cell activity was anisotropic: the coordination

59 ed by ClC-a, is exclusively expressed in the stellate cell and is required for Drosophila kinin-media

60 e, reduces asymmetrical orientation of spiny stellate cell dendrites, and functionally impairs thalam

61 anscriptome of rat PMFs, compared to hepatic stellate cell HSC-derived myofibroblasts in culture, ide

62 Cells showed decreased fibrogenesis, hepatic stellate cell infiltration, Kupffer cells and inflammato

63 We find that in cerebellar stellate cell interneurons of mice, the composition and

64 activity and isoprenylation are required for stellate cell LD loss and induction of activation marker

65 LE) on the activation of human liver hepatic stellate cell line LX-2 cells.

66 This mechanism was confirmed in a hepatic stellate cell line stably that endogenously expresses RX

67 ted PRHs was applied to cultured rat hepatic stellate cell line, HSC-T6, with or without Flu-pretreat

68 involving the TRAIL receptors in the hepatic stellate cell line, LX2.

69 ulation; coculture of hepatocyte and hepatic stellate cell lines significantly increased expression o

70 fibrogenic program in hepatocyte and hepatic stellate cell lines through ROS, NFkappaB, and TGFbeta1

71 f hepatocyte markers, oval cell markers, and stellate cell markers.

72 ndence for the exponential term that matches stellate cell membrane properties, a low degree of fluct

73 ns observed with collagen matrices including stellate cell morphologies, cell-mediated realignment of

74 tate transaminase, alanine transaminase, and stellate cell proliferation by up to 50-100%.

75 ctin mRNA), whereas EX increased the hepatic stellate cell senescence marker CCN1 (P < 0.01 vs. O-SED

76 ffects of neuroligin deletions on cerebellar stellate cell synapses by electrophysiology in acute sli

77 t cell synapses, but not at distal dendritic stellate cell synapses.

78 iber (PF) to PC synapses and DSI at putative Stellate cell to PC synapses.

79 Mechanistically, PTX3 mediated the hepatic stellate cell wound-healing response.

80 flammation accompanied with elevated hepatic stellate cell-derived TnC and Toll-like receptor 4 expre

81 These results demonstrated that hepatic stellate cell-induced MDSCs concurrently suppress both T

82 or olive glycinergic synapse, and the basket/stellate cell-Purkinje GABAergic synapse in the cerebell

83 Primary hepatic stellate cell-seeded hydrogels stiffened in situ at late

84 owever, the molecular mechanisms for hepatic stellate-cell activation by HCV-infected hepatocytes are

85 lly contributed to climbing-fiber and basket/stellate-cell synapse functions, such that inhibitory sy

86 gins increased the size of inhibitory basket/stellate-cell synapses but simultaneously severely impai

87 Barrel cortex layer IV spiny stellate cells (bSCs) are the primary recipients of asce

88 poptosis resistance in primary human hepatic stellate cells (hHSC).

89 type 2 (CCR2) is expressed by active hepatic stellate cells (HSC) and is a key monocyte recruitment s

90 inib reduced EGFR phosphorylation in hepatic stellate cells (HSC) and reduced the total number of act

91 Hepatic stellate cells (HSC) are a major source of the immunoreg

92 Hepatic stellate cells (HSC) are the major source of extracellul

93 Recently, human hepatic stellate cells (HSC) have been reported to induce monocy

94 nvolvement in liver fibrogenesis and hepatic stellate cells (HSC) regulation is under study.

95 iorates liver fibrosis by inhibiting hepatic stellate cells (HSC), and loss of miR-200a is associated

96 nse (UPR) both promote activation of hepatic stellate cells (HSC), however the link between the two s

97 incipally regulated by activation of hepatic stellate cells (HSC).

98 factor (CCN2) drives fibrogenesis in hepatic stellate cells (HSC).

99 (FAK) plays a key role in promoting hepatic stellate cells (HSCs) activation in vitro and liver fibr

100 cipally expressed in quiescent mouse hepatic stellate cells (HSCs) and directly suppressed production

101 Hepatic stellate cells (HSCs) and portal fibroblasts (PFs) are b

102 liver fibrosis remission by killing hepatic stellate cells (HSCs) and producing interferon (IFN)-gam

103 Hepatic stellate cells (HSCs) are key players in the development

104 -1alpha (HIF-1alpha) is activated in hepatic stellate cells (HSCs) by hypoxia and regulates genes imp

105 kinase receptor, is up-regulated in hepatic stellate cells (HSCs) during chronic liver injury.

106 Effects of LPS on fibrogenic hepatic stellate cells (HSCs) from WT and TLR4-KO mice were asse

107 Hepatic stellate cells (HSCs) have been identified as the main f

108 Retinoid-storing hepatic stellate cells (HSCs) have recently been described as a

109 Activation of hepatic stellate cells (HSCs) in response to injury is a key ste

110 Hepatic stellate cells (HSCs) induce hepatic inflammation and im

111 Hepatic stellate cells (HSCs) inhibit T cells, a process that co

112 We answered the questions of whether hepatic stellate cells (HSCs) interact with CD4+ T cells during

113 Activation of hepatic stellate cells (HSCs) is a critical step in the developm

114 er disease mediated by activation of hepatic stellate cells (HSCs) leads to liver fibrosis.

115 erating cholangiocytes and activated hepatic stellate cells (HSCs) participate in the promotion of li

116 Hepatic stellate cells (HSCs) play a major role increasing IHVR

117 Hepatic stellate cells (HSCs) play critical roles in liver fibro

118 and pro-fibrogenic environment with hepatic stellate cells (HSCs) remodeling the extracellular matri

119 lls to the liver to remove activated hepatic stellate cells (HSCs) significantly and ameliorate liver

120 e demonstrated previously that mouse hepatic stellate cells (HSCs) suppress T cells via programmed de

121 rix proteins, such as collagen I, by hepatic stellate cells (HSCs) that culminates in cirrhosis.

122 hese secreted cytokines may activate hepatic stellate cells (HSCs) toward fibrosis.

123 Hepatic stellate cells (HSCs) were recently identified as liver-

124 Hepatic stellate cells (HSCs) were treated with or without adipo

125 increased LPA levels, activation of hepatic stellate cells (HSCs), and amplification of profibrotic

126 soidal endothelial cells (LSECs) and hepatic stellate cells (HSCs), are the first liver cells to enco

127 In cultured hepatic stellate cells (HSCs), disrupting Hedgehog signaling blo

128 s were performed with primary rodent hepatic stellate cells (HSCs), Kupffer cells (KCs), and hepatocy

129 directly targeting Gli3 in activated hepatic stellate cells (HSCs), reduces expression of Gli3 and pr

130 transcriptome signature of activated hepatic stellate cells (HSCs), the primary collagen-secreting ce

131 sm of this resistance by focusing on hepatic stellate cells (HSCs), which are known to regulate Treg

132 fibrosis is marked by activation of hepatic stellate cells (HSCs).

133 elial neoplasia, or PDAC, as well as hepatic stellate cells (HSCs).

134 luding laminin (Ln)-332, produced by hepatic stellate cells (HSCs).

135 pecial focus on the STAT3 pathway in hepatic stellate cells (HSCs).

136 omes could regulate the phenotype of hepatic stellate cells (HSCs).

137 factor-beta (PDGFB) is a mitogen for hepatic stellate cells (HSCs).

138 Kupffer cells (KCs), neutrophils, or hepatic stellate cells (HSCs).

139 deposition of collagen by activated hepatic stellate cells (HSCs).

140 as retinyl esters in the retina and hepatic stellate cells (HSCs).

141 liferation and activation of resting hepatic stellate cells (HSCs).

142 med in vitro studies on immortalized hepatic stellate cells (LX-2).

143 up to 21 days using human cell lines hepatic stellate cells (LX2), hepatocellular carcinoma (Sk-Hep-1

144 Recent findings implicate pancreatic stellate cells (PSC) as prominent mediators of inflammat

145 ber 17 (SLC22A17) in human pancreatic cancer stellate cells (PSC), key mediators of the PDAC stroma.

146 oplasia, which is orchestrated by pancreatic stellate cells (PSCs) and accounts for the majority of t

147 rix proteoglycan overexpressed by pancreatic stellate cells (PSCs) and pancreatic ductal adenocarcino

148 demonstrate that mouse and human pancreatic stellate cells (PSCs) are a source of IL-4/IL-13.

149 Pancreatic stellate cells (PSCs) are key mediators in the productio

150 Normal pancreatic stellate cells (PSCs) are regarded as quiescent, only to

151 Persistent activation of pancreatic stellate cells (PSCs) can perturb the biomechanical homo

152 Pancreatic stellate cells (PSCs) differentiate into cancer-associat

153 version of quiescent to activated pancreatic stellate cells (PSCs) drives the severe stromal reaction

154 activation of myofibroblast-like pancreatic stellate cells (PSCs) plays a predominant role in the fo

155 Conversely, TLR9 ligation induces pancreatic stellate cells (PSCs) to become fibrogenic and secrete c

156 er of myofibroblasts or activated pancreatic stellate cells (PSCs)).

157 nalling between pancreatic acinar (PACs) and stellate cells (PSCs).

158 a common phenomenon of activated pancreatic stellate cells (PSCs)/fibroblasts, the major stromal cel

159 ffer (KC), sinusoidal endothelial (LSEC) and stellate cells (SC) are major cellular components of the

160 s (BCs) in the mouse cochlear nucleus with T-stellate cells (SCs), which do have normal overshooting

161 tigate Kv2 channel functions in mEC layer II stellate cells (SCs).

162 Addition of hepatic stellate cells allowed generation of myeloid-derived sup

163 Smooth-muscle actin expression by stellate cells and CD34 expression by liver sinusoidal e

164 mpanied by enhanced activation of pancreatic stellate cells and elevated levels of serum retinoic aci

165 We found that Sema7A is expressed in spiny stellate cells and GABAergic interneurons and that its a

166 is an emerging new target expressed on liver stellate cells and hepatocytes that regulates the respon

167 ro experiments were performed in rat hepatic stellate cells and hepatocytes.

168 ression (LTD) between cortical layer 4 spiny stellate cells and layer 2/3 pyramidal cells requires th

169 We identify potent MMIC activity in hepatic stellate cells and liver sinusoidal endothelial cells.

170 eceptor, CD74, that is released from hepatic stellate cells and that binds MIF, neutralizing its sign

171 r escalated by bradykinin-induced signals in stellate cells and thus killing of stellate cells by bil

172 cinar cells but the effects of bile acids on stellate cells are unexplored.

173 ignals in stellate cells and thus killing of stellate cells by bile acids might have important implic

174 oid and cholesterol metabolism are linked in stellate cells by the LD-associated protein Rab18.

175 more dramatic Ca(2+) signals and necrosis in stellate cells compared to the adjacent acinar cells in

176 wn to reside in the principal cells, whereas stellate cells control the anion conductance, but by an

177 on of miR-200b in cholangiocytes and hepatic stellate cells decreased the expression of miR-200b, ang

178 ivation of the autophagic pathway in hepatic stellate cells during Brucella infection could have an i

179 tes in lung myofibrogenesis as suggested for stellate cells during liver fibrosis.

180 rikingly, electrophysiological recordings in stellate cells from these PV-Cre/NL123 cKO mice revealed

181 the organization of glutamatergic input from stellate cells in layer 2 and from the hippocampus, with

182 cellular electrophysiological properties of stellate cells in layer II of MEC change systematically

183 Stellate cells in layer II of the mEC project to the hip

184 0 was much higher in hepatocytes and hepatic stellate cells in liver biopsies from patients with fibr

185 s in acinar cells, had only minor effects on stellate cells in lobules.

186 cells (NFkappaB) in hepatocytes and hepatic stellate cells in monoculture; however, they do not acco

187 Voltage clamp recordings from mEC stellate cells in rat brain slices showed that GTx inhib

188 receive a spatially broad inhibition from D-stellate cells in the AVCN, and a spatially confined inh

189 tor function at parallel fibre synapses onto stellate cells in the cerebellum using whole-cell patch-

190 duced fibrosis and the numbers of pancreatic stellate cells in the tumor stroma and altered the types

191 e major cerebellar neuroligin isoforms, from stellate cells in triple NL123 conditional knock-out mic

192 pathophysiological effects of bile acids on stellate cells in two experimental models: ex vivo (mous

193 on of miR-200b in cholangiocytes and hepatic stellate cells in vitro, we evaluated angiogenesis and f

194 We recently demonstrated that hepatic stellate cells induce the differentiation of myeloid-der

195 niaturized and integrated with human hepatic stellate cells inside microfluidic devices.

196 Furthermore, T-stellate cells integrate D-stellate inhibition from an a

197 responses by random voltage fluctuations in stellate cells is significantly limited.

198 pairment in inhibitory synaptic responses in stellate cells lacking NL123 despite a nearly complete s

199 esponses in medial entorhinal cortical (MEC) stellate cells of rats, which express strong sub-thresho

200 , mutation or RNAi-mediated knockdown in the stellate cells of the tubule of TAR2 (tyrR, CG7431) resu

201 to monitor TGF-beta1 release from activated stellate cells over the course of 20 h.

202 parate putative pyramidal cells and putative stellate cells recorded extracellularly in layer II of t

203 Overexpression of miR-29 in activated stellate cells reduced stromal deposition, cancer cell v

204 ver, bile acid-elicited signalling events in stellate cells remain unexplored.

205 Transplanted stellate cells repopulated the damaged rat liver by cont

206 ell types show phase precession but putative stellate cells show steeper slopes of phase precession a

207 put image-based screen using primary hepatic stellate cells that identified the antifungal drug itrac

208 tion of GSG1L into mouse cultured cerebellar stellate cells that lack this protein increased the inwa

209 ivation of the autophagic pathway in hepatic stellate cells to create a microenvironment that promote

210 AIL pathway can mediate apoptosis of hepatic stellate cells to promote the resolution of liver fibros

211 DNA damage, whereas proliferation of hepatic stellate cells was stimulated by KCa3.1 inhibition.

212 Primary pancreatic stellate cells were activated in vitro by C5a.

213 howed that macrophages and activated hepatic stellate cells were the main cell types expressing PTX3

214 Astrocytes are stellate cells whose appearance can resemble a pointed s

215 We previously demonstrated that pancreatic stellate cells within pancreatic ductal adenocarcinoma (

216 e tracing to follow transplanted rat hepatic stellate cells, a resident liver mesenchymal cell popula

217 In stellate cells, a voltage-dependent increase in membrane

218 rosis in a yin-yang interaction with hepatic stellate cells, and are a key component of tumor-promoti

219 es in the majority of pyramidal cells, spiny stellate cells, and interneurons within the extrastriate

220 fibrogenic activation of attenuated hepatic stellate cells, and limits fibrosis reversal.

221 sinophils, neutrophils, macrophages, hepatic stellate cells, and lymphocytes all identified as major

222 dothelin-induced vasoconstriction by hepatic stellate cells, and not platelet accumulation or coagula

223 etwork that includes macrophages, pancreatic stellate cells, and prominent cytokines that are present

224 a subset of TGF-beta target genes in hepatic stellate cells, and the cooperation between the JAK1-STA

225 ted excitatory synaptic responses, which, in stellate cells, are largely extrasynaptic, without a cha

226 companied by increased activation of hepatic stellate cells, but hepatic mediators of inflammation we

227 ities of hepatocytes, Kupffer cells, hepatic stellate cells, endothelial cells, and circulating immun

228 ), which is secreted by activated pancreatic stellate cells, has important functions in chronic pancr

229 mor-derived JAG1 signaling activated hepatic stellate cells, increasing their recruitment to vasculat

230 olate induced cytosolic Ca(2+) elevations in stellate cells, larger than those elicited simultaneousl

231 idenced by chloride ion movement through the stellate cells, leading to depolarization of the transep

232 tumor stroma had fewer activated pancreatic stellate cells, lower levels of periostin, and alteratio

233 es employing Tg technology to target hepatic stellate cells, myofibroblasts, liver sinusoidal endothe

234 Contrary to the stellate cells, pyramidal cells show weaker temporal cod

235 ory projection cell classes, the bushy and T-stellate cells, receive a spatially broad inhibition fro

236 brosis, attenuated the activation of hepatic stellate cells, reduced frequencies of Th9, Th17 and Th1

237 Together with our recent findings on stellate cells, we propose a general mechanism by which

238 CCN1 also induced Jag1 expression in hepatic stellate cells, whereupon they interacted with hepatic p

239 The inflammatory cells activate hepatic stellate cells, which are the major source of myofibrobl

240 hat the activation of perisinusoidal hepatic stellate cells, which is a key event mediating the augme

241 signaling may lead to activation of hepatic stellate cells, which is required for fibrosis.

242 d treatment caused necrosis predominantly in stellate cells, which was abolished by removal of extrac

243 n the overall bile acid uptake in pancreatic stellate cells.

244 ramidal cells were superimposed on scattered stellate cells.

245 asic effect on EPSC amplitudes recorded from stellate cells.

246 y phenotype in pancreatic normal, cancer and stellate cells.

247 ctivates fibrosis-related markers in hepatic stellate cells.

248 liver, their expansion supported by hepatic stellate cells.

249 onic stem cells, gastric tumors, and hepatic stellate cells.

250 al signaling, and Crbp1 levels in VA storing stellate cells.

251 ng protein Crbp1 (RBP1) levels in VA-storing stellate cells.

252 sis is limited compared with that of hepatic stellate cells.

253 onstellate principal cells (NSPCs) and in no stellate cells.

254 he microfluidic devices containing activated stellate cells.

255 4F nanoparticles were incubated with hepatic stellate cells.

256 ell as primary human hepatocytes and hepatic stellate cells.

257 s marker activation in primary human hepatic stellate cells.

258 (+) -dependent bile acid uptake mechanism in stellate cells.

259 only signalling in acinar cells but also in stellate cells.

260 Early postnatally, layer-2 pyramidal but not stellate-cells co-localized with doublecortin - a marker

261 2 emerged around birth while reelin-positive stellate-cells were scattered throughout development.

262 art receive sympathetic innervation from the stellate ganglia (STG).

263 ctance directly in neurons isolated from the stellate ganglia of spontaneously hypertensive rats (SHR

264 before and after left, right, and bilateral stellate ganglia stimulation and norepinephrine infusion

265 my was performed and the heart and bilateral stellate ganglia were exposed.

266 enes required for ACh synthesis increased in stellate ganglia, which contain most of the sympathetic

267 Left stellate ganglion (LSG) hyperactivity promotes ischemia

268 Performance of stellate ganglion blocks at the bedside in the ICU is fe

269 ather than fluoroscopy, to perform bilateral stellate ganglion blocks at the patient's bedside in the

270 t efferent cardiac sympathetic branch of the stellate ganglion in Zucker diabetic fatty rats revealed

271 and functional development of layer IV spiny stellate glutamatergic neurons receiving sensory input,

272 Furthermore, T-stellate cells integrate D-stellate inhibition from an area that spans twice the fr

273 gins are selectively essential in cerebellar stellate interneurons for enabling the function of extra

274 tudied the role of neuroligins in cerebellar stellate interneurons that participate in a well defined

275 alyzed the role of neuroligins in cerebellar stellate interneurons.

276 regulation of NMDAR responses in cerebellar stellate interneurons.

277 esions were composed of hyperautofluorescent stellate lesions arranged in an open or closed ring with

278 Ethanol caused stellate lesions with patchy areas of normal myocardium,

279 imulating proliferation of desmin(+) hepatic stellate-like cells and enforcing a pro-fibrotic vascula

280 Primary or immortalized human hepatic stellate (LX2) cells were exposed to exosomes derived fr

281 ined the cellular properties of layer II mEC stellate neurons (mEC-SCs) in rTg4510 mice, a rodent mod

282 lammatory markers and enhanced [Ca(2+) ]I in stellate neurons (P < 0.05).

283 Our findings identify MeA stellate neurons as an important component in the respon

284 eonatal ventricular myocytes and sympathetic stellate neurons from normal (WKY) and pro-hypertensive

285 Here, we show that Ocean cells, excitatory stellate neurons in the medial EC layer II projecting in

286 of the dendritic branches in layer IV spiny stellate neurons is reduced.

287 mine the effects of the mutation on layer II stellate neurons of the medial entorhinal cortex (mEC),

288 es were observed in MeA bipolar neurons, BLA stellate neurons or in lateral amygdala stellate neurons

289 e dendritic spine density of mGluR5 KO spiny stellate neurons was significantly higher than in wild-t

290 , decreased [Ca(2+) ]i evoked responses from stellate neurons, and also reduced indicators of brainst

291 ind that a subpopulation of cells, so-called stellate neurons, exhibits clear temporal coding.

292 ructural remodeling of medial amygdala (MeA) stellate neurons.

293 BLA stellate neurons or in lateral amygdala stellate neurons.

294 elopment of functional connectivity in spiny stellate neurons.

295 ortex layer II contains pyramidal island and stellate ocean cells.

296 OPL and HFL, cavities were elongated with a stellate pattern, whereas in the INL they were rounded a

297 the morphology of widefield amacrine cells (stellate, semilunar, and thorny amacrine cells).

298 ent circuit between these cells and L4 spiny stellates (SSNs) that disappears by the end of the L4 cr

299 from 47.5+/-2.8 ms to 78.1+/-9.8 ms; P<0.01) stellate stimulation and strongly correlated with whole

300 revealed choline acetyltransferase (ChAT) in stellate sympathetic neurons and vesicular ACh transport

301 ame clinical presentation characterized by a stellate ulceration over the upper extremities and repor