ライフサイエンスコーパス: astrocytic

1 d with a sharp increase in neuronal, but not astrocytic, 2DG-IR uptake.

2 mory and suggest that AD-linked increases in astrocytic A2A receptor levels contribute to memory loss

3 or protein (hAPP) showed increased levels of astrocytic A2A receptors.

4 These results show that the dysfunction of astrocytic A2AR, by controlling GLT-I activity, triggers

5 of neuronal uPA to astrocytic uPAR promotes astrocytic activation and that astrocytes activated by u

6 g of neuronal uPA to astrocytic uPAR induces astrocytic activation by a mechanism that does not requi

7 Furthermore, astrocytic activation decreased the firing rate of CeM n

8 inding is necessary and sufficient to induce astrocytic activation in the ischemic brain and that ast

9 In summary, we show that uPA/uPAR-induced astrocytic activation mediates a cross talk between astr

10 ronal activity release ATP, which propagates astrocytic activation, stimulates release of vasoactive

11 ) model, with an additional layer simulating astrocytic activation.

12 The astrocytic alkalinization is shown to be highly correlat

13 r results support a model in which elevating astrocytic alphaBc confers neuroprotection through a pot

14 Interestingly, astrocytic alphaBc overexpression was neuroprotective ag

15 owledge for the first time, insight into how astrocytic and endothelial activation of antiviral statu

16 njury (SCI) is characterized by formation of astrocytic and fibrotic scars, both of which are necessa

17 Neuropathological examination showed astrocytic and microglial activation and neuronal loss.

18 ystrophic neurites and glial responses, both astrocytic and microglial.

19 neural circuit function, it seems as though astrocytic and neuronal biology continue to advance in p

20 Our calcium-imaging data show that astrocytic and neuronal calcium levels increase after br

21 ution of specific gut bacterial taxa towards astrocytic and neuronal changes in brain function using

22 ations in the mRNA and protein expression of astrocytic and neuronal proteins necessary for optimal e

23 for the clinical care of adult patients with astrocytic and oligodendroglial gliomas, including gliob

24 that OPCs have the potential to develop both astrocytic and oligodendroglial tumors given loss of p19

25 ovascular decline and complement activation, astrocytic Apoe dramatically decreased in aged mice, a d

26 ecule, this suggests a possible link between astrocytic Apoe, age-related neurovascular dysfunction a

27 models, we show that increased expression of astrocytic apoE4, but not apoE3, during the seeding stag

28 athophysiological outcomes of IgG binding to astrocytic AQP4 are poorly understood.

29 ost patients, an IgG autoantibody binding to astrocytic aquaporin 4, the principal water channel of t

30 or Lrp4, in response to agrin, in modulating astrocytic ATP release and synaptic transmission.

31 Importance: A novel astrocytic autoantibody has been identified as a biomark

32 Nonetheless, whether mHtt affects astrocytic BDNF in the HD brain remains unknown.

33 This key metabolic role of astrocytic beta2ARs may represent a novel target mechani

34 ing neurovascular coupling (NVC) via several astrocytic Ca(2+) -dependent signalling pathways such as

35 Cortical PA vascular responses and astrocytic Ca(2+) dynamics were measured using an in vit

36 PAs; studies were supplemented with in vivo astrocytic Ca(2+) imaging.

37 Astrocytic Ca(2+) responses were corroborated in vivo, w

38 signals that mimicked the stimulation-evoked astrocytic Ca(2+) responses.

39 yrR or Wtrw expression in astrocytes blocked astrocytic Ca(2+) signalling and profoundly altered olfa

40 Astrocytic Ca(2+) signalling has been proposed to modula

41 s Oct-TyrR and Wtrw as key components of the astrocytic Ca(2+) signalling machinery, provides direct

42 to explore whether neuronal activity evokes astrocytic Ca(2+) signals at glutamatergic synapses of a

43 adenosine triphosphate (ATP) elicited global astrocytic Ca(2+) signals that mimicked the stimulation-

44 n imaging revealed global stimulation-evoked astrocytic Ca(2+) signals with distinct latencies, rise

45 concentrations and a consequent increase in astrocytic Ca(2+) through Na(+)/Ca(2+) exchange.

46 ivation of glutamate transport and increased astrocytic Ca(2+) through reversed Na(+)/Ca(2+) exchange

47 od pressure evoked a significant increase in astrocytic Ca(2+).

48 Here, we show that the suppression of astrocytic calcineurin/NFATs helps to protect synaptic f

49 We find that astrocytic calcium activity precedes spontaneous circuit

50 nous MrgA1Rs expressed in astrocytes tripled astrocytic calcium oscillation frequency in both the pre

51 l (blood-brain barrier), ATPase activity and astrocytic cell functions contribute to MDD and suicide,

52 xogenous expression of PICK1 in the grade IV astrocytic cell line U251 reduces their capacity for anc

53 l 3-kinase (PI3K) pathways were evaluated in astrocytic cell models in the presence and absence of LR

54 gic, and cholinergic markers and markers for astrocytic cells and fibers and connexin 43 puncta.

55 SVG astrocytic cells were pretreated with TIMBD or resveratr

56 ol and choline are hyperammonemia-associated astrocytic changes, while diffusion tensor imaging (DTI)

57 R spectroscopy and hyperammonemia-associated astrocytic changes.

58 These results show that astrocytic clearance of extracellular glutamate is slowe

59 Blockade of the astrocytic CN/NFAT pathway in rats using adeno-associate

60 The blockade of astrocytic CN/NFAT signaling in a common mouse model of

61 However, the impact of astrocytic CN/NFAT signaling on neural function/recovery

62 The results reveal astrocytic CN/NFAT4 as a key pathologic mechanism for dr

63 Together, the results implicate the astrocytic CN/NFAT4 pathway as a key mechanism for disru

64 e of the Ca(2+) transients by 30-40% in both astrocytic compartments.

65 Here we report that astrocytic complement activation also regulates Abeta dy

66 ted activity-dependent upregulation of major astrocytic components of the astrocyte-neuron lactate sh

67 t microbial taxa are related to neuronal and astrocytic consequences of cirrhosis-associated brain dy

68 In contrast, synapses with astrocytic contacts were smaller after conditioned inhib

69 ocytes are unknown despite the fact that the astrocytic CREB is also activity-driven and neuroprotect

70 in mice results in a switch from neuronal to astrocytic d-serine release.

71 sion demonstrates that neuronal, rather than astrocytic d-serine, modulates synaptic plasticity.

72 Astrocyte-specific elimination of the astrocytic d-serine-synthesizing enzyme serine racemase

73 rylation may account for the facilitation of astrocytic death.

74 The SCZ glial chimeras also showed delayed astrocytic differentiation and abnormal astrocytic morph

75 ntify a novel function of YAP in neocortical astrocytic differentiation and proliferation, and reveal

76 ence for YAP regulation of mouse neocortical astrocytic differentiation and proliferation.

77 beta1-integrin increases GFAP expression and astrocytic differentiation by cultured EZCs without alte

78 in YAP-deficient NSCs partially rescued the astrocytic differentiation deficit in response to BMP2.

79 d reveal a BMP2-YAP-SMAD1 pathway underlying astrocytic differentiation in the developing mouse neoco

80 By contrast, retinal astrocytic differentiation was accelerated by the exposu

81 While astrocytic differentiation was not impaired in FTD NPCs

82 gen from the retinal circulation may promote astrocytic differentiation, in part by triggering oxygen

83 nal vascular development but also suppressed astrocytic differentiation, reducing the abundance of di

84 YAP in NSCs was required for neocortical astrocytic differentiation, with no apparent role in sel

85 ors, and undergo less proliferation and less astrocytic differentiation.

86 MP2 induction and stabilization of SMAD1 and astrocytic differentiation.

87 he brains of PD patients, and that decreased astrocytic Dlp1 likely represents a relatively early eve

88 Astrocytic EAAT2 buffers basal glutamate activation of A

89 se data shed new light on the important role astrocytic EAAT2 plays on buffering nTS excitation and o

90 (CSF) both at the choroid plexus and at the astrocytic end feet and defects in the synthesis of cere

91 n the choroid plexus but is expressed in the astrocytic end feet and ependymal cells.

92 w that AQP4 polarization in the perivascular astrocytic end feet was impaired after TBI, which was mo

93 e changes were associated with detachment of astrocytic end-feet from cerebral microvessels, leakage

94 ensity, blood-brain barrier (BBB) integrity, astrocytic end-feet, and the expression of astrocytic ga

95 cular space of preexisting vessels, displace astrocytic endfeet from endothelial or vascular smooth m

96 We conclude that NO can modulate astrocytic energy metabolism in the short term, reversib

97 utamate concentration occurs in part through astrocytic excitatory amino acid transporters (EAATs).

98 Astrocytic exosomes carry heat shock proteins that can r

99 Conversely, injection of astrocytic exosomes into the striatum of HD140Q KI mice

100 We found that mHtt is not present in astrocytic exosomes, but can decrease exosome secretion

101 citatory glutamatergic neurotransmission and astrocytic extracellular glutamate uptake and induces de

102 c commitment at the point of oligodendrocyte-astrocytic fate decision.

103 ng oligodendrocytes (OLs) while promoting an astrocytic fate in vitro.

104 with intact axons and instead divert into an astrocytic fate.

105 to direct non-astrocytic progenitors toward astrocytic fate.

106 ization requires AQP4-bound IgG to engage an astrocytic Fcgamma receptor (FcgammaR).

107 The influence that neurons exert on astrocytic function is poorly understood.

108 In turn, astrocytic GA production induces a neurotoxic phenotype

109 eport a previously unrecognized role for the astrocytic GABA transporter, GAT-3.

110 , astrocytic end-feet, and the expression of astrocytic gap junction and endothelial adherens junctio

111 The LPS-induced astrocytic GAP43 expression was mediated by Toll-like re

112 These proneurotoxic effects of astrocytic GAP43 knockdown were accompanied by attenuate

113 In sum, the present study suggests that astrocytic GAP43 mediates glial plasticity during astrog

114 Hence, astrocytic GAP43 upregulation may serve to indicate bene

115 Through this mechanism, increases in astrocytic GAT-3 activity due to GABA released from inte

116 Genomic analysis has connected altered astrocytic gene expression with synaptic deficits in a n

117 uncovers a wide programme of neuron-induced astrocytic gene expression, involving Notch signalling,

118 Separately, hundreds of astrocytic genes are acutely regulated by synaptic activ

119 Moreover, the groups of astrocytic genes induced by neurons or neuronal activity

120 iously found that Mertk and its ligand Gas6, astrocytic genes involved in phagocytosis, are upregulat

121 lood-brain barrier (BBB) and then across the astrocytic glia limitans (GL).

122 clinical cohort of patients with high-grade astrocytic glioma.

123 Neuropathological analysis showed diffuse astrocytic gliosis and activated microglia in the white

124 halamus have severe neuronal loss and marked astrocytic gliosis in every case, whereas the entorhinal

125 suggest the pharmacological relevance of NTS astrocytic GLP-1R activation for food intake and body we

126 ollectively, data demonstrate a role for NTS astrocytic GLP-1R signaling in energy balance control.

127 gic signaling, we tested the hypothesis that astrocytic GLP-1R signaling regulates energy balance in

128 er body weight, and seizures suggesting that astrocytic GLT-1 is of major importance.

129 In conclusion, astrocytic GLT-1 performs critical functions required fo

130 However, the contribution of astrocytic GLT-1 to glutamate uptake into synaptosomes i

131 noticeably glt-1, the ortholog of mammalian astrocytic GLT1 (EAAT2).

132 Unexpectedly, NH4(+) had no effect on astrocytic glucose consumption.

133 tle, leading to a CREB-dependent increase in astrocytic glucose metabolism and elevated lactate expor

134 Furthermore, astrocytic glutamate activates neuronal GluN2B-containin

135 ntiation involved astrocyte GABAB receptors, astrocytic glutamate release, and presynaptic metabotrop

136 abolic enzyme levels in the VMH, 4) examined astrocytic glutamate reuptake mechanisms, and 5) used (1

137 d glutamate was also associated with reduced astrocytic glutamate transport in the VMH.

138 n was present: neuronal activation triggered astrocytic glutamate transport via excitatory amino acid

139 obal and prefrontal cortical blockade of the astrocytic glutamate transporter (GLT-1) induces anhedon

140 Astrocytic glutamate transporter excitatory amino acid t

141 xFAD mice led to increased expression of the astrocytic glutamate transporter GLT-1 and to attenuated

142 ized glutamate signaling dynamics, increased astrocytic glutamate transporter levels and alleviated m

143 The gene for EAAT2, the major astrocytic glutamate transporter, generates two carrier

144 developmental disorders, while alteration in astrocytic glutamate uptake is a core feature of multipl

145 As astrocytic glutamate uptake is a fundamental and essenti

146 Insufficiency of astrocytic glutamate uptake is a major element in the pa

147 ered EAAT expression, our findings show that astrocytic glutamate uptake is dynamic on a fast time-sc

148 el experimentally by showing that inhibiting astrocytic glutamate uptake using TFB-TBOA nearly quadru

149 ed excitability was associated with impaired astrocytic glutamate uptake.

150 citability resulting from impaired supply of astrocytic glutamine for neuronal GABA synthesis, and ep

151 y stimulation before and after inhibition of astrocytic glutathione and PgE2 synthesis.

152 st upon activation with a subsequent delayed astrocytic glycolysis increase.

153 We examined the impact of astrocytic Gq-GPCR and IP3R-dependent Ca(2+) signaling o

154 However, the roles of astrocytic Gs-coupled receptors in cognitive function ar

155 ese findings establish a regulatory role for astrocytic Gs-coupled receptors in memory and suggest th

156 Chemogenetic activation of astrocytic Gs-coupled signaling reduced long-term memory

157 r telangiectasia type 2 and solitary retinal astrocytic hamartoma in one patient.

158 , macular telangiectasia type 2 and solitary astrocytic hamartoma was detected as a unique and rare o

159 ke surface of the tumour typical for retinal astrocytic hamartoma.

160 Retinal astrocytic hamartomas arose in the nerve fiber layer in

161 121 patients who had a primary diagnosis of astrocytic HGG (51 World Health Organization [WHO] grade

162 rse outcome in patients with newly diagnosed astrocytic HGG.

163 the use of different therapeutic regimens in astrocytic high-grade glioma (HGG), the prognosis for pa

164 Proaggregant Tau causes neuronal and astrocytic hypoactivity and presynaptic dysfunction inst

165 Moreover, astrocytic IL-1beta plays a role in the enhanced synapti

166 unknown, and it is unclear whether impairing astrocytic infiltration of the neuropil alters synaptic

167 Moreover, an astrocytic inflammatory response, which reduces the surv

168 SH also blunted the astrocytic inhibition of IKA in NTS neurons and increase

169 corresponding mechanisms of seizure-induced astrocytic injury have not been documented.

170 We report that astrocytic insulin signaling co-regulates hypothalamic g

171 Collectively, our findings reveal a neuronal/astrocytic interaction in the spinal cord by which neuro

172 t Tweak induces motoneuron death, stimulates astrocytic interleukin-6 release and astrocytic prolifer

173 Here we explore the relationship between astrocytic intracellular pH dynamics and the synchronous

174 extracellular volume partly through impaired astrocytic ion and water transport.

175 Accordingly, astrocytic IR ablation reduces glucose-induced activatio

176 directly CNS glucose levels in mice lacking astrocytic IRs indicates a role in glucose transport acr

177 Hypothalamus-specific knockout of astrocytic IRs, as well as postnatal ablation by targeti

178 The existence of an astrocytic lactate reservoir and its quick mobilization

179 gs suggest that NO modulates the size of the astrocytic lactate reservoir involved in neuronal fuelin

180 Local astrocytic lactate shuttling was not required.

181 An acute increase in astrocytic lactate was also observed in acute hippocampa

182 integrity at embryonic/neonatal stage, while astrocytic laminin maintains vascular integrity in adult

183 tibody and RNAi, we further demonstrate that astrocytic laminin, by binding to integrin alpha2 recept

184 of dendritic spines and shafts, and on some astrocytic leaflets, in both hippocampus and cerebellum.

185 preferentially in PSDs, and in perisynaptic astrocytic leaflets, provides morphologic evidence that

186 addition to the traditional presynaptic and astrocytic locations.

187 Intriguingly, astrocytic LPL deficiency also triggered increased ceram

188 Likewise, astrocytic LPL deletion reduced the accumulation of lipi

189 these results suggest that both neuronal and astrocytic MAGL contribute to 2-AG clearance and prevent

190 (CF) to PC synapses, while both neuronal and astrocytic MAGL significantly contributes to the termina

191 ed the relative contribution of neuronal and astrocytic MAGL to the termination of DSE and DSI in Pur

192 ation into neurons, proper expression of the astrocytic marker GFAP and corticogenesis.

193 g of neurons and increased expression of the astrocytic marker GFAP in the cortex of 7-day old pups.

194 Notch signalling, which drives and maintains astrocytic maturity and neurotransmitter uptake function

195 ll death of patient-derived motor neuron and astrocytic-mediated neurotoxicity in co-culture assays.

196 neuropathic pain sensitization by releasing astrocytic mediators (e.g. cytokines, chemokines and gro

197 vating FcgammaR's gamma subunit and involves astrocytic membrane loss of an inhibitory FcgammaR, CD32

198 zation is shown to be highly correlated with astrocytic membrane potential changes during seizure-lik

199 gammaR engagement for internalization of two astrocytic membrane proteins critical to CNS homeostasis

200 , (b) brain glucose uptake and neuronal- and astrocytic metabolism, and (c) synaptic plasticity.

201 Blocking the astrocytic mGluR5-signaling pathway suppressed mechanica

202 amate by astrocytes regulate the movement of astrocytic mitochondria and suggest a mechanism by which

203 cerebral ischaemia in mice induced entry of astrocytic mitochondria into adjacent neurons, and this

204 s after OGD or NMDA, and blocked the loss of astrocytic mitochondria.

205 Taken together, our results suggest that astrocytic mitochondrial Dlp1 is a key protein in mitoch

206 als with NPT, there was dissociation between astrocytic morphological features and axo-spinous synapt

207 ayed astrocytic differentiation and abnormal astrocytic morphologies.

208 ce was: 1p/19q loss, EGFR amplification, and astrocytic morphology, which resulted in the identificat

209 GAT-3 activity results in a rise in astrocytic Na(+) concentrations and a consequent increas

210 E3 knockout reduces functional expression of astrocytic NBCe1.

211 ring glucose and lactate trafficking through astrocytic networks.

212 from interdependent and mutually supportive astrocytic-neuronal signaling.

213 Furthermore, in the absence of astrocytic NL2, the formation and function of cortical e

214 inergic neurons and this inhibition required astrocytic Oct-TyrR and Wtrw.

215 ased reader will follow our argumentation on astrocytic or microglial P2X7Rs being the primary target

216 We substantiated the astrocytic origin of SEPs through paired neuron-astrocyt

217 odel is constrained by relative neuronal and astrocytic oxygen and glucose utilization, by the concen

218 niques, we evaluated the mechanisms by which astrocytic PAR1s modulate the activity of presynaptic va

219 (CSF), or both that yielded a characteristic astrocytic pattern of mouse tissue immunostaining; (2) c

220 Rapid astrocytic pH changes are highly temporally correlated w

221 different cell-pair combinations reveal that astrocytic pH dynamics are more closely related to netwo

222 r short and long sleep loss, suggesting that astrocytic phagocytosis may represent the brain's respon

223 r damage.SIGNIFICANCE STATEMENT We find that astrocytic phagocytosis of synaptic elements, mostly of

224 Astrocytic phagocytosis, mainly of presynaptic component

225 o identify a nuclear marker pathognomonic of astrocytic phenotype, we assessed differential RNA expre

226 The effects of AE3 knockout on astrocytic pHi homeostasis in MAc-related assays require

227 Here, we used a conditional astrocytic phosphorylated signal transducer and activato

228 The early prominence of the astrocytic plaques in relation to sparse neuronal lesion

229 ticobasal degeneration and the pathognomonic astrocytic plaques were the most prominent lesion type i

230 els enable the high conductance state of the astrocytic plasma membrane, which ensures the driving fo

231 g oxygen dependent HIF-2alpha degradation in astrocytic precursors.

232 apses were always located within 1 mum of an astrocytic process, but none were ensheathed by those pr

233 ensheathing of synapses and vasculature with astrocytic processes and adhere to the adjacent processe

234 Therefore, structural relationships between astrocytic processes and dendritic spines undergo activi

235 t caused a delayed loss of mitochondria from astrocytic processes and increased colocalization of mit

236 Fine astrocytic processes are in tight contact with neurons a

237 de that stimulation-evoked Ca(2+) signals in astrocytic processes at CA3-CA1 synapses of adult mice (

238 lso induced mitochondrial confinement within astrocytic processes in close proximity to synapses.

239 ume measurements of synapses and surrounding astrocytic processes in mouse frontal cortex after 6-8 h

240 ere coordinated with changes in perisynaptic astrocytic processes in the border region between head a

241 ical Ca(2+) events occurring within the fine astrocytic processes of mature animals.

242 ignaling-dependent mitochondrial dynamics in astrocytic processes remains unclear.

243 walk into the model containing neuronal and astrocytic processes to study the spatial distribution o

244 s of neurons in area CA1 and mitochondria in astrocytic processes were blocked by ionotropic glutamat

245 ecently, mitochondria have been localized to astrocytic processes where they shape Ca(2+) signaling;

246 otransmission: the extracellular space, fine astrocytic processes, and neuronal terminals.

247 orter EAAT2, which is primarily localized on astrocytic processes, facilitates glutamate clearance fr

248 sibly even as a source of calcium signals in astrocytic processes.

249 omologous identified neurons and surrounding astrocytic processes.

250 nd dramatic increases in Ca(2+) signaling in astrocytic processes.

251 ulates the levels of intracellular Ca(2+) in astrocytic processes.

252 ctively, increases mitochondrial mobility in astrocytic processes.

253 P enhance the motility of synapse-associated astrocytic processes.

254 ead of differentiated astrocytes, but behind astrocytic progenitor cells (APCs) and immature astrocyt

255 ever, only Notch is sufficient to direct non-astrocytic progenitors toward astrocytic fate.

256 ed fewer neocortical astrocytes and impaired astrocytic proliferation and, consequently, death of neo

257 mulates astrocytic interleukin-6 release and astrocytic proliferation in vitro.

258 stologic evaluation of neuronal survival and astrocytic proliferation was performed on day 14.

259 However, YAP in astrocytes was necessary for astrocytic proliferation.

260 We tested the hypothesis that astrocytic prostaglandin E2 (PgE2) plays a key role for

261 control may be caused by thrombin acting on astrocytic protease-activated receptors (PAR1) in the hi

262 inal hydrolase (UCH-L1) and glial fibrillary astrocytic protein (GFAP) in acute stroke patients and h

263 brain, increased plasma levels of S100B, an astrocytic protein, and down-regulation of tight junctio

264 Our study suggests that astrocytic Rab3a is a potential therapeutic target for H

265 Here we show that astrocytic rather than neuronal beta2ARs in the hippocam

266 Astrocytic release of extracellular mitochondrial partic

267 p-me signal that activates a neuroprotective astrocytic response, which fails in ALS, and therefore r

268 each cell type, with Tnfr1 required for the astrocytic response.

269 Preventing astrocytic scar formation significantly reduced this sti

270 scar-forming astrocytes, or ablating chronic astrocytic scars all failed to result in spontaneous reg

271 Astrocytic scars are widely regarded as causal in this f

272 these data suggest that mGlu3 can influence astrocytic signaling and modulate betaAR-mediated effect

273 Blockade of astrocytic signaling by overexpression of ATP-degrading

274 ls that enable the selective manipulation of astrocytic signaling pathways in vivo.

275 a unidimensional process involving neuronal-astrocytic signaling to local blood vessels to a multidi

276 apses of adult mice (1) differ from those in astrocytic somata and (2) are modulated by glutamate and

277 dent transient astrocytic volume changes and astrocytic structural elaboration.

278 The earliest change was astrocytic swelling, substantiating that in MLC the prim

279 evoked vasoconstriction was blunted when the astrocytic syncytium was loaded with BAPTA (chelating in

280 en high Ca(2+) or ATP were introduced to the astrocytic syncytium.

281 astrocyte population, associated with marked astrocytic synthesis of the chemokines CXCL1 and CCL2 in

282 e hypoxic injury via a mechanism mediated by astrocytic thrombospondin-1 (TSP1) and synaptic low-dens

283 d by ERK1/2-regulated STAT3 phosphorylation, astrocytic thrombospondin-1 (TSP1) and synaptic low-dens

284 , neurons and neuronal activity regulate the astrocytic transcriptome with the potential to shape ast

285 st administered after stroke reduces the OPC astrocytic transformation and improves poststroke oligod

286 ing of extracellular glutamate, we find that astrocytic transients in glutamate co-occur with shifts

287 lize glutamate uptake but also restore other astrocytic transporter activities afflicted with HD.

288 Our results suggest that activation of astrocytic TRPV1 activates endogenous neuroprotective ma

289 Our data suggest that astrocytic TRPV4 channels are key molecular sensors of h

290 CK1 expression is down-regulated in grade IV astrocytic tumor cell lines and also in clinical cases o

291 erlie the particularly invasive phenotype of astrocytic tumor cells are unclear.

292 Astrocytic tumor cells infiltrate the surrounding CNS ti

293 PICK1 expression plays an important role in astrocytic tumorigenesis.

294 atively regulates neoplastic infiltration of astrocytic tumors and that manipulation of PICK1 is an a

295 Astrocytic tumors are the most common form of primary br

296 c injury and that binding of neuronal uPA to astrocytic uPAR induces astrocytic activation by a mecha

297 We found that binding of neuronal uPA to astrocytic uPAR promotes astrocytic activation and that

298 ic reticulum cisternae that shadow neuronal, astrocytic, vascular, and axonal structures; interface w

299 nisms that included AQP4-dependent transient astrocytic volume changes and astrocytic structural elab

300 utoantibodies against aquaporin-4 (AQP4), an astrocytic water channel.