ライフサイエンスコーパス: astrocyte

1 ain barrier, including endothelial cells and astrocytes.

2 om Schwann cells and share similarities with astrocytes.

3 2 alpha subunit was deleted in GFAP-positive astrocytes.

4 l groups of interest (GOI), e.g., neurons vs astrocytes.

5 teraction between TRPV4 and Cx43 channels in astrocytes.

6 o hippocampal dentate gyrus-like neurons and astrocytes.

7 ithin the individual territories of Disc1-KD astrocytes.

8 irus into neural cells such as microglia and astrocytes.

9 molecular classes while sparing normal human astrocytes.

10 ured human astrocytic cells and rat cortical astrocytes.

11 4 water channel expressed on the end-feet of astrocytes.

12 lgi was not affected in Abeta(25-35)-exposed astrocytes.

13 duced impaired gap junction coupling between astrocytes.

14 and proteinase K-resistance levels in these astrocytes.

15 neurons neighboring ephrin-B1-overexpressing astrocytes.

16 targets two cell types, oligodendrocytes and astrocytes.

17 Ps), which normally never differentiate into astrocytes.

18 cdh-gammaC4 is expressed in both neurons and astrocytes.

19 n in cortical neurons compared with cortical astrocytes.

20 ate into cells that are similar to mammalian astrocytes.

21 while this support was lost by EVs from aged astrocytes.

22 was associated with upregulation of reactive astrocytes.

23 its interaction with histone deacetylases in astrocytes.

24 depend on major Ca(2+)-dependent cascades in astrocytes.

25 h in cortex and in single neurons but not in astrocytes.

26 from the retino-hypothalamic tract and from astrocytes.

27 Astrocytes, a highly heterogeneous population of glial c

28 Astrocytes, a major cell type found throughout the centr

29 plays a pivotal role in the LPS-upregulated astrocyte activation and proliferation, supporting their

30 inflammation, impaired neuroprotection, and astrocyte activation associated with delirium duration,

31 Our findings reveal that DMS astrocyte activation differentially regulates MSNs' acti

32 CNS prion infection coincided with enhanced astrocyte activation in the brain during the preclinical

33 Consistent with this, astrocyte activation with G(q) designer receptors exclus

34 as reduced blood-brain barrier dysfunction, astrocyte activation, and interleukin-1beta, interleukin

35 O-KO mice exhibited significantly attenuated astrocyte activation, astrocytic aromatization, and decr

36 ations in pathways and genes associated with astrocyte activation, neuroinflammation, and oxidative s

37 voltage-gated Ca(2+) channels contribute to astrocyte activation, we generated an inducible conditio

38 ctive loss of dopamine neurons and increased astrocyte activation, whereas nTg mice with MPTP exposur

39 ealed that apoE4 in VMCs was associated with astrocyte activation, while apoE3 was linked to angiogen

40 F2 signaling, which is a known suppressor of astrocyte activation.

41 lammatory effects by reducing microglial and astrocytes activation as well as suppressing cerebral cy

42 romotes greater axonal survival and inhibits astrocyte activity in the optic nerve.

43 gamma range (30-50 Hz) followed by a delayed astrocyte activity that dampens the steady-state gamma a

44 Herein, we provide evidence that astrocytes aged in culture develop a spontaneous pro-inf

45 an hippocampus gives rise to new neurons and astrocytes all through adulthood.

46 Disc1-KD in astrocytes also led to decreased expression of the gluta

47 h vehicle-treated animals and also regulated astrocyte and microglial reactivity.

48 The perfect coordination of neuron/astrocyte and neuron/oligodendrocyte entities was termed

49 that evolves in space and time within single astrocytes and across astrocytic networks.

50 transporter up-regulation in both the mouse astrocytes and brain tissue.

51 ulk transcriptome analyses of CD49f(+) hiPSC-astrocytes and demonstrate that they perform key astrocy

52 on-specific transcriptional dependencies for astrocytes and identify astrocytic NFIA as a key transcr

53 oplastic cells, including endothelial cells, astrocytes and immune cells, constituting a complex and

54 1, but not SMRT, was detected in a subset of astrocytes and in the microglia.

55 t little is known about the heterogeneity of astrocytes and its regulation.

56 eview, we discuss the complementary roles of astrocytes and microglia in building the brain, includin

57 st-RT accompanied by increased colabeling of astrocytes and microglia.

58 e GABA uptake transporters (GATs) located on astrocytes and neurons.

59 ferent distributions and intensities between astrocytes and neurons.

60 revealed that FGF15 is generated by thalamic astrocytes and not retino-recipient neurons.

61 most FGF1-responsive cell type at Day 1, but astrocytes and oligodendrocyte lineage cells subsequentl

62 mple) neuronal cultures by co-culturing with astrocytes and oligodendrocyte precursor cells (complex

63 These NPCs generate both forms of macroglia: astrocytes and oligodendrocytes, and can form neurospher

64 We explore mechanisms of crosstalk between astrocytes and other cells in the CNS in the context of

65 oreover, miR-223 was found to be enriched in astrocytes and secreted via exosomes, and antipsychotics

66 ses neurotransmission through stimulation of astrocytes and the consequent A(1) receptor activation.

67 EMENT This report establishes a link between astrocytes and the development of excitatory and inhibit

68 tsynapse, but also on cue-induced changes in astrocytes and the extracellular matrix adjacent to the

69 ctive and critical for induction of reactive astrocytes and their ability to produce astrocyte-derive

70 phages linked to subacute infarcts, reactive astrocytes, and damaged blood vessels in multi-infarct d

71 nd nonneuronal (oligodendrocytes, microglia, astrocytes, and endothelial) cell types.

72 interleukin-1beta expression, activation of astrocytes, and microglia.

73 rane reporter-transduced D1- and D2-MSNs and astrocytes, and MMP-2,9 gelatinase activity adjacent to

74 matory conditions, EVs released by activated astrocytes appear to mediate or exacerbate the pathologi

75 These disease-associated astrocytes appeared at early disease stages and increase

76 eactive astrogliosis, and mislocalization of astrocyte aquaporin-4 (AQP4).

77 Astrocytes are a large and diverse population of morphol

78 earch adds to the accumulating evidence that astrocytes are active and integral players in synaptic c

79 There is evidence that astrocytes are acutely sensitive to decreases in cerebra

80 Astrocytes are an integral component of the neurovascula

81 art methods also in challenging images where astrocytes are clustered together.

82 Astrocytes are emerging as critical regulators of striat

83 The data obtained in this study suggest that astrocytes are integral components of the brainstem mech

84 We conclude that parenchymal astrocytes are latent neural stem cells and that targete

85 Overall, our data show that astrocytes are malleable, using context-specific respons

86 Astrocytes are neural parenchymal cells that ubiquitousl

87 We next found that astrocytes are neuroprotective to seeded aggregation wit

88 HNSPCs that differentiate into astrocytes are of interest for specific neurological dis

89 indings indicate that excitatory neurons and astrocytes are organized into distinct lineage-associate

90 Astrocytes are the most abundant cell type in the centra

91 Astrocytes are thought to play a pivotal role in couplin

92 CD49f(+) hiPSC-astrocytes are thus a valuable resource for investigatin

93 New methods for investigating human astrocytes are urgently needed, given their critical rol

94 s H(2)O(2) from severe but not mild reactive astrocytes as a key determinant of neurodegeneration in

95 ization, and function of AQP4, using primary astrocytes as a model system.

96 ed the mechanosensory signaling in brainstem astrocytes, as these cells reside alongside the cardiova

97 al that PDK2 ablation or inhibition in mouse astrocytes attenuates diabetes-induced hypothalamic infl

98 anners, and upregulated the proliferation of astrocytes based on increased (3)H-thymidine update.

99 restricted and active populations of HIV(+) astrocytes based on the viral promoter activity.

100 In contrast to neurons, astrocytes become less synchronized during non-rapid eye

101 Astrocyte-biased cells were successfully enriched from h

102 roperties for label-free enrichment of human astrocyte-biased cells.

103 Astrocyte-biased hNSPCs differ from other cell types in

104 Enriched astrocyte-biased human cells enable future experiments t

105 pression of DISC1 in astrocytes could impair astrocyte bioenergetics, leading to abnormalities in syn

106 al abnormalities that could be attributed to astrocyte bioenergetics.

107 t harboring the HIV genome profoundly alters astrocyte biology and that strategies that keep the viru

108 d to systematically document and interrogate astrocyte biology in vivo.

109 harboring the HIV genome profoundly altered astrocyte biology, resulting in a proinflammatory phenot

110 nteractions with brain endothelial cells and astrocytes, blood-brain barrier extravasation, angiogene

111 e intermingling of cells at the Schwann cell-astrocyte boundary, enabling growth of neurites over the

112 und that idebenone stimulated respiration by astrocytes but reduced the respiratory capacity of neuro

113 y combining two-photon microscopy to monitor astrocyte calcium and electrocorticogram to record neuro

114 Cortical astrocyte calcium signaling also altered the acute stimu

115 reactive astrocytes, where the reactivity of astrocytes can be manipulated as mild (GiDm) or severe (

116 The arborizations of the astrocytes can extend across neuronal functional domains

117 , we describe an immortalized mouse neuronal astrocyte cell line (C8D1A) that can be infected with mu

118 , 9 studies did not find any effect of BD on astrocyte cells, whereas 8 studies found a decrease and

119 d rodents provide new insight into microglia-astrocyte communication in homeostasis and disease.

120 t govern astrocyte-synapse adhesions and how astrocyte contacts control synapse formation and functio

121 Astrocytes contribute to the pathogenesis of multiple sc

122 Astrocytes control multiple processes in the nervous sys

123 indicate that altered expression of DISC1 in astrocytes could impair astrocyte bioenergetics, leading

124 aggregation and toxicity compared with their astrocyte counterparts.

125 dditionally, treatment with D-serine reduces astrocyte counts in the MEA, alters their reactive statu

126 ) and interleukin-6 [IL-6]) and astrogliosis/astrocyte damage (glial fibrillary acidic protein [GFAP]

127 d neurons were enlarged and both neurons and astrocytes demonstrated increased S6 phosphorylation.

128 However, the precise role of astrocyte-derived E2 in the injured brain remains unclea

129 Transcriptome analysis further revealed that astrocyte-derived E2 was critical for the induction of t

130 estigated by quantifying Cproteins in plasma astrocyte-derived exosomes (ADEs) of subjects with sport

131 ATF6 then induces mesencephalic astrocyte-derived neurotrophic factor (MANF), an ER-resi

132 tive astrocytes and their ability to produce astrocyte-derived neurotrophic factors, BDNF and IGF-1,

133 ole for the cytolytic complement proteins in astrocyte destruction in NMO is well established, little

134 humanized glial chimeric mice by engrafting astrocytes differentiated from human-induced pluripotent

135 Astrocytes differentiated from patient-derived neuronal

136 results suggested that n-3 PUFAs facilitate astrocyte differentiation, and may mimic effects of some

137 During astrocyte differentiation, we found that n-3 PUFAs incre

138 AT3 O-GlcNAc at Threonine 717 as a driver of astrocyte differentiation.

139 derstand the putative regional properties of astrocyte DISC1, we assessed whether knockdown of Disc1

140 Although not electrically excitable, astrocytes display a complex repertoire of intracellular

141 pha2-Na/K ATPase is conditionally deleted in astrocytes display episodic paralysis.

142 artments containing astrocytes; in contrast, astrocytes do not migrate into neuronal domains signifyi

143 ny-stimulating factor (GM-CSF) signalling in astrocytes drives the expression of MAFG and MAT2alpha a

144 xpression of the membrane-bound ephrin-B1 in astrocytes during postnatal day (P) 14-28 period would a

145 lly, targeting this signaling exclusively in astrocytes during prion disease is alone sufficient to p

146 Astrocyte dysfunctions are also linked to synapse pathol

147 ein normally expressed in perivascular brain astrocyte end feet that is essential for neurovascular d

148 behavior along vessels corresponded to when astrocyte endfeet more fully ensheath vessels.

149 l ages associate with vascular areas void of astrocyte endfeet, and the developmental shift in microg

150 cellular and functional level and disrupted astrocyte-endothelial interactions in both animal models

151 Moreover, there is emerging evidence that astrocytes exhibit regional heterogeneity, and the mecha

152 seq demonstrated that even in a healthy CNS, astrocytes express TAM phagocytic receptors, which were

153 myotrophic lateral sclerosis (ALS), in which astrocytes expressing mutant superoxide dismutase-1 (mut

154 Uptake of vesicles into astrocytes follows a more classical pathway involving dy

155 harmacologic depletion of fibrinogen reduced astrocyte formation within the SVZ after cortical injury

156 of 5hmC that is found in neurons but not in astrocytes from 3xTg mice (an AD mouse model).

157 gic neurons, oligodendrocytes, and microglia/astrocytes) from three different brain regions (anterior

158 a valuable resource for investigating human astrocyte function and dysfunction in health and disease

159 .g., shock and kill) would be detrimental to astrocyte function and possibly augment their contributi

160 Disruptions in astrocyte function following loss of NFIA are most prono

161 d with respect to the activation of striatal astrocyte G protein-coupled receptor (GPCR) signaling.

162 ic delivery of energy substrates by reducing astrocyte gap junction coupling with dominant negative c

163 nd measured how metabolites mobilize through astrocyte gap junctions composed of connexin 43 (Cx43).

164 By performing astrocyte gene expression analyses following 14 experime

165 How astrocytes grow and integrate into neural circuits remai

166 lyses to compare gene expression patterns of astrocyte harboring active versus restricted long termin

167 uited for such investigations, but bona fide astrocytes have not been described in this system.

168 l-mediated release of signaling molecules by astrocytes having an excitatory action on the CNS sympat

169 , glycogen-derived bioenergetic resources in astrocytes help promote tissue survival in response to f

170 ed rapid progress in the characterization of astrocyte heterogeneity and its control by astrocyte int

171 yme (BACE1), APP, and Abeta in human primary astrocytes (HPAs) exposed to Tat.

172 ditionally reducing intracellular calcium in astrocytes impairs the homeostatic response to sleep dep

173 The ventral astrocyte in particular, whose territory can extend well

174 ody of evidence supporting an active role of astrocytes in brain information processing.SIGNIFICANCE

175 function are needed to evaluate the role of astrocytes in brain physiology and dysfunction.

176 ticle, we provide an overview of the role of astrocytes in CNS inflammation, highlighting recent disc

177 Here we modeled human interlaminar astrocytes in humanized glial chimeric mice by engraftin

178 hese findings in light of emerging roles for astrocytes in immune cell crosstalk.

179 We suggest that including astrocytes in mechanistic, theoretical, and computationa

180 re studies and will help unravel the role of astrocytes in PML pathogenesis.IMPORTANCE Animal models

181 regardless of diagnosis and was localised to astrocytes in some brains.

182 consequences, we chemogenetically activated astrocytes in the DMS using GFAP promoter-driven express

183 gs demonstrate a crucial role for AANAT1 and astrocytes in the regulation of monoamine bioavailabilit

184 unction, far less is known about the role of astrocytes in this brain area.

185 Furthermore, melanopsin-activated astrocytes in wild-type mice enhanced the firing rate of

186 neurons migrate into compartments containing astrocytes; in contrast, astrocytes do not migrate into

187 As astrocytes initiated neurogenesis, they became transcrip

188 ttle is known regarding the initial phase of astrocyte injury.

189 rgely unknown how GABAergic interneurons and astrocytes interact and contribute to stable performance

190 s in synaptic communication, and that neuron-astrocyte interactions are key cellular processes involv

191 Microglia-astrocyte interactions represent a delicate balance affe

192 f astrocyte heterogeneity and its control by astrocyte interactions with other cells in the central n

193 ediate negative effects of altered microglia-astrocyte interactions.

194 Strikingly, cultured mouse astrocytes isolated from the parafacial respiratory grou

195 Furthermore, direct restoration of the astrocyte lactate supply alone rescued stress-impaired s

196 Astrocyte layer features, established in the early postn

197 chanistically, LRP4 promotes Abeta uptake by astrocytes likely by interacting with ApoE.

198 We find that NRCAM is expressed in cortical astrocytes, localizes to perisynaptic contacts and is re

199 lls were identified as a subset of activated astrocytes located predominately in the white matter of

200 We report that cultured mouse astrocytes maintain mitochondrial pyruvate in the low mi

201 Similarly, 17 out of 51 studies evaluating astrocytes markers, 9 studies did not find any effect of

202 STATEMENT There is evidence suggesting that astrocytes may function as intracranial baroreceptors th

203 Astrocytes may function as mediators of the impact of no

204 Therefore, astrocytes mediate the dopamine- and amphetamine-induced

205 ptor type 5 (mGluR5) signaling and that this astrocyte-mediated response is necessary for A1R-mediate

206 ish that silent synapses are generated by an astrocyte-mediated synaptogenic mechanism in response to

207 Many astrocyte microdomain Ca(2+) transients are spatio-tempo

208 opose that local ROS production can activate astrocyte microdomain Ca(2+) transients through TrpML, a

209 ssed in multiple brain cell types, including astrocytes, microglia, and vascular mural cells (VMCs).

210 iochemical analysis using markers of myelin, astrocytes, microglia, neurons, globoid cells, and immun

211 microvascular endothelial cells, pericytes, astrocytes, microglia, oligodendrocytes and neurons to m

212 ein is present in neuronal and non-neuronal (astrocytes, microglia, vascular endothelial cells) cells

213 supplementation was associated with reduced astrocyte/microglia activation and downregulation of the

214 One process by which astrocytes modulate homeostasis is the release of functi

215 to the striatum, we discovered that striatal astrocytes mount context-specific molecular responses at

216 the shuttling of glucose and lactate through astrocyte networks, creating a barrier for neuronal acce

217 lls, but hardly detectable in non-neoplastic astrocytes, neural stem cells or normal brain.

218 and identify a proteome that is enriched at astrocyte-neuron junctions in vivo, which includes neuro

219 We investigated astrocyte-neuronal network interactions in vivo by combi

220 of monSTIM1 in either excitatory neurons or astrocytes of mice brain is able to induce Ca(2+)-depend

221 nockdown of Disc1 (Disc1-KD) in mature mouse astrocytes of the prefrontal cortex (PFC) or the hippoca

222 nical stimulation-evoked Ca(2+) responses in astrocytes of the rat brainstem were blocked by (1) anta

223 and bright labeling of thousands of neurons, astrocytes, or microglia in each brain, revealing their

224 Astrocytes orchestrate neural development by powerfully

225 Through data mining, we also identified astrocyte pathways in Huntington's disease (HD) that wer

226 Astrocytes perform classical innate immune functions, wh

227 here were composed of six brain cell types: Astrocytes, pericytes, endothelial cells, microglia cell

228 ignaling pathway, as well as the A2 reactive astrocyte phenotype after ischemia.

229 The heterogeneity of astrocyte populations underlies the diversity in their f

230 Conditional deletion of VMAT2 in astrocytes postnatally produces loss of PFC DA homeostas

231 CHI3L1 is expressed by a subset of activated astrocytes predominately located in white matter.

232 a suppressed TLR2/4-mediated upregulation of astrocyte proliferation, supporting an autocrine/paracri

233 an autocrine/paracrine role of TNF-alpha on astrocyte proliferation.

234 Immunoblotting results revealed that the astrocytes propagated 22L prions well over all six passa

235 AD genetic risk factors and in microglia and astrocyte protein markers associated with an anti-inflam

236 Astrocyte reactivity associated with brain metastases im

237 Thus, the astrocyte reactivity state resulting from UPR over-activ

238 reverse the diminishment in neuroprotective astrocyte reactivity, and attenuate neuronal damage in F

239 1066 to determine the role of STAT3-mediated astrocyte reactivity, specifically, in brain metastasis.

240 The activation of DMS astrocytes reduced the frequency of spontaneous excitato

241 The conventional view is that neurons or astrocytes release vasodilatory factors that act directl

242 work analysis infers the interaction between astrocyte-released amyloid precursor protein (APP) and d

243 development, and this is mediated in part by astrocyte-released thrombospondins (TSPs) and activation

244 ired to maintain the protective functions of astrocytes relevant to the development of motor deficits

245 mechanisms by which Abeta modulates Cx43 in astrocytes remain elusive.

246 Notably, CD49f(+) hiPSC-astrocytes respond to inflammatory stimuli, acquiring an

247 In addition to homeostatic roles, astrocytes respond to neurotransmitters with calcium tra

248 Therefore, cortical astrocytes respond to sensory inputs and regulate sensor

249 s in identifying that the majority of HIV(+) astrocytes restrict HIV expression and were resistant to

250 upled conversion of NSCs into differentiated astrocytes restrict the stem cell pool with age.

251 Here, we report that the majority of human astrocytes restricted R/G-HIV-1 gene expression early du

252 of Cx43 endocytosis in Abeta(25-35)-exposed astrocytes resulted in their retention at the cell surfa

253 roteomic analysis of EVs from young and aged astrocytes revealed peptide repertoires unique to each a

254 may present a promising strategy to promote astrocyte-secreted prosurvival signals.

255 Astrocyte shape varies more than previously reported; ma

256 th accompanying improvement of HD-associated astrocyte signaling pathways, including those related to

257 f ADEVs in the blood is useful for detecting astrocyte-specific biomarkers in different neurological

258 anced excitation of CA1 pyramidal neurons in astrocyte-specific ephrin-B1 KO male mice, which coincid

259 Furthermore, astrocyte-specific Trpa1 disruption in a mouse brainstem

260 is in the above experiments, indicating that astrocytes stand by in case of microglial impairment.

261 In cultured primary astrocytes stimulated with lipopolysaccharide, condition

262 Furthermore, selective striatal astrocyte stimulation of the G(i)-GPCR pathway in vivo c

263 ammation, highlighting recent discoveries on astrocyte subsets and the mechanisms that control them.

264 It is now clear that multiple astrocyte subsets or activation states (plastic phenotyp

265 Our findings are evidence for specialized astrocyte subtypes between and within brain regions.

266 identifies five transcriptomically distinct astrocyte subtypes in adult mouse cortex and hippocampus

267 owever, the molecular mechanisms that govern astrocyte-synapse adhesions and how astrocyte contacts c

268 ed scheme of neuropil division among the six astrocytes that populate each hemi-segment is not possib

269 ncreases calcium (Ca(2+)) levels in striatal astrocytes through activation of metabotropic glutamate

270 eveal hypoxia-monitoring function exerted by astrocytes through an O(2)-regulated protein trafficking

271 ly, they observe preferential sensitivity of astrocytes to altered doses of imprinted loci.

272 -step conversion of isolated mouse and human astrocytes to functional neurons by depleting the RNA-bi

273 ing the contribution of SVZ-derived reactive astrocytes to lesion scar formation.

274 t stem cell (iPSC)-derived motor neurons and astrocytes to model early cell type-specific features of

275 phenotype is also accomplished by converting astrocytes to neurons using antisense oligonucleotides t

276 ivity limits the ability of neurons, but not astrocytes, to use idebenone as an electron donor to sup

277 However, it has been shown that astrocytes undergo morphologic changes in response to br

278 After stroke, however, striatal astrocytes undergo neurogenesis in mice, triggered by de

279 Astrocytes use multiple modes of communication to intera

280 tically induced cellular activity in the DMS astrocytes using calcium imaging.

281 ion of arborization territory for identified astrocytes was great enough that a standardized scheme o

282 Subsequently, the STAT3 pathway in astrocytes was inhibited with WP1066 to determine the ro

283 antitative analysis of fluorescent images of astrocytes, we introduce a new automated image processin

284 that extracellular vesicles (EVs) from young astrocyte were sufficient to convey support for oligoden

285 Newborn astrocytes were derived from WT, Tnfalpha(-/-), Il1alpha

286 Newborn astrocytes were found all along the dorso-ventral axis,

287 However, actively infected astrocytes were inducible, leading to increased expressi

288 Also, mature oligodendrocytes and reactive astrocytes were only detected in complex cultures upon t

289 We found that neurons and astrocytes were sparsely infected, but choroid plexus ep

290 , a newly developed animal model of reactive astrocytes, where the reactivity of astrocytes can be ma

291 duce the expression of IFITM3 in neurons and astrocytes, which binds to gamma-secretase and upregulat

292 of these changes on distinct targets such as astrocytes, which exhibit norepinephrine-dependent Ca(2+

293 ion acutely increases Ca(2+) events in NAcSh astrocytes, while decreasing astrocytic Ca(2+) blocks co

294 were restored by optogenetic stimulation of astrocytes with melanopsin.

295 We challenged astrocytes with three mouse-adapted prion strains (22L,

296 city of reliable tools with which to explore astrocytes within the adult vertebrate CNS in vivo.

297 he nature of the recently discovered role of astrocytes within the SCN network.

298 First, we found that astrocytes within the TME (TuAstrocytes) were trans-diff

299 ular sensory modalities, suggesting that the astrocyte would respond to neuronal activity in any of t

300 Higher glutamine export from astrocytes would increase extracellular D-serine, provid