ライフサイエンスコーパス: neuronal

1 h astrocyte networks, creating a barrier for neuronal access to an astrocytic energy reservoir in the

2 tress-induced helplessness and increased NAc neuronal activation at night.

3 Microglia respond to neuronal activation by suppressing neuronal activity, an

4 inflammation and activation of GABAergic and neuronal activation in mice regardless of cirrhosis comp

5 found that sevoflurane caused an increase in neuronal activation in primary somatosensory cortex of y

6 sh the role of the apparently avian-specific neuronal activation in the VMH of zebra finch parents.

7 e a circuit framework through which dopamine neuronal activation shifts from reward delivery to cue o

8 ries at the single-cell level in response to neuronal activation.

9 al bioenergetics is dynamically coupled with neuronal activities, which are altered by hypoxia-induce

10 However, hyperactive shifts in neuronal activity (kainate status epilepticus and CaMKII

11 er rates in cultured brain cells under basal neuronal activity and found that protein turnover is inf

12 normally positive effects of estrogen on SF1 neuronal activity and glucose balance control to paradox

13 d mice exhibited normal synaptic density and neuronal activity as measured by density of VGLUT2(+) pu

14 naptic loss, motor neuron death, and reduced neuronal activity in spinal sensory-motor circuits.

15 tations, such as synaptic scaling, stabilize neuronal activity in the face of perturbations.

16 imaging, we detected evoked and spontaneous neuronal activity in the mouse visual cortex, with fluor

17 To test these hypotheses, we recorded neuronal activity in the orbitofrontal and anterior cing

18 te that modulation of chronic stress-induced neuronal activity limits microglia-mediated neuronal rem

19 hese subcortical structures, we recorded CDh neuronal activity of macaque monkeys before and during u

20 However, how neuronal activity regulates synaptic vesicle recycling i

21 study reveals that 4-AP-induced increase of neuronal activity restores synaptic connectivity and fun

22 GABBR2 inhibits neuronal activity through G protein-coupled second-messe

23 Intrinsic neuronal activity was assessed using resting-state blood

24 proposed modulatory effect of irradiation on neuronal activity without causing cellular death require

25 espond to neuronal activation by suppressing neuronal activity, and ablation of microglia amplifies a

26 The absence of PlexA1, neuronal activity, Bax and Bak, or caspase-9 leads to th

27 vels, it modulates synaptic transmission and neuronal activity, but at much higher levels mediates ne

28 Our work reveals a neuronal activity-regulated role for microglia in modify

29 indicate that NKCC1b is required to maintain neuronal activity-related solute homeostasis at the axon

30 ion, and therefore possibly able to modulate neuronal activity.

31 nal enhancers that appear to be modulated by neuronal activity.

32 F4G1 function and chemogenetic inhibition of neuronal activity.

33 invisible to standard methods of monitoring neuronal activity.

34 Neuronal alpha-synuclein activates microglia, which in t

35 been shown to induce the production of toxic neuronal amyloid protein and also enhance neurotoxicity.

36 icing of the Bak1 microexon is essential for neuronal and animal survival.

37 The roles that neuronal and glial progenitors and mature cells play in

38 s work identifies a simultaneous activity of neuronal and lymphoid CB(2)that protects against spontan

39 Neuronal and muscle cells of the 2 glands in particular

40 latently infected with KSHV express several neuronal and NE genes.

41 nide treatment was associated with increased neuronal and network excitability after injury, includin

42 of the mechanism(s) of action of tDCS at the neuronal and systems levels, the establishment of the co

43 at are significantly enriched in osteoblast, neuronal, and mitochondrial functions.

44 applies to simplified models of ecological, neuronal, and traffic networks.

45 ated that EBOV can induce satellite cell and neuronal apoptosis and microglial activation in infected

46 depletion of BAK1 proteins uniquely repress neuronal apoptosis.

47 Whether the NR controls neuronal assemblies, a hallmark of information exchange

48 her, our results identify an mTOR-responsive neuronal autophagy pathway, wherein RILP integrates the

49 tle is known about which PATs are present in neuronal axons, although long-distance trafficking of pa

50 particles and sorting of these virions into neuronal axons.

51 formation transfer could help illuminate the neuronal basis of the conscious state.

52 However, mice lacking both neuronal beta1 and beta4 spectrin show exacerbated nervo

53 rowth factor (NGF) regulates many aspects of neuronal biology by retrogradely propagating signals alo

54 the loss of Ascl1 yielded a similar delay in neuronal birth, suggesting that Ascl1 cannot rescue the

55 ic reduction in nascent protein synthesis in neuronal cell bodies and dendrites.

56 s by which mutant huntingtin (mHTT) leads to neuronal cell death in Huntington's disease (HD) are not

57 sible for unchecked inflammation that causes neuronal cell death, systemic stress, and lethal immunod

58 The Mfsd7c-KO brain exhibited hypoxia and neuronal cell death.

59 We have developed a new human neuronal cell model of HD, using neural stem cells (ReNc

60 f this study was to morphologically identify neuronal cell types of the CX in the honeybee Apis melli

61 In neuronal cell-based models of mTOR hyperactivity, 7 corr

62 that microglial cells constitute ~7% of non-neuronal cells in different brain structures as well as

63 Interestingly, PRV infection of neuronal cells leads not only to a nonspecific depletion

64 g to these motifs in vivo, we analysed human neuronal cells using ChIP-seq and ATAC-seq technologies.

65 ligands to target the construct to specific neuronal cells utilizing only native components of the n

66 is, genotoxicity, and ultimately necrosis of neuronal cells.

67 lpha) cause dominantly inherited adult-onset neuronal ceroid lipofuscinosis (ANCL), a rapidly progres

68 Thus, modification of neuronal cholesterol trafficking and of lipid rafts by N

69 ent and presynaptic function in a developing neuronal circuit in its native environment is unclear.

70 Here, we identify a neuronal circuit in the nematode Caenorhabditis elegans

71 Here we study the neuronal circuitry that allows larval Drosophila melanog

72 veals important regulatory components of the neuronal circuitry that underlies female aggressive soci

73 ly contribute to developmental refinement of neuronal circuits and associated behaviors.

74 In this review, I discuss newly discovered neuronal circuits in primates that represent uncertainty

75 Dysfunction of neuronal circuits is an important determinant of neurode

76 aine to the dura prevented activation of all neuronal classes but not the initiation or maintenance o

77 Here we recorded spiking activity in 435 neuronal clusters evoked by acoustic stimuli in the peri

78 n-wide functional imaging, we identify three neuronal clusters in the anterior hindbrain that are wel

79 Action potentials are a key component of neuronal communication and their precise timing is criti

80 Decreased neuronal complexity three months after peripheral immune

81 r a stimulus has disappeared is considered a neuronal correlate of working memory.

82 activity of prefrontal neurons constitutes a neuronal correlate of working memory.

83 t the existence of gonadal steroid-sensitive neuronal crosstalk remains undefined.

84 d evolution of neuronal culture networks and neuronal culture cluster networks by estimating the impo

85 e investigate the structure and evolution of neuronal culture networks and neuronal culture cluster n

86 Here, we investigated, in rat hippocampal neuronal cultures derived from embryos of unknown sex, w

87 d the uptake of D-serine in synaptosomes and neuronal cultures of mice of either sex, while increasin

88 ealed a disease duration-related increase in neuronal cytoplasmic inclusions in the dentate gyrus and

89 Semi-quantitative analysis of neuronal cytoplasmic inclusions in the hippocampus and p

90 macrostructural change characterises global neuronal damage, investigating microstructural alteratio

91 oid cells 2 (sTREM2), as well as a marker of neuronal damage, neurofilament light chain (NfL), using

92 ) on Cx43 expression and function leading to neuronal damage, underlying mechanisms by which Abeta mo

93 efficient migration of microglia to sites of neuronal damage.

94 This may be attributed to axon degeneration/neuronal death and sustained neuroinflammation.

95 Suppression of early-stage neuronal death by AAV-YAPdeltaC reduces the later-stage

96 e that is expressed by Muller glia following neuronal death, is required for Muller glia to progress

97 ortem and HD mouse striata, correlating with neuronal death.

98 that D(1)R-induced cell death signaling and neuronal degeneration, are mitigated by an H(3)R antagon

99 Ganglionitis, characterized by neuronal degeneration, necrosis, and mononuclear leukocy

100 onal myelination and metabolic adaptation to neuronal degeneration.

101 modulate BDNF-dependent gene expression and neuronal dendritic growth mediated by the CREB transcrip

102 nger photoperiods are associated with higher neuronal density and decreased depressive-like behaviour

103 ize neurons and is associated with increased neuronal density.

104 e is tightly regulated and central to normal neuronal development and survival.

105 een distinct RBPs and alternative 5' UTRs in neuronal development and underscore the risk of post-tra

106 scam2 is a cell surface protein required for neuronal development in Drosophila; it can promote neura

107 ent, however, if Gli3 plays a role in GnRH-1 neuronal development is unclear.

108 h the dynamic AGO2-RNA association for human neuronal development.

109 Zinc and copper are involved in neuronal differentiation and synaptic plasticity but the

110 represses the expression of region-specific neuronal differentiation genes, thereby controlling the

111 nly observed in individuals with CHARGE, and neuronal differentiation is reduced in CHARGE patient-de

112 em to study changes driving and accompanying neuronal differentiation.

113 nscriptional regulatory networks controlling neuronal differentiation.

114 d interventions can guide them through their neuronal differentiation.

115 es an intrinsic temporal program to increase neuronal diversity.

116 GNIFICANCE STATEMENT We examine how coherent neuronal dynamics arise from optogenetic stimulation in

117 We studied intracortical neuronal dynamics during transitions of loss of consciou

118 a general mechanism for generating coherent neuronal dynamics without the need for an oscillatory ge

119 es of LB formation and their contribution to neuronal dysfunction and degeneration.

120 Disruption of autophagy is associated with neuronal dysfunction and neurodegeneration.

121 istic role for both Abeta and tau in driving neuronal dysfunction seen in AD.

122 exposed phosphatidylserine (PS) represents a neuronal "eat-me" signal involved in microglial-mediated

123 cent tracking of nanoparticles together with neuronal electrical activity recording at the submillise

124 forms, but recently, photonic techniques for neuronal emulation have emerged given their unique prope

125 Dynamin 1 is a neuronal endocytic protein that participates in vesicle

126 apture the proteomic microenvironment of the neuronal endolysosomal network by knocking in (KI) an en

127 formation of hundreds of cell-type-specific neuronal enhancers that appear to be modulated by neuron

128 to its innervation of a particular region or neuronal ensemble in the NAcSh.

129 s are updated through dynamic recruitment of neuronal ensembles on the basis of excitability and func

130 dentate gyrus contain functionally distinct neuronal ensembles, genetically defined by the Fos- or N

131 course have greater hemispheric asymmetry in neuronal epigenomes than those with a short disease cour

132 NALCN-mediated currents regulate neuronal excitability linked to respiration, locomotion

133 estigated changes in synaptic plasticity and neuronal excitability of BLA neurons in vitro in the lef

134 now find a role for the APP family in neuronal excitability, synaptic plasticity, and memory i

135 ase the GlyR-associated currents and enhance neuronal excitability.

136 lation that uses mechanical energy to affect neuronal excitability.

137 arkers (alpha-synuclein and syntenin-1) from neuronal exosomes.

138 Our data support a role for altered neuronal expression and activity of KPNA7 in a rare type

139 In hermaphrodites, neuronal expression is initially highly restricted and t

140 It also suggests that the neuronal fate selector function of GATAs is modulated by

141 be due, at least in part, to suppression of neuronal FGF2 signaling, which is a known suppressor of

142 evealed a total of 33 brain neuropils and 30 neuronal fiber tracts including six distinct tracts betw

143 In cortex that is recruited to the seizure, neuronal firing rates increase and waveforms become long

144 Sun et al. discover that neuronal firing rates of hippocampal place cells code fo

145 ot alter the running speed-dependent gain in neuronal firing rates.

146 Using a novel method to track neuronal firing, we analyzed microelectrode array record

147 for counteracting MOR-mediated inhibition of neuronal firing.

148 ses (NDDs) comprise conditions with impaired neuronal function and loss and may be associated with a

149 conclusion, electrophysiological analysis of neuronal function in rodent retinal explants is useful f

150 n examines the extended role of autophagy in neuronal function, plasticity, and memory.

151 g effects of background genetic variation on neuronal function, the regulatory effects of MORs on syn

152 aling in neurons and plays critical roles in neuronal function.

153 nal, and other membranes highly important in neuronal function.

154 stabilizes ECs, and are important for proper neuronal function.

155 izations of the astrocytes can extend across neuronal functional domains.

156 Neuronal functions of GSK3 are typically attributed to o

157 Thus, the neuronal functions of tra-1 are not limited to hermaphro

158 P sets with distinct molecular processes and neuronal functions.

159 gliotransmitters that regulate synaptic and neuronal functions.

160 epigenetic control of enhancers that modify neuronal functions.

161 In a separate sample, we investigated the neuronal gene expression associated with CUD by using RN

162 tered and glial-enriched miRNA that controls neuronal gene expression is regulated by antipsychotics.

163 esults highlight the unique role of eRNAs in neuronal gene regulation and demonstrate that eRNAs can

164 ction of NONO in regulation of TET1-targeted neuronal genes, offering new functional and mechanistic

165 be the equilibrium ensemble of structures of neuronal GIRK2 as a function of the C8-PIP(2) concentrat

166 We identified and profiled both neuronal (glutamatergic and GABAergic) and nonneuronal (

167 d protein that was initially discovered as a neuronal guidance cue.

168 P/Abeta, but not tau, in the emergence of EC neuronal hyperactivity and impaired theta rhythmicity.

169 Here we show that chronic neuronal hyperexcitability, induced by M-type potassium

170 roadly in the C. elegans nervous system, and neuronal IL-17-MALT-1 signaling regulates multiple pheno

171 We find that neuronal IL-33 instructs microglial engulfment of the ex

172 degeneration (~45%) exhibit TDP-43 positive neuronal inclusions, suggesting a role for this protein

173 n of fusogens in the nervous system disrupts neuronal individuality, which, in turn, leads to a chang

174 h the administration of GSK2656157 abrogated neuronal induction of IFNbeta, switched microglial polar

175 r's disease (AD), its reflection on regional neuronal injury in the context of amyloid pathology rema

176 activity, but at much higher levels mediates neuronal injury through oxidative stress.

177 ion (n = 115, 39.4%) mainly for treatment of neuronal injury, and improved immune and inflammatory mo

178 l fluid microRNAs that control inflammation, neuronal injury, autophagy and vesicular transport genes

179 ity and restored pancreatic islet cell mass, neuronal innervation and microbiome composition.

180 s resulted in substantial alterations in the neuronal input-output function.

181 , including unique phenomena associated with neuronal interactions.

182 material fibres allows nitric oxide-mediated neuronal interrogation in vivo.

183 Assessing neuronal involvement in ictal events is pivotal to under

184 tered APP processing could contribute to the neuronal iron elevation and oxidative burden that featur

185 age-activated potassium current generated by neuronal Kv7 channels.

186 Mutations that truncate the C terminus of neuronal Kv7/KCNQ channels are linked to a spectrum of s

187 rgic neuronal loss and the presence of intra-neuronal Lewy body (LB) inclusions with aggregated alpha

188 lism in neurons and indicates that directing neuronal lipid synthesis away from TG synthesis and towa

189 isease (PD) is characterized by dopaminergic neuronal loss and the presence of intra-neuronal Lewy bo

190 Therefore, neuronal loss rather than inflammation was critical for

191 ching as evaluated by immunocytochemistry of neuronal markers.

192 uggests that primary cilia are important for neuronal maturation and function in cells of the SC and

193 ion genes, thereby controlling the timing of neuronal maturation.

194 al development, including axon outgrowth and neuronal maturation.

195 Moreover, we elucidated the neuronal mechanism of RLN3/RXFP3 signaling in PVN in mal

196 We benchmark available neuronal media and show that BPI enhances fluorescence s

197 rm lipid-stabilized pores that might disrupt neuronal membranes and ion homeostasis.

198 This neuronal memory mechanism does not rely on persistent ac

199 with nontransgenic wild-type mice, mice with neuronal Mfn2 overexpression also exhibited alleviated b

200 iants and reveal how glioblastoma alters the neuronal microenvironment.

201 r material, and knockdown of Cep85l causes a neuronal migration defect in mice.

202 n, and this is required for proper GABAergic neuronal migration into the substantia nigra pars reticu

203 me activity is important for neuritogenesis, neuronal migration, and neurodevelopment.

204 nt in the nasal mucosa and subsequent GnRH-1 neuronal migration.

205 d engineering are expanding the use of human neuronal models in vitro.

206 es with maintaining HSV-1 latency in certain neuronal models of latency.

207 tive dendritic measurements, descriptions of neuronal morphologies were still possible.

208 Diverse sensory neurons exhibit distinct neuronal morphologies with a variety of axon terminal ar

209 ing that preclinical/prodromal YAP-dependent neuronal necrosis represents a target for AD therapeutic

210 The spontaneous neuronal network activities were monitored with an integ

211 yte calcium and electrocorticogram to record neuronal network activity in the somatosensory cortex du

212 o sensory inputs and regulate sensory-evoked neuronal network activity maximizing its dynamic range.

213 We investigated astrocyte-neuronal network interactions in vivo by combining two-p

214 d VGLUT3 is key for the function of specific neuronal networks involved in motor coordination, emotio

215 Multielectrode recordings of neuronal networks revealed hyperexcitability and altered

216 To investigate the role of neuronal NF-kappaB activity in pathogenesis of amyotroph

217 ects of energy balance (e.g. oxytocin (OXT), neuronal nitric oxide synthase 1 (NOS1), melanocortin 4-

218 accompanied by biomarker evidence of ongoing neuronal or astrocytic injury/activation or induction of

219 Previous research has suggested that neuronal oscillations at different frequency bands are a

220 rated along the terminal tree, computing the neuronal output, which propagates toward the CNS, thus s

221 the mTOR pathway activity and the resulting neuronal overgrowth phenotype.

222 No effect on neuronal pathfinding was detected.

223 KV and host interactions inducing ocular and neuronal pathogenesis are unclear.

224 ircadian rhythms, although the molecular and neuronal pathways implicated have not been fully elucida

225 s of tcf12 in zebrafish larvae perturbs GnRH neuronal patterning with concomitant attenuation of the

226 Prominent among neuronal phenotypes was a decreased mitochondrial conten

227 intracellular transport, cell motility, and neuronal physiology.

228 ling genes, including S100a10 (p11), linking neuronal plasticity to the antidepressant response.

229 ological and pathological processes, such as neuronal plasticity, development, and viral invasion.

230 RUFY3 is implicated in the establishment of neuronal polarity and axon elongation.

231 GABAergic medium spiny neurons are the main neuronal population in the striatum.

232 ecent studies revealed a novel glutamatergic neuronal population in the VP [VP neurons expressing the

233 To advance the measurement of distributed neuronal population representations of targeted motor ac

234 ey regulator of a previously uncharacterized neuronal population within the PVH that impinges upon mu

235 neous neural subtypes rather than a specific neuronal population.

236 lly and in complexes: whether particular SCN neuronal populations act as pacemakers, and if so, by wh

237 nding whether these processes affect similar neuronal populations and whether they have similar effec

238 we tested the discrimination performance of neuronal populations at five levels of the auditory syst

239 trains, we performed comparative analysis of neuronal populations in A1 of adult (~ 10 weeks) C57BL/6

240 king noise decreased sound discrimination of neuronal populations in each auditory structure, but col

241 der, an area that gives rise to a variety of neuronal populations including the dorsal raphe (DR) nuc

242 and 2) What do we know about the neuronal populations involved?

243 n each auditory structure, discrimination by neuronal populations was slightly decreased when tone-vo

244 ral cortex necessary for generating expanded neuronal populations.

245 states are encoded by distinct hypothalamic neuronal populations.

246 tial using transfected HEK293T cells, rodent neuronal preparations, and behavioural and electrophysio

247 We identified neuronal Prkag3 mRNA as a mechanistic substrate for NMD

248 Hemispheric asymmetry in neuronal processes is a fundamental feature of the human

249 aller with a reduced number of proliferating neuronal progenitors while mutant ugdh zebrafish do not

250 dings demonstrate that subtle differences in neuronal projection patterns can have a significant effe

251 uroendrocrine system and mediated by sensory neuronal prolactin receptor.

252 receptor (beta(2)-AR) signaling and mediated neuronal protection through an arginase 1-polyamine axis

253 rombospondins (TSPs) and activation of their neuronal receptor, alpha2delta-1.

254 the present investigation used multichannel neuronal recording and tract tracing methods to examine

255 NAcC neuronal recordings revealed a stronger representation o

256 st their therapeutic targeting for promoting neuronal recovery.IMPORTANCE Brain injury induced by acu

257 ms members of the TGF-beta family, including neuronal regeneration-related protein (NREP) and growth

258 tes of spinal cord injury (SCI) and generate neuronal relays across lesions that can provide function

259 onal program modulates the expression of key neuronal remodeling genes, including S100a10 (p11), link

260 neuronal activity limits microglia-mediated neuronal remodeling in the medial PFC, and subsequent be

261 ttle is known about how OR antagonism shapes neuronal representations in the detection layer of the o

262 The potential for neuronal representations of external stimuli to be modif

263 Neuronal representations of spatial location and movemen

264 ity is that animals use disembodied internal neuronal representations of time to decide when to initi

265 with the application of ultrasound; (2) the neuronal response rate to ultrasound is dependent on pul

266 ics by fiber photometry, we observe that the neuronal response to conditioned context cues evolves ov

267 and delayed-visual experience) and compared neuronal responses to natural scene features in relation

268 Additionally, neuronal RNAi-mediated knockdown of Cdk8 in flies result

269 We tested this prediction by mapping neuronal selectivity(7) and photoablating(9,10) neurons

270 TRP channel complexes regulate diversity in neuronal sensitization and may provide a therapeutic tar

271 basic physiological principles that underlie neuronal signaling in the AOB remain elusive.

272 XBP-1s therefore remodels neuronal signaling to coordinately modulate intestinal p

273 ubunit complexes that play a crucial role in neuronal signaling.

274 coordinate the assembly-disassembly cycle of neuronal SNARE complexes.

275 Here, we provide estimates of neuron number, neuronal soma size, and volume of the different layers a

276 hted (downregulated) genes were enriched for neuronal, specifically interneuronal, affiliations and c

277 anding the effects of anesthesia on cortical neuronal spiking and information transfer could help ill

278 tly, clusters are permanently switched on by neuronal spiking, switched off by strong hyperpolarizati

279 nduced pluripotent stem cells (iPSC)-derived neuronal stem cell lines were generated from individuals

280 iking interneurons comprise ~1% of the total neuronal striatal population, are enriched dorsolaterall

281 hresholded voltage and its rate of change in neuronal structures subject to spatio-temporal synaptic

282 Using this approach on other neuronal subclasses should ultimately accelerate the com

283 characterization of individual somatosensory neuronal subclasses within a mixed population.

284 versification of motor neurons into distinct neuronal subsets by ensuring the maintenance of Isl1 exp

285 disorders; however, the genetically-defined neuronal subtypes and projections that govern these beha

286 r results show that neurochemically distinct neuronal subtypes in the primary auditory cortex have di

287 In mice, we identified several neuronal subtypes that stably express gene modules acros

288 r cofactors to refine the differentiation of neuronal subtypes.SIGNIFICANCE STATEMENT Predisposition

289 ulthood, despite the lack of requirement for neuronal survival.

290 r the same phenomenon occurs at conventional neuronal synapses due to the difficulties in collecting

291 o investigate the astrocytic activity-driven neuronal synaptic events and behavioral consequences, we

292 Abnormal changes of neuronal Tau protein, such as phosphorylation and aggreg

293 spective, following this arc of inquiry from neuronal to neuron-glial mechanisms by which activity an

294 t they are involved in three main processes: neuronal transmission, immuno-reactivity, and developmen

295 ata highlight an integral role for CaMKII in neuronal TRPV4-associated Ca(2+) responses, the importan

296 odel of T1D produce Abs directed against the neuronal type III intermediate filament protein peripher

297 We predict that an intermediate neuronal type should temporally integrate the output of

298 Many neuronal types occur as pairs that are similar in most r

299 Neuronal VAChT staining and airway narrowing in response

300 gnificantly improves both motor function and neuronal viability.