ライフサイエンスコーパス: neuronal

1 sal hippocampus inputs to LS showed enhanced neuronal activation (as measured by Fos expression) duri

2 Furthermore, explicit pairing of TH(VTA) neuronal activation with a forepaw stimulus of a particu

3 link normalization mechanisms to correlated neuronal activity and attention, showing that normalizat

4 However, direct measures of spontaneous neuronal activity and functional integrity of these impa

5 s) is widely used for remote manipulation of neuronal activity in freely moving animals.

6 been linked to the temporal irregularity of neuronal activity in the central nervous system.

7 tions of undernourishment, during which POMC neuronal activity is decreased.

8 ral evolution and cellular substrates of the neuronal activity patterns associated with spontaneous s

9 f specific CREB/CRTC1-dependent genes during neuronal activity remain largely unclear.

10 PET with (18)F-FDG captures neuronal activity that is in steady state at a longer ti

11 apability of a given brain area to propagate neuronal activity to other regions in a given brain stat

12 ron, Padamsey et al. (2017) demonstrate that neuronal activity triggers lysosomal fusion with the pla

13 iciently retrieves more membrane at elevated neuronal activity when ATP consumption within nerve term

14 These frequencies appear to aggregate local neuronal activity, but it is unclear how this relationsh

15 FOXP1 SUMOylation is tightly controlled by neuronal activity, in which synapse to nucleus signallin

16 ith a Drd3 agonist, which increases Drd3(LS) neuronal activity, normalizes the social dysfunctions of

17 s various physiological processes, including neuronal activity, vascular tone, inflammation, and ener

18 nderstand how gene deletions lead to altered neuronal activity, we investigated the synaptic and netw

19 eleasing factors to influence blood flow and neuronal activity.

20 e LDT, together with a decrease in LDT basal neuronal activity.

21 of 1-hydroxymidazolam consistently inhibited neuronal activity.

22 acts and enables confined recruitment of the neuronal activity.

23 d volume (CBV) as a proxy of drug effects on neuronal activity.

24 ty, whereas gain of GIRK function can reduce neuronal activity.

25 namic signals in assessing changes in evoked neuronal activity.SIGNIFICANCE STATEMENT Neurovascular c

26 multaneously activating other MAP kinases in neuronal and endocrine cells.

27 oduction of an intergenic transcript linking neuronal and immune Fpr genes.

28 ght be relevant to many aspects of disrupted neuronal and synaptic function, increased permeability t

29 in diabetes-mediating adverse effects to the neuronal and vascular components of the retina.

30 istered to neonatal animals cause widespread neuronal apoptosis and later neurocognitive impairment.

31 ice exhibit decreased neurogenesis, enhanced neuronal apoptosis, and an increased ratio of excitatory

32 a role for paracrine factors in induction of neuronal apoptosis.

33 or function, as well as with preservation of neuronal architecture.

34 ing, from a unidimensional process involving neuronal-astrocytic signaling to local blood vessels to

35 Here, we report that induction of neuronal autophagy enhances BACE1 turnover, which is sup

36 rtance of MT flexibility in N-C coupling and neuronal-branching regulation during neuronal migration.

37 s are involved in cellular responses such as neuronal bursting activity and cardiac rhythm.

38 sensitivity, to quantify the interaction of neuronal Ca(2+)-Sensor proteins with their targets opera

39 that their luciferase profiles reflect their neuronal calcium and in some cases firing profiles in wa

40 ations in phagocytic capacity and effects on neuronal calcium signaling.

41 lia (which associate almost exclusively with neuronal cell bodies) to understand glia-soma interactio

42 l day 30 Snord116p-/m+ mice the reduction in neuronal cell body size was associated with decreased ne

43 st that birth may be an important trigger of neuronal cell death and identify transient cell groups t

44 We focus on the hippocampus neuronal cell death, as well as the potential link betwe

45 Individual neuronal cell types predominantly express a single FXG t

46 activity had slower replication in mammalian neuronal cells and reduced virulence in 2-day-old mice.

47 Overexpression of functional NMDAR in non-neuronal cells results in cell death by excitotoxicity,

48 cell death in fibroblasts, cardiomyoblasts, neuronal cells, and primary cardiomyocytes.

49 tion and accumulation of protein deposits in neuronal cells.

50 ansmission of ORF7-deficient virus among the neuronal cells.

51 gous mutations in the PGRN gene present with neuronal ceroid lipofuscinosis.

52 es trafficking of a subset of these GPCRs to neuronal cilia.

53 ur understanding of the relationship between neuronal circuit function and symptoms of schizophrenia,

54 A map of a neuronal circuit in a marine worm reveals how simple net

55 ration); and within these two ends, specific neuronal circuits control the actual rhythmic pattern of

56 ory, and it is crucial for the refinement of neuronal circuits during development.

57 The discovery is that neuronal circuits operating reflexively regulate innate

58 reflect profound disruptions of activity in neuronal circuits that mediate awareness and cognition.

59 Immune cell activation stimulates neuronal circuits that regulate innate and adaptive immu

60 nt approaches have been utilized to decipher neuronal circuits, including electron microscopy (EM) an

61 nt modifications of synaptic strength within neuronal circuits.

62 nvolvement of individual neurons within each neuronal class.

63 e brain, causing persistent modifications of neuronal communication thought to provide the cellular b

64 xample of GAP/GEFs localized within multiple neuronal compartments and determine an additional 110 in

65 ide sufficient sensitivity for imaging small neuronal compartments, such as single dendritic spines i

66 participates in the establishment of precise neuronal connections during development.

67 circumstances: during development to refine neuronal connections, after injury to clear damaged neur

68 n between axons and dendrites, therefore the neuronal connectivity map not only depicts the underlyin

69 itment of MMP-2 by a previously unrecognized neuronal constituent.

70 By bioprinting neuronal constructs, one can precisely control the micro

71 eases, emphasizing the importance of precise neuronal control of effector pathways.

72 red after extended wake, yet, the underlying neuronal correlates have been difficult to identify.

73 c mice in vivo and in cell lines and primary neuronal culture derived from timed pregnant rats in vit

74 in non-neuronal mammalian cells, in primary neuronal culture, in brain slices of mouse and monkey, a

75 In neuronal cultures lithium attenuates iron efflux by lowe

76 In productively infected neuronal cultures, epinephrine treatment significantly i

77 well as publicly available transcriptomes of neuronal cultures.

78 mbinant ApoE (E2, E3, E4) also leads to some neuronal damage and death compared with the absence of A

79 ng factors for the induction of tau-mediated neuronal damage.

80 e pharmacologic inhibition of ASIC1a reduces neuronal death following ischemic stroke in rodents.

81 tivity caused by OGD/ischemia contributes to neuronal death in hippocampal neurons via diverse effect

82 utic intervention aimed at the prevention of neuronal death in neurodegenerative diseases.

83 es slightly shorter than those causing acute neuronal death; under these conditions, cytosolic Zn(2+)

84 JNK signaling pathway.SIGNIFICANCE STATEMENT Neuronal degeneration occurs in disparate circumstances:

85 nd regulatory relationships that orchestrate neuronal delamination and may inform mechanisms underlyi

86 lso mediate forward secretory trafficking in neuronal dendrites and spines through a specialized GA-i

87 Dendritic spines are protrusions along neuronal dendrites that harbor the majority of excitator

88 stroglial and microglial activation, reduced neuronal density, perivascular CD3-positive T-lymphocyte

89 We assessed neuronal-dependent and -independent contributions by act

90 pic glutamate receptors that are crucial for neuronal development and higher cognitive processes.

91 ngements and contains many genes crucial for neuronal development and migration.

92 d in the brain, where they play key roles in neuronal development and neurotransmission.

93 at this notion is not a general principle of neuronal development by documenting the timing of mitosi

94 ntegration of adult-born neurons, similar to neuronal development during embryogenesis.

95 ys a pivotal role in brain, where it affects neuronal development, function, and disease.

96 rowth cone motility and axon guidance during neuronal development.

97 yses we found that (1) MYT1L is required for neuronal differentiation and identified ID1, a HLH inhib

98 loss leads to aberrations in proliferation, neuronal differentiation and migration in the embryonic

99 at carbofuran inhibits NSC proliferation and neuronal differentiation by altering TGF-beta signaling.

100 vidual BMPs promote progenitor patterning or neuronal differentiation by their activation of differen

101 eased to regulate MOR gene expression during neuronal differentiation of P19 cells, suggesting a cons

102 the microtubule-actomyosin interfaces during neuronal differentiation.

103 e insulin-like peptides, which induce lamina neuronal differentiation.

104 disrupted wild type NSCs demonstrate delayed neuronal differentiation.

105 ies of Zeb2 are required for EDN3 to prevent neuronal differentiation.

106 of clinical importance within the context of neuronal diseases caused by an impaired glyoxalase syste

107 We found an unexpectedly high degree of neuronal diversity in the LTMR-RZ: seven excitatory and

108 SID can capture neuronal dynamics in vivo within a volume of 900 x 900 x

109 ccurate on the working memory task and their neuronal dynamics indicated that encoding operations wer

110 ease, genetic knockdown of PIP4K ameliorated neuronal dysfunction and degeneration as assessed using

111 ognitive decline, increasingly attributed to neuronal dysfunction induced by amyloid-beta oligomers (

112 are largely unknown but could contribute to neuronal dysfunction.

113 aicin-evoked cough responses consistent with neuronal dysfunction.

114 ral circuit mechanisms underlying persistent neuronal encoding within this network remain unresolved.

115 y neuronal glycolysis.SIGNIFICANCE STATEMENT Neuronal energy levels are critical for proper CNS funct

116 ittle is known about specific changes within neuronal ensembles activated during the recall of drug-e

117 ese properties specifically on cue-activated neuronal ensembles.

118 e, which is synthesized from L-serine by the neuronal enzyme serine racemase (SR).

119 sults reveal an input-dependent control over neuronal excitability and dendritic complexity in the de

120 ariants can act as autoreceptors to regulate neuronal excitability and dopamine release, but the role

121 demonstrate that Scn8a plays a vital role in neuronal excitability and provide insight into the mecha

122 We found substantial derangements in both neuronal excitability and short-term synaptic plasticity

123 Although widespread drug-induced changes in neuronal excitability have been observed, little is know

124 cing and suggests that associated changes in neuronal excitability, particularly in developing neuron

125 hol application had heterogeneous effects on neuronal excitability, with both excitation and suppress

126 mportant role for CaV1.3 L-CDF in regulating neuronal excitability.

127 leep assays indicate that mir-92a suppresses neuronal excitability.

128 synthesized Daunorubicin is an inhibitor of neuronal excitability.

129 hibitor of AMPH-dependent trafficking of the neuronal excitatory amino acid transporter 3 (EAAT3) blo

130 Here we use zebrafish larvae with pan-neuronal expression of GCaMP6s, combined with light shee

131 ucts expressed during latency cooperate with neuronal factors to maintain latency.

132 We reveal that neuronal function and integrity decline rapidly with age

133 htly regulated CAMK2 auto-phosphorylation in neuronal function and neurodevelopment.

134 Neuraminidases 3 and 4 regulate neuronal function by catabolizing brain gangliosides.

135 of molecular targets or compounds that alter neuronal function can lead to therapeutic advances that

136 ability as evidenced by the rapid decline in neuronal function during ischemic attacks and acute seve

137 ) might be the major deleterious species for neuronal function in these diseases.

138 ole of PD-L1 and PD-1 in regulating pain and neuronal function is unclear.

139 use and human and known to play key roles in neuronal function.

140 xonal projection morphology, and a switch in neuronal function.

141 is mellifera, has been suggested to have non-neuronal functions.

142 uts from multiple sources to generate normal neuronal functions.SIGNIFICANCE STATEMENT Critical perio

143 Neuronal genome tagging in vivo by Mef2c-Dam adenine met

144 allial developmental origin (Tbr1, Sp8), and neuronal/glial antigens for phenotype characterization.

145 Instead, either ambient monocarboxylates or neuronal glycolysis was sufficient to supply requisite s

146 by bulk but not local monocarboxylates or by neuronal glycolysis.SIGNIFICANCE STATEMENT Neuronal ener

147 usally linked to abnormal synaptic function, neuronal growth and survival are unknown.

148 mammalian target of rapamycin signaling and neuronal growth.

149 Understanding the mechanisms that control neuronal GSK3beta is critical.

150 tential paracrine mechanism that coordinates neuronal homeostasis and inflammation in the CNS.

151 ting lipids including cholesterol to support neuronal homeostasis and synaptic integrity.

152 This observed neuronal homeostasis is maintained by new neurons formed

153 o Alzheimer's disease that is independent of neuronal hypometabolism, predates changes in brain perfu

154 siological processes, namely cardiovascular, neuronal, immune, respiratory, gastrointestinal, liver,

155 ceptor is the culprit of COX-2/PGE2-mediated neuronal inflammation and degeneration remains largely u

156 and microglial exosomal miR-124-3p inhibited neuronal inflammation in scratch-injured neurons.

157 Neuronal inhibition can occur via synaptic mechanisms or

158 Proteolytic neuronal injury biomarkers (alphaII-spectrin breakdown p

159 lood molecules into the brain contributes to neuronal injury during stroke and other cerebrovascular

160 Neuronal injury often leads to devastating consequences

161 of beta-amyloidosis and neurodegeneration or neuronal injury to more fully characterise the heterogen

162 Here we describe a new method for neuronal labelling by electrophoretic dye delivery from

163 normal cell junctions, generating an ectopic neuronal layer that resembles cerebral cortex abnormalit

164 For each ten percent increase in total neuronal loss, average thresholds across patients at eac

165 This deposition is accompanied by neuronal loss, spongiform change, astrogliosis, and cons

166 develop inclusions associated with extensive neuronal loss.

167 ch as neurofibrillary tangles and widespread neuronal losses.

168 tein 2 (LAMP-2) immunolabeling showed higher neuronal lysosomal counts in brain of 12-months-old APP(

169 ich were reported to be the brightest in non-neuronal mammalian cells, in primary neuronal culture, i

170 The neuronal MAP tau is also not sensitive to tubulin acetyl

171 ysine residues and has been shown to disrupt neuronal maturation and OR expression in the developing

172 Markers of neuronal maturity were first expressed 3 months after gr

173 er the ability to bridge different scales of neuronal measurement by interpreting population response

174 Our findings represent a possible neuronal mechanism for a direct influence of the respira

175 In this study, we elucidated the neuronal mechanism underlying the response at an anatomi

176 tein target for anesthetics is assumed to be neuronal membrane receptors and ion channels, however ne

177 heat superparamagnetic nanoparticles on the neuronal membrane.

178 evidence points to critical effects on intra-neuronal microtubules, a target of interest due to their

179 , Lpd contributes to neuronal morphogenesis, neuronal migration during development and its C. elegans

180 ctrum of brain malformations due to impaired neuronal migration in the developing cerebral cortex.

181 of RG cells to provide a stable scaffold for neuronal migration, and suggest that the transition in m

182 formation requires the precise regulation of neuronal migration, axon guidance, and dendritic arboriz

183 affecting auto-phosphorylation also affected neuronal migration, highlighting the importance of tight

184 ing and neuronal-branching regulation during neuronal migration.

185 A reproducible neuronal model of human origin would facilitate studies

186 e suggest that SHANK3 has a critical role in neuronal morphogenesis in placodal neurons and that earl

187 n central nervous system, Lpd contributes to neuronal morphogenesis, neuronal migration during develo

188 Absence of FMRP results in abnormal neuronal morphologies in a selected manner throughout th

189 Disruption of neuronal morphology contributes to the pathology of neur

190 However, how neuronal morphology is maintained in the adult brain rem

191 cell surface molecules, and determinants of neuronal morphology that is differentially expressed in

192 sed, we found 7 displaying a major impact in neuronal morphology when inactivated in mice.

193 ing molecules pertinent for excitability and neuronal morphology.

194 evolutionary selection of donor L1s driving neuronal mosaicism.

195 ed the temporal gene expression changes in a neuronal mRNA pool during an olfactory long-term associa

196 Further, it adds the neuronal Munc13 proteins and the synaptic vesicle primin

197 Epileptic seizures represent altered neuronal network dynamics, but the temporal evolution an

198 t mediator of early cortical development and neuronal network formation in the brain.

199 e Fbxl3(+/+) but not the Fbxl3(Afh/Afh) vSCN neuronal network.

200 Functionally, mPFC neuronal networks appeared to be affected in a PKA-depen

201 cells that probably started to connect into neuronal networks soon afterward.

202 er the underlying structural connectivity in neuronal networks.

203 cyte morphogenesis through interactions with neuronal neurexins.

204 crucial for secretory vesicle biogenesis in neuronal/neuroendocrine cells.

205 Neuronal nicotinic acetylcholine receptors (nAChRs) are

206 regulating the expression and clustering of neuronal nicotinic acetylcholine receptors (nAChRs) rema

207 Y), and the nitric oxide synthesizing enzyme neuronal nitric oxide synthase (nNOS) in nerve fibers of

208 This NO stems from neuronal NOS (nNOS), but not endothelial (eNOS).

209 cell body size was associated with decreased neuronal nucleolar size.

210 ly 100 putatively functional ones located in neuronal OCRs, including rs1198588, at a leading risk lo

211 ion is essential to more accurately approach neuronal operations of human multisensory integration.

212 The role of neuronal oscillations in human somatosensory perception

213 These dorsoventral differences in neuronal output and spatial representation could arise d

214 o prime mature follicles to be responsive to neuronal ovulatory stimuli, thus providing mechanistic i

215 P2X7R has also been implicated in neuronal pathologies, in which it may influence neuronal

216 bed for the rat, thus, elucidating potential neuronal pathways involved in the regulation of the HPA

217 f the microbiota induces positive effects on neuronal pathways that are able to slow down the progres

218 conditions, however, animals use alternative neuronal pathways to adapt to the metabolic challenges o

219 Thus, entrainment of vasomotion links neuronal pathways to functional connections.

220 quires selective modulation of dysfunctional neuronal pathways.

221 ed proteins discretely expressed in specific neuronal pathways; these accessory proteins provide a ne

222 ainst alphaSyn-induced cell death in a human neuronal PD model.

223 lease of the AMPA receptor clustering factor neuronal pentraxin 1 from presynaptic terminals by signa

224 y of compounds that affect the age-dependent neuronal physiology.

225 Restoring neuronal PINK1 function strikingly reduces amyloid-beta

226 investigated the effect of excitotoxicity on neuronal PKD1 activity.

227 spines are dynamic structures which regulate neuronal plasticity and have crucial roles in myriad bra

228 P).SIGNIFICANCE STATEMENT Activity-dependent neuronal plasticity is the cellular basis for learning a

229 the pathophysiology of schizophrenia and in neuronal plasticity suggests that facilitation of NMDAR

230 e conjoint influence of these two factors on neuronal plasticity.

231 The neuronal population of the subthalamic nucleus (STN) has

232 nent CB subtype-1 receptor (CB1R) expressing neuronal population throughout development.

233 gRP) in mice, we have demonstrated that this neuronal population tonically suppresses splanchnic SNA

234 viding two-photon imaging access to cortical neuronal populations at single-cell or single dendritic

235 er activity and NFIA expression in glial and neuronal populations.

236 n disturbs the migration of serotonin (5-HT) neuronal precursors, leading to altered global serotoner

237 s functional diversity for the regulation of neuronal processes by the NRG/ErbB pathway are discussed

238 rmediaries between peripheral immune events, neuronal processing, and potentially cognition.

239 rofiles, and may be mildly conserved for the neuronal profiles.

240 ned, but postulated pathways include loss of neuronal progenitor cells, damage to the developing vasc

241 u isoform expression, mitotic progression in neuronal progenitors and post-mitotic neuronal survival.

242 Although the importance of neuronal progenitors in vascular development within the

243 ippocampal proliferative cells by inhibiting neuronal proliferation and triggering the formation of m

244 es memory-related processes by controlling a neuronal proliferation/differentiation switch of ID-bHLH

245 a detailed analysis of the connectivity and neuronal properties of lamprey pretectal cells.

246 Neuronal protein 3.1 (P311), a conserved RNA-binding pro

247 Tau is a multifaceted neuronal protein that stabilizes microtubules (MTs), but

248 between signal correlations, associated with neuronal receptive fields, and noise correlations, assoc

249 l recycling and sorting of several important neuronal receptors.

250 esses initially considered exclusively under neuronal regulation.

251 mice were used to assess microglia-mediated neuronal remodeling and dendritic spine density in the m

252 opportunities to explore in conjunction with neuronal rescue and repair strategies.

253 4 h postinfection (hpi), suggesting a unique neuronal response to viral infection.

254 lds, and noise correlations, associated with neuronal response variability.

255 Within the LGN, neuronal responses are often suppressed by stimuli that

256 ionships affect neocortical oscillations and neuronal responses is poorly understood.

257 ta were used to expose a pair of distinctive neuronal responses to the stimulation.

258 pired by the known anatomical structures and neuronal responses within the bee brain and subsequently

259 ss is characterized by rapid fluctuations in neuronal responses.

260 of mRNAs that are translated in dendrites by neuronal ribosomes.

261 a plays an essential, noncompensated role in neuronal saltatory migration in vivo and highlights the

262 fMRI also reflects fine-grained patterns of neuronal selectivity.

263 However, terminally differentiated, neuronal SH-SY5Y cells release significantly less extrac

264 rom a suction electrode directly through the neuronal sheath of nerves and ganglia in insects.

265 y neurons, and that experimental ablation of neuronal Shh expression causes loss of taste receptor ce

266 tters from the synaptic cleft to terminate a neuronal signal and enable subsequent neurotransmitter r

267 This neuronal signal-mediated mechanism holds potential for d

268 ology has led to the recognition of distinct neuronal signaling pathways linking Abeta to synaptotoxi

269 channels (CaCCs) encoded by TMEM16A control neuronal signalling, smooth muscle contraction, airway a

270 s in the SCN2A gene that disrupt the encoded neuronal sodium channel NaV1.2 are important risk factor

271 tivation resembling the properties of F1.Q54 neuronal sodium channels.

272 Neurons express many neuronal-specific proteins that regulate membrane traffi

273 f neofunctionalization is the acquisition of neuronal specificity by immune formyl peptide receptors

274 Here we used MEAs to record neuronal spiking activity in the human middle temporal g

275 se lateral PFC-STN coherence and altered STN neuronal spiking.

276 y increases in the expression of hypoexcited neuronal state in the ventral SCN at night and enhances

277 oteomic analyses of infected human, primary, neuronal stem and monocytic cells revealed effects on ne

278 These data support a model in which a single neuronal stem cell can produce a large number of interne

279 is highly modulated and oscillating circuit, neuronal structures appear to be governed by a space-fil

280 Conditional KO of Prlr from neuronal subpopulations expressing the neurotransmitters

281 d that acute stress preferentially activates neuronal subpopulations that express the neuropeptide ge

282 st two talks discuss novel developmental and neuronal subtype-specific contributions to the excitator

283 Mounting evidence points to specialized neuronal subtypes within the serotonergic neuronal syste

284 P7C3 aminopropyl carbazoles promote neuronal survival by enhancing nicotinamide adenine dinu

285 t to understand the mechanisms that regulate neuronal survival in deaf ears.

286 that unlike Nna1, CCP5 is not essential for neuronal survival in mouse.

287 Neuronal survival is necessary for the proper function o

288 ion in neuronal progenitors and post-mitotic neuronal survival.

289 of axonal transport, a critical function for neuronal survival.

290 ronal pathologies, in which it may influence neuronal survival.

291 Neuronal synapses are adhesions specialized for communic

292 and degeneration of the nigral-dopaminergic neuronal system exacerbates motor deficit.

293 ed neuronal subtypes within the serotonergic neuronal system, borne out in functional studies, for th

294 iates ternary SNARE complex formation in the neuronal system.

295 regional co-expression of genes enriched for neuronal terms.

296 the presence of Lewy bodies (LBs) in certain neuronal tissues.

297 In primates, we combined neuronal tracer injections into various arms of the circ

298 The mammalian brain contains diverse neuronal types, yet we lack single-cell epigenomic assay

299 etic variants of Neuregulin 1 (NRG1) and its neuronal tyrosine kinase receptor ErbB4 are associated w

300 When light falls within a neuronal visual receptive field (RF) the resulting activ