ライフサイエンスコーパス: spine

1 n nonneoplastic and malignant lesions in the spine.

2 iseases is magnetic resonance imaging of the spine.

3 rogressive disease can lead to fusion of the spine.

4 atio analysis within the thoracic and lumbar spine.

5 is-dependent structural changes of dendritic spines.

6 ric anatomic visualization of embalmed human spines.

7 vated calcium transients in apical dendritic spines.

8 ondria within spatially restricted dendritic spines.

9 a small reduction in the numbers of synaptic spines.

10 terfaces of the parallel-in-register amyloid spines.

11 on of cytoskeleton proteins in dendrites and spines.

12 f CB (1) -KO with no changes in PC dendritic spines.

13 dant in postsynaptic compartments, including spines.

14 short stubby, long stubby and short mushroom spines.

15 ethods for fluorescent labeling of dendritic spines.

16 -term maintenance of dendrites and dendritic spines.

17 compartments like primary cilia or dendritic spines.

18 nd processed for quantification of dendritic spines.

19 lowed by glia (37.7 +/- 2.5%), and dendritic spines (14.3 +/- 2.6%) in the matrix of the mouse striat

20 ning regimen that effectively enforced local spine a priori knowledge during training.

21 ther, our results suggest that the dendritic spine abnormalities are primary developmental defects in

22 Further, these perpetual NMII-driven spine actin dynamics in BLA neurons may contribute to th

23 fication of a previously unknown ability for spine actin dynamics to persist days after stimulation a

24 re contained in axon terminals and dendritic spines adjacent to the synaptic membrane, which support

25 characterized by the presence of a segmented spine along its main axis.

26 ntation and reduced positioning to dendritic spines along with increased caspase 3 cleavage in dendri

27 The majority of large spines also contains synaptopodin (SP), an actin-modulat

28 rformed single-unit recordings and dendritic spine analyses on striatal medium spiny neurons (MSNs) i

29 le-binding protein tau, is required for this spine anchoring of GSK3alpha and mediates GSK3alpha-indu

30 AHEI (score: 25-86) was also associated with spine and all hip sites (P <0.02), whereas MeDS (0-9) wa

31 hord define the evolutionary identity of the spine and demonstrate how simple shifts in development c

32 progressive limb-girdle weakness with rigid spine and disabling contractures.

33 men with or without low BMD underwent lumbar spine and hip bone densitometry and a complete periodont

34 to the abdomen, forming an angle between the spine and LES.

35 ing to the IGF 11778 anterior inferior iliac spine and lumbar vertebrae structure and identifications

36 nts a family of inflammatory diseases of the spine and peripheral joints.

37 embryonic development give rise to the adult spine and summarize recent advances in the field, largel

38 as associated with SCFA-dependent changes in spine and synapse densities.

39 Lumbar spine and whole body BMD z-scores remained below baselin

40 two-stage decay functions, SP-negative (SP-) spines and all spines of SP-deficient animals showed sin

41 entified changes in pyramidal cell dendritic spines and axon initial segments consistent with compens

42 portion of synapses established on dendritic spines and dendritic shafts.

43 of them were excitatory, targeting dendritic spines and displaying a macular shape, regardless of the

44 shape that consists of extremely tall neural spines and elongate chevrons, which forms a large, flexi

45 The proximal domains exhibit spines and en passant-like processes and are proposed he

46 s and related signaling to protect dendritic spines and processes from Abeta-induced injury.

47 microglia are absent, abGCs develop smaller spines and receive weaker excitatory synaptic inputs.

48 eased MMP-9 activity around D1-MSN dendritic spines and synapse-proximal astroglial processes.

49 ice enabled thorough evaluation of dendritic spines and synapses on pathway-identified SPNs.

50 can induce tau mislocalization to dendritic spines and synaptic deficits in cultured rat hippocampal

51 ering osteoblast migration to the developing spine, and increasing sensitivity to somitogenesis defec

52 the Asp-Phe-Gly (DFG) motif, the regulatory spine, and the gatekeeper residue to kinase regulation.

53 ond primary dendrite, acquired more mushroom spines, and had enlarged mossy fiber presynaptic termina

54 nding to Galphai1, localization to dendritic spines, and inhibitory actions on LTP induction, while v

55 ization of DG granule cell dendritic arbors, spines, and synapses, whereas it restricts the survival

56 -term spine stability: SP clusters stabilize spines, and the presence of SP indicates spines of high

57 yskinesis test, head, shoulder, and thoracic spine angle were measured at baseline, post-test, and fo

58 In large spines, ER frequently forms a spine apparatus, while smaller spines contain just a sin

59 ted neurons displayed spine loss and altered spine architecture.

60 Disorders of the spine are among the most common indications for neurosur

61 Imaging standards for brain and spine are defined.

62 Dendritic spines are tiny membranous protrusions on the dendrites

63 inking PKCalpha and structural plasticity of spines are unknown.

64 The generality of stacking spines as conduits for effector-dependent, interdomain c

65 ion and elevated calcium levels in dendritic spines as important local-circuit alterations driven by

66 The vertebral column or spine assembles around the notochord rod which contains

67 include the use of MRI of the brain and the spine, assessment of clinical status, and the use of cor

68 functions to increase the number of bulbous spine-associated synapses at retinogeniculate connection

69 es vertebral malformation and curving of the spine axis at those sites.

70 cation for the injuries of the thoracolumbar spine, based on MRI in a large group of patients.

71 0.029 +/- 0.006 g/cm2, P <0.001), and lumbar spine BMD (0.025 +/- 0.007 g/cm2, P = 0.001).

72 At 48 weeks, lumbar spine BMD with ZOL was 11% higher than placebo (n = 60;

73 Kir2.1, we validate the practical utility of SPINE by constructing and comparing domain insertion per

74 ium responses invade dendrites and dendritic spines by active backpropagation.

75 , L-type Ca(2+) channel activation, enhanced spine Ca(2+) transients, nuclear translocation of a CaM

76 demonstrated how the stabilization of the R-spine can be used as a strategy to greatly increase the

77 Dendritic spines change shape in response to input signals, thereb

78 time-lapse two photon imaging to examine how spines change their structure during LTD induced by acti

79 ently forms a spine apparatus, while smaller spines contain just a single tubule of smooth ER.

80 se organotypic tissue cultures we found that spines containing SP survived considerably longer than s

81 SPINE could help explore the relationship between domain

82 culated that the presence of SP within large spines could explain their long lifetime.

83 Accordingly, in dstyk mutants the spine curves increasingly over time as vertebral bone fo

84 t agents capable of blocking severe juvenile spine deformity.

85 expression correlates with reduced dendritic spine densities in selected cortical regions of developi

86 , proliferation of type 1 NSCs and dendritic spine densities of adult-born neurons reverted to normal

87 In addition, dendritic spine densities of adult-born neurons were significantly

88 Dendritic spine density (DSD) is significantly different based on

89 lpha2 cKO mice exhibited decreased dendritic spine density and abnormal spine morphology in hippocamp

90 on for 24 hr selectively increased dendritic spine density and AMPA-receptor-mediated EPSCs in wild-t

91 pregnation labeling showed reduced dendritic spine density and destabilized spines of hippocampal pyr

92 polymerization pathway, leading to increased spine density and improved flexible behavior.

93 e phases and found a congruence of dendritic spine density and spatial memory deficits, with reduced

94 m potentiation (LTP) and increased dendritic spine density and synaptic markers compared with aged WT

95 entified striatonigral MSNs, and (2) altered spine density and thin-spine morphology on striatal MSNs

96 culum) and MSNs (i.e., dendritic complexity, spine density and typology, and excitatory inputs).

97 aptic plasticity but had increased dendritic spine density compared with young WT.

98 In addition, SorCS2 regulates dendritic spine density in CA2 neurons where SorCS2 expression is

99 However, reduced cortical spine density in knockouts persists into adulthood.

100 synaptic plasticity, along with an increased spine density in layer V pyramidal neurons, were detecte

101 polarization and coincident decreased distal spine density in striatal direct pathway striatal projec

102 re neurotropic and reduce neuronal dendritic spine density in vivo.

103 aptic pathology characterized by a decreased spine density of neighboring healthy neurons in an APP-d

104 ty and spatial memory deficits, with reduced spine density only in mice stressed during high estradio

105 eaning rat pups display increased BLA neuron spine density paralleled with enhanced evoked synaptic r

106 e airway caused the most prominent dendritic spine density reduction, yet intraperitoneal injection o

107 nic social defeat, D2-MSNs exhibit increased spine density that is correlated with enhanced social av

108 ents on both apical and basal dendrites, and spine density was increased in secondary branches and di

109 mplified dendritic arbors, reduced dendritic spine density, and diminished excitatory synaptic transm

110 Glut1/PSD95 colocalization, higher dendritic spine density, and enhanced evoked AMPAR and NMDAR EPSCs

111 eater apical dendritic branching complexity, spine density, and inhibition, indicative of enhanced de

112 neurons, old adult-born neurons had greater spine density, larger presynaptic terminals, and more pu

113 Ror2 and Ryk receptors to enhance dendritic spine density, leading to nociceptive sensitization.

114 ive function, synaptic plasticity, dendritic spine density, microglial morphology, and brain mitochon

115 t, in adulthood attenuates learning, memory, spine density, synaptic plasticity (L-LTP), and potentia

116 l injection of these amyloids did not affect spine density.

117 stress, NAc MSNs exhibit increased dendritic spine density.

118 nced mEPSC frequency and increased dendritic spine-density.

119 neurons leads to perturbations in dendritic spine development and hypoconnectivity, which mirror neu

120 uole biogenesis, notochord morphogenesis and spine development through mTORC1/TFEB pathway.

121 which is critical for synapse and dendritic spine development.

122 d stabilizes ankyrin-G to maintain dendritic spine development.

123 ervical, as compared to patients with lumbar spine disease.

124 Calcium surges are observed in synaptic spines during an EPSP and back-propagating action potent

125 The stabilization of dendrites and spines during neuronal maturation is essential for prope

126 tic spines in a non-random manner, targeting spines during periods of high synaptic activity.

127 a critical role of CXCL12/CXCR4 signaling in spine dynamics and cognitive flexibility, suggesting tha

128 , the relationship between altered dendritic spine dynamics and neuropathic pain may serve as a struc

129 and outline the potential for modulation of spine dynamics by targeting two proteins, srGAP3 and Rac

130 estigations in vivo of spinal cord dendritic spine dynamics in the context of injury and disease.

131 e ongoing, steady-state changes in dendritic spine dynamics in the dorsal horn associated with periph

132 ful utility of intravital study of dendritic spine dynamics in the superficial dorsal horn; (2) that

133 NMII inhibition, METH-induced changes to BLA spine dynamics were reversed by a single systemic inject

134 y myeloid cells, restores cortical dendritic spine dynamics, and improves the animals' neurological f

135 ture-function relationship between dendritic spine dysgenesis and the presence of neuropathic pain.

136 xial and proximal weakness, scoliosis, rigid spine, dysmorphic facies, cutaneous involvement, respira

137 e of sleep in experience-dependent dendritic spine elimination of layer 5 pyramidal neurons in the vi

138 MD- or FC-induced spine elimination was significantly reduced after total

139 calcium spikes prevented MD- and FC-induced spine elimination.

140 ocation of MAP2 was coupled with LTP-induced spine enlargement.

141 In large spines, ER frequently forms a spine apparatus, while sma

142 lighting specific transitions during teleost spine evolution.

143 Whereas the survival time courses of SP+ spines followed conditional two-stage decay functions, S

144 ion of MAP2, present in dendritic shafts, to spines following LTP stimulation.

145 ve reported downsizing and loss of dendritic spines following sleep deprivation.

146 s, enhances synaptic viability and dendritic spine formation, and increases turnover of neurotransmit

147 pinal neurons, where they regulate dendritic spine formation, axon elongation, and pontine midline cr

148 t guides symmetrical growth of vertebrae and spine formation.

149 lysis to quantify thin, mushroom, and stubby spines from CA1 dendrites, distinguishing between branch

150 s severely biased and sparse for some genes, SPINE generated high-quality libraries for all genes tes

151 four ion channel genes, we demonstrate that SPINE-generated libraries are enriched for in-frame inse

152 conclude that the brief ER visits to active spines have the important function of preventing runaway

153 -induced cocaine reinstatement and increased spine head diameter (d(h)).

154 g training approaches for the muscles of the spine in microgravity, this study examined the effects o

155 We analyzed dendritic spines in 4-week-old (P28) and 12-week-old (P84) male an

156 Here we show that the ER visits dendritic spines in a non-random manner, targeting spines during p

157 nt a concise review of the role of dendritic spines in neuropathic pain and outline the potential for

158 and reduction in the width of the dendritic spines in Postnatal day 21 to 12-month-old LD animals.

159 ed caspase 3 cleavage in dendritic shaft and spines in response to oligomycin A.

160 oduces half of the cells and the majority of spines in the dentate gyrus.

161 at a subset of spatially clustered dendritic spines in the motor cortex.

162 The density and head diameter of dendritic spines in the MSNs of Het mice were also reduced.

163 itochondrial alterations within postsynaptic spines in the pre-BotC neurons.

164 For example, dendritic spines in the primate dorsolateral prefrontal cortex (dl

165 ncreasing the net trafficking of AMPARs into spines, including in non-motor brain regions.

166 ons for endocarditis, central nervous system/spine infections, osteomyelitis, and septic arthritis we

167 ely reviewed the patients with thoracolumbar spine injuries who underwent magnetic resonance imaging

168 tal role of caspase 3 signaling in mediating spine injury and the modulation of caspase 3 activation

169 Astronauts are at increased risk of spine injury.

170 The spine is a defining feature of the vertebrate body plan.

171 nalysis of a zebrafish mutant, spondo, whose spine is dysmorphic, prompted us to reconstruct paleonto

172 SPINE is the first technology to enable saturated domain

173 Structural plasticity of dendritic spines is a key component of the refinement of synaptic

174 Actin cytoskeleton remodeling in spines is a key element of their formation and growth.

175 type glutamate receptor (NMDAR) to dendritic spines is essential for excitatory synaptic transmission

176 that baseline AMPAR expression in individual spines is highly dynamic with more dynamics in primary v

177 tural and functional plasticity of dendritic spines is the basis of animal learning.

178 The growth and stabilization of dendritic spines is thought to be essential for maintaining long-t

179 tion of these vacuoles in zebrafish leads to spine kinking.

180 The spine-LES angle was smaller in patients with achalasia (

181 and DCE perfusion MRI performed at the same spine level as biopsy.

182 ts were also generated on discrete dendritic spine-like structures on the melanocytes.

183 balanced nuclear import/export and dendritic spine localization are essential for RGS14 functions.

184 the short M-Si bonds, a nearly linear M-Si-M spine, long M-C bonds, and the presence of two planar te

185 ting that HAND - or other diseases driven by spine loss - may be reversible and upturned by targeting

186 ges, oligomycin A-insulted neurons displayed spine loss and altered spine architecture.

187 one of primary visual cortex (V1b) undergoes spine loss and changes in neuronal responsiveness follow

188 Trem2(ko) mice also exhibited more dendritic spine loss around plaque and more neurofilament light ch

189 phosphorylation, and has effects preventing spine loss both up and downstream of RhoA activation.

190 This event leads to a decrease in dendritic spine loss by reducing dendritic localization of hTau-S1

191 we did not observe the previously described spine loss during ODP in either genotype, our results re

192 aspase 3 activation may benefit neurons from spine loss in diseases, at least, in those with F1Fo ATP

193 demonstrated dendritic atrophy and dendritic spine loss in dorsal striatum D1-MSNs from mice with rep

194 l elements and blocked CUS-induced dendritic spine loss in the medial PFC.

195 r this caspase signaling plays a key role in spine loss when severe mitochondrial functional defects

196 ce of osteoporosis at baseline at the lumbar spine (LS) and femoral neck (FN) was 17.6% and 7.2%, res

197 erinatally infected with HIV with low lumbar spine (LS) BMD (Z score < -1.5) were randomized to recei

198 n, Tet3 cKO mice exhibit increased dendritic spine maturation in the ventral CA1 hippocampal subregio

199 synapse development, dendritic arborization, spine maturation, and prevention of apoptosis of some ne

200 the maintenance of a straight body axis and spine morphogenesis in adult zebrafish.

201 We, therefore, analyzed the dendritic spine morphologies in pyramidal neurons of the hippocamp

202 data show that PCDH7 can regulate dendritic spine morphology and synaptic function, possibly via int

203 creased dendritic spine density and abnormal spine morphology in hippocampus.

204 MSNs, and (2) altered spine density and thin-spine morphology on striatal MSNs; both phenomena mimick

205 use viral labeling to characterize dendritic spine morphology specifically in dopamine D2 receptor ex

206 and manipulations of Bin1 lead to changes in spine morphology, AMPA receptor surface expression and t

207 l synaptic plasticity and abnormal dendritic spine morphology, but little is known about how these ar

208 lters gene expression patterns, and disrupts spine morphology.

209 N-acylhydrazone and selenophene residues as spine motifs, yielding metabolically stable inhibitors w

210 ic currents accompanied changes in dendritic spine nano-architecture, and single-synapse currents, ev

211 se should be assessed using MRI of brain and spine, neurological examination, and anti-inflammatory o

212 Dendritic spine number and morphology are altered as a consequence

213 ng cold and vibrotactile sensations down the spine of subjects in temporal conjunction with a chill-e

214 aptic density and endosomes within dendritic spines of CA2 neurons.

215 taining SP survived considerably longer than spines of equal size without SP.

216 nervated all layers of A25, mostly targeting spines of excitatory neurons.

217 ize spines, and the presence of SP indicates spines of high stability.

218 the effect of sleep deprivation on dendritic spines of hippocampal CA1 neurons using genetic methods

219 suppresses synaptic plasticity in dendritic spines of hippocampal neurons.

220 ced dendritic spine density and destabilized spines of hippocampal pyramidal neurons 4 weeks after in

221 d calcium transients in the apical dendritic spines of pyramidal neurons.

222 functions, SP-negative (SP-) spines and all spines of SP-deficient animals showed single-phase expon

223 Here, we quantified dendrites and dendritic spines of supragranular pyramidal neurons in tissue from

224 MIA increases plastic dendritic spines of the intrinsically bursting neurons and their i

225 , presynaptic mitochondria, and in dendritic spines of xCT(-/-) mice.

226 r motile processes to interact with mushroom spines on abGCs, and when microglia are absent, abGCs de

227 EM sleep alters the structural remodeling of spines on ABN dendrites and impairs memory consolidation

228 transiently required for the development of spines on apical, but not basal, secondary dendrites.

229 to induce plasticity at individual dendritic spines on hippocampal CA1 neurons from mice and rats of

230 CXCL12 preferentially regulates plastic thin spines on layer II/III pyramidal neurons of the medial p

231 Formation of dendritic spines on newborn neurons was also impaired following de

232 s via Fn14 to restrict the number of bulbous spines on relay neurons, leading to the elimination of a

233 the abdomen or pelvis or CT of the cervical spine or neck with unsuspected findings highly suspiciou

234 en or pelvis and 18 CT scans of the cervical spine or neck.

235 dium spiny neurons, the density of dendritic spines, or the density or ultrastructure of corticostria

236 e profiled the in vivo dynamics of dendritic spines over time on the same superficial dorsal horn (la

237 for the differentiation of these sources of spine pain and potential complicating features, permitti

238 There are many potential aetiologies of spine pain with similar clinical presentation, including

239 ssess the cause and complicating features of spine pain.

240 ord protein, Calymmin, as a key regulator of spine patterning in zebrafish.

241 mbryonic brain, suggesting that the aberrant spine phenotype could be a developmental defect in LD.

242 In striking contrast, NMDA-induced spine plasticity in Fmr1(-/y) mice was no longer depende

243 Together, our data indicate dendritic spine plasticity is MSN subtype specific, improving our

244 However, it remains unclear if the dendritic spine plasticity is MSN subtype specific.

245 microglial IL-33 receptor leads to impaired spine plasticity, reduced newborn neuron integration, an

246 ing C1q, we found that the densities of most spine populations on basal and proximal apical dendrites

247 centra and bifurcated anterior dorsal neural spines (present in piatnitzkysaurids).

248 nonapoptotic caspase signaling in mediating spine pruning.

249 halamocortical synapse numbers and increased spine pruning.

250 Current and previous spine radiographs were also reviewed.

251 bolic rates, grazing, growth, calcification, spine regeneration, and gonad production under constant,

252 Spine regrowth was reduced under all hypoxia treatments,

253 eraction in the spinal dorsal horn prevented spine remodeling and significantly reduced inflammatory

254 have highlighted the importance of dendritic spine remodeling in driving synaptic plasticity within t

255 d Rac1 activation and deficits in structural spine remodeling.

256 Assess occurrence of the dendritic spine scaffolding protein Drebrin as a pathophysiologica

257 Genetic analyses of patients with severe spine segmentation defects have implicated several human

258 non-ionotropic NMDAR signaling to drive both spine shrinkage and LTD.

259 (NMDAR), independent of ion flow, in driving spine shrinkage and LTD.

260 in driving synaptic weakening and dendritic spine shrinkage during synaptic plasticity.

261 TD and AMPA receptor internalization, but no spine shrinkage in either wildtype or Fmr1(-/y) mice.

262 Spine shrinkage was initiated by non-ionotropic (metabot

263 ic NMDAR signaling pathway driving dendritic spine shrinkage, including the interaction between NOS1A

264 Kv7.3, and Kv7.5) on layer III dendrites and spines, similar to M1Rs.

265 rmational changes in the NMDAR to changes in spine size and synaptic strength.

266 hout all nuclei of the BNC and had aspiny or spine-sparse dendrites.

267 nd NMDAR-mediated Ca(2+)-currents during the spine spike, and ultrastructural data prove NMDAR presen

268 nd nebulin repeats of LASP2 are required for spine stability and dendritic arbor complexity.

269 plicate SP as a major regulator of long-term spine stability: SP clusters stabilize spines, and the p

270 stinct role in dendritic arbor and dendritic spine stabilization.

271 y-induced pain triggers changes in dendritic spine steady-state behavior in the spinal cord dorsal ho

272 ns of an ecological model species, the three-spined stickleback.

273 Here we show that in three-spined sticklebacks (Gasterosteus aculeatus), fish that

274 effects in a freshwater population of three-spined sticklebacks Gasterosteus aculeatus by independen

275 rea CA1 of the hippocampus, but an effect on spine structural plasticity remains to be determined.

276 resence or absence of PKCalpha during single-spine structural plasticity.

277 smission, synaptic plasticity, and dendritic spine structure.

278 Surgery was performed by spine surgeons who used conventional microdiskectomy tec

279 he combination of navigation and robotics in spine surgery has the potential to accurately identify a

280 e of the most common procedures performed in spine surgery.

281 p to one year (Y1) after cervical and lumbar spine surgery.

282 ycyte processes and at their endfeet such as spines, swelling, en passant boutons, boutons, or claws.

283 is required to maintain NMDARs at dendritic spine synapses and mediates the direct extracellular int

284 dominant negative approach against myosin V, spine synapses became stronger compared to controls.

285 reventing runaway potentiation of individual spine synapses, keeping most of them at an intermediate

286 ng reorganizes L2 into a nucleobase-stacking spine that sequesters the SDS, linking effector recognit

287 lized actin-rich structures called dendritic spines that receive and integrate most excitatory synapt

288 Of note, SP-positive (SP+) spines that underwent pruning first lost SP before disap

289 asurements of the mandible and linear mental spine to clivus.

290 a ventrally curved mid to anterior presacral spine to hinder the dorsal slope of the whole presacral

291 a two-photon uncaging of glutamate causes GC spines to release GABA both synchronously and asynchrono

292 Time-lapse confocal imaging showed that spine translocation of MAP2 was coupled with LTP-induced

293 eptors specifically in the neurons with MAP2 spine translocation.

294 microglia depletion confirmed that elevated spine turnover and the generation of presynaptic filopod

295 absorptiometry images at the L1 to L4 lumbar spine using TBS software.

296 h and region-specific analysis revealed that spine volume was greater in primary dendrites of apical

297 h, right and left crus of the diaphragm, and spine were segmented in each CT scan slice images to con

298 These spines were also present in intact human skin.

299 HTau-S199-P mislocalizes to dendritic spines, which induces synaptic dysfunction at the early

300 Immunohistochemistry on NAcore labeled spines with ChR2-EYFP virus, showed increased immunoreac

301 ing risk of major osteoporotic (hip, pelvis, spine, wrist, and proximal humerus) fractures individual