ライフサイエンスコーパス: LTM

1 LTM and/or HTM increased gene expression of VEGF, TIMP3,

2 LTM and/or HTM increased inflammation by upregulating TN

3 LTM improved growth performance on d14, HTM improved gro

4 LTM interacts with the TOPLESS corepressor and with seve

5 LTM is supported by structural synaptic plasticity; howe

6 LTM permitted classification of 131 patients (58%) into

7 LTM total lifetime practice hours (TLPH) did not signifi

8 LTM was applied to an anti-TNF-alpha antibody, D2E7, whi

9 LTMs had less striatal gray matter, greater cortico-stri

10 Since both AD-ITM and AD-LTM require MAPK activity, these collective findings sug

11 ceptors: -2.6 nA, -21 pA pF(-1); both Adelta-LTMs and nociceptors: -1.3 nA, approximately -14 pA pF(-

12 at such increased expression does not affect LTM after retrieval.

13 Although LTM is sustained by structural synaptic plasticity, how

14 Among LTMs, greater practice experience was associated with sl

15 erm memory (LTM) by itself, flies develop an LTM.

16 The use of an LTM assembly that utilizes the principle of resistive wi

17 After scanning, subjects performed an LTM test on words presented during both WM conditions.

18 Together, these results suggest an LTM consolidation model in which transient neural activi

19 haracteristics during walking on the FTM and LTM.

20 ously demonstrated to augment normal LTF and LTM.

21 Although L-LTP and LTM are normal in mTOR(+/-) mice, application of a low c

22 Problematically, both LTP and LTM are unaffected in both constitutive and conditional

23 ce indicating that mTORC1 promotes L-LTP and LTM is controversial.

24 Thus, the role of mTORC1 in L-LTP and LTM is unclear.

25 subthreshold for WT mice-prevented L-LTP and LTM only in mTOR(+/-) mice.

26 of PKMzeta that interferes with both LTP and LTM.

27 e and its restoration rescued both L-LTP and LTM.

28 for synapse-specific expression of L-LTP and LTM.

29 sting that appetitive middle-term memory and LTM are mechanistically linked.

30 so required in adult DPM neurons for MTM and LTM formation.

31 argeting neuropeptides essential for MTM and LTM.

32 ral peptides need to be degraded for MTM and LTM.

33 Abeta expression detrimental to both MTM and LTM.

34 in states) may influence both nociceptor and LTM excitability.

35 in states) may influence both nociceptor and LTM excitability.expression and/or properties (e.g. in c

36 ing was associated with both enhanced WM and LTM for faces, as well as baseline activity shifts in a

37 ase A (PKA) activity correlates with Aplysia LTM, the analysis focuses on a positive feedback loop in

38 entally advantageous marine mollusk Aplysia, LTM for sensitization can be induced by the presentation

39 Appetitive LTM has some mechanistic similarity to aversive LTM in t

40 l motivational drive that enables appetitive LTM retrieval.

41 Furthermore, appetitive LTM requires activity in the dorsal paired medial neuron

42 However, appetitive LTM is completely disrupted by the radish mutation that

43 entary aversive and safety memories augments LTM performance after spaced training by making the odor

44 On average, LTMs showed slower baseline respiration rate (RR) than C

45 has some mechanistic similarity to aversive LTM in that it can be disrupted by cycloheximide, the dC

46 sting transcriptional changes and behavioral LTM.SIGNIFICANCE STATEMENT: In the present paper, we sig

47 We go on to show that apart from being LTM defective, creb1/crh-1-null animals show defects in

48 -4.6 nA,-33 pA pF(-1); cutaneous Aalpha/beta LTMs: -2.2 nA, -20 pA pF(-1); Abeta-nociceptors: -2.6 nA

49 Of the Aalpha/beta-LTM units, muscle spindle afferents had the fastest CV a

50 eptive, 10 C-, 8 Adelta- and 178 Aalpha/beta-LTM, 18 C- and 19 Adelta- unresponsive, and 4 C-cooling

51 or sharp/pricking-type pain) and Aalpha/beta-LTMs (tactile sensations and proprioception).

52 or sharp/pricking-type pain) and Aalpha/beta-LTMs (tactile sensations and proprioception).

53 evidence for specific dissociations between LTM and LTP.

54 neurobiological metrics, differences between LTMs and MNPs may be attributable to pre-existing differ

55 t into LTM, whereas CaMKIIalpha-HM4D blocked LTM formation.

56 rapamycin reduces L-LTP and partially blocks LTM, recent genetic and pharmacological evidence indicat

57 Conversely, if memories are erased, BM-LTM should be reduced to resemble untrained levels.

58 he amnesia is due to a retrieval failure, BM-LTM should remain at levels comparable to trained, unimp

59 the brain mechanisms of long-term memory (BM-LTM).

60 Here we review the use of BM-LTM in a number of studies that induced amnesia by targe

61 roup experienced greater gains in total body LTM (0.45 kg; 95% CI: 0.07, 0.84 kg), leg LTM (0.22 kg;

62 timulus-guided visuospatial attention and by LTM-guided visuospatial attention.

63 ors: -1.3 nA, approximately -14 pA pF(-1); C-LTMs: -0.4 nA, -7.6 pA pF(-1); and C-nociceptors: -0.26

64 the magnitude of a previously characterized LTM trace, which is manifested as increased calcium infl

65 r inhibition of DNMT eliminates consolidated LTM.

66 20E either enhanced or suppressed courtship LTM, depending on the timing of its administration.

67 ernable ring, while 2 (Aalpha/beta cutaneous LTMs) had weakly stained rings.

68 lanogaster store protein synthesis-dependent LTM (PSD-LTM) as well as protein synthesis-independent,

69 onsolidated into protein-synthesis-dependent LTM remains unclear.

70 l outcomes were compared between 3 different LTM subgroups.

71 ve model for the role of dCREB in Drosophila LTM.

72 fundamental mechanism underlying Drosophila LTM.

73 We found that the swing phase during LTM walking was slightly enhanced as well as some specif

74 the specific actions of ELAV proteins during LTM formation remained to be understood.

75 talk between these two brain regions during LTM formation.

76 ehensively identified genes regulated during LTM consolidation.

77 uts from these MBONs are all required during LTM retrieval.

78 KII autophosphorylation is in fact to enable LTM formation after a single training trial, possibly by

79 se a specific function for CaMK2N1; enabling LTM maintenance after retrieval by inhibiting T286 autop

80 nverted early LTP into late LTP and enhanced LTM.

81 processing in the reorder condition enhanced LTM by strengthening inter-item associations.

82 ther mTORC2 or actin polymerization enhances LTM.

83 rtial training cannot subsequently establish LTM.

84 w that it impairs maintenance of established LTM, but only if retrieval occurs.

85 synapses after retrieval of contextual fear LTM.

86 determines effective training intervals for LTM formation.

87 essential intertrial signaling mechanism for LTM induction.

88 tivation, a necessary signaling molecule for LTM induction, at 45 min after a single TS.

89 smission from MB-V3 neurons is necessary for LTM retrieval; and (v) RNAi-mediated down-regulation of

90 related with effective training patterns for LTM.

91 ease in apc/ebp gene expression required for LTM formation requires the addition of TGFbeta signaling

92 ortens the inter-trial interval required for LTM induction, whereas overexpression of constitutively

93 ing that CaMKII activity is not required for LTM storage.

94 of pretranslational processing required for LTM, which relies on the stabilization of a newly synthe

95 rain are reported now as essential sites for LTM formation, while mushroom bodies are claimed to be u

96 RH-1e-expressing neurons during training for LTM formation abolishes the LTM of the animal.

97 to random Brownian or ATP-dependent forces (LTM).

98 a massed training protocol, but cannot form LTM after a single trial.

99 ase of new items, which are independent from LTM retrieval, masked priming reduced PRC activity and p

100 However, LTMs self-reported lower attentional impulsivity, but hi

101 ory (LTM), and hSyn-HM4D completely impaired LTM formation.

102 oteins (ORBs) in any of these MBONs impaired LTM.

103 ion of CaMK2N2 in dorsal hippocampus impairs LTM formation, but not LTM maintenance, suggesting that

104 rotein translation) in MB-V3 neurons impairs LTM.

105 g protein synthesis in MB-V3 neurons impairs LTM; (ii) MB-V3 neurons show enhanced neural activity af

106 Neither the target of Notch activity in LTM formation nor the underlying mechanism of regulation

107 plicating alphaCaMKII autophosphorylation in LTM formation rather than storage.

108 contrast, produced the anticipated block in LTM formation.

109 Null mutants in creb1/crh-1 are defective in LTM formation across phyla.

110 ysone signaling is reduced were defective in LTM, and that an elevation of 20E levels was associated

111 of the mutants tested revealed a deficit in LTM compared to the robust LTM observed in control flies

112 ntrinsic and synaptic plasticity involved in LTM formation.

113 ntial part of the neural network involved in LTM formation.

114 at a number of these targets are involved in LTM.

115 the requirement of a secreted TrkB ligand in LTM formation at molecular, synaptic, and behavioral lev

116 e recruited for the stabilization of mRNA in LTM formation.

117 the potential importance of ELAV proteins in LTM formation has previously been reported, the specific

118 y whether there is a prior representation in LTM, and not whether the stimulus involves letters or fa

119 get-predictive spatial information stored in LTM triggers spatiotopic modulation of preparatory activ

120 d in various biological processes, including LTM.

121 duced LTF in the CNS, and tail shock-induced LTM but is not necessary for short-term synaptic facilit

122 vel two-trial training pattern which induces LTM in Aplysia, we show that the first of two training t

123 n of resting intervals required for inducing LTM is regulated by activity levels of the protein tyros

124 By using a paradigm that integrates LTM and attentional orienting, we first demonstrate that

125 Intensive LTM training after hemisection was found to change featu

126 (STM) but not LTM, can be consolidated into LTM by exposing animals to novel but not familiar enviro

127 mation of a subthreshold learning event into LTM, whereas CaMKIIalpha-HM4D blocked LTM formation.

128 brain consolidates early labile memory into LTM.

129 dy LTM (0.45 kg; 95% CI: 0.07, 0.84 kg), leg LTM (0.22 kg; 95% CI: 0.02, 0.42 kg), and muscle strengt

130 3 treatments supplemented with 0 (NTM), low (LTM) and high (HTM) TM levels in the same basal diet.

131 d through lean red meat on lean tissue mass (LTM), muscle size, strength and function, circulating in

132 e (including low-threshold mechanoreceptive (LTM) and cooling units).

133 nd cutaneous low-threshold mechanoreceptive (LTM) neurons, 50 had no discernable ring, while 2 (Aalph

134 by cutaneous low threshold mechanoreceptors (LTMs).

135 ciceptive or low-threshold-mechanoreceptors (LTMs) and as having C-, Adelta- or Aalpha/beta-conductio

136 Separately, long-term meditators (LTMs) did not perform differently than meditation-naive

137 resentations in subjects long-term memories (LTM) and that face stimuli used in prior experiments wer

138 rocesses that facilitate long-term memories (LTM) but also the suppression of inhibitory processes th

139 the formation of long-term olfactory memory (LTM).

140 the mechanisms supporting long term memory (LTM) access/retrieval in language and music.

141 Both the formation of long-term memory (LTM) and dendritic spine growth that serves as a physica

142 Both the formation of long-term memory (LTM) and late-long-term potentiation (L-LTP), which is t

143 ddle-term memory (MTM) and long-term memory (LTM) and that their expression is required in the mushro

144 selectively impaired both long-term memory (LTM) and the late phase of hippocampal long-term potenti

145 study of humans engaged in long-term memory (LTM) and working memory tasks.

146 the hippocampus for recent long-term memory (LTM) but then become increasingly independent of the hip

147 of molecular processing in long-term memory (LTM) by describing a novel form of pretranslational proc

148 is not capable of inducing long-term memory (LTM) by itself, flies develop an LTM.

149 n Morris Water Maze (MWM), long-term memory (LTM) contextual fear testing, and rotarod test when comp

150 mTORC2 (A-443654) reverses long-term memory (LTM) deficits in both aged mice and flies.

151 om neuroimaging studies of long-term memory (LTM) encoding have contributed to the view that the vent

152 trials in the induction of long-term memory (LTM) for sensitization in Aplysia californica.

153 DLPFC should contribute to long-term memory (LTM) formation by strengthening associations among items

154 11A is required for social long-term memory (LTM) formation during adolescence and adulthood.

155 Long-term memory (LTM) formation is a critical survival process by which a

156 APK isoforms important for long-term memory (LTM) formation.

157 ture involved in olfactory long-term memory (LTM) formation.

158 EC) that are necessary for long-term memory (LTM) formation.

159 not affect contextual fear long-term memory (LTM) formation.

160 on working memory (WM) and long-term memory (LTM) has not yet been investigated.

161 ormal short-term (STM) and long-term memory (LTM) in a novel object recognition task, but exhibit imp

162 t role in the formation of long-term memory (LTM) in adults, implying that memory formation requires

163 eviously, we reported that long-term memory (LTM) in Aplysia can be reinstated by truncated (partial)

164 use LTF is a substrate for long-term memory (LTM) in Aplysia, we examined the requirement of a secret

165 shown to be necessary for long-term memory (LTM) in Aplysia.

166 for middle-term (MTM) and long-term memory (LTM) in the dorsal paired medial (DPM) neurons, a pair o

167 ity.SIGNIFICANCE STATEMENT Long-term memory (LTM) induced by repeated trials spaced over time is know

168 A property of long-term memory (LTM) induction is the requirement for repeated training

169 Long-term memory (LTM) is believed to be stored in the brain as changes in

170 y (STM) is intact, whereas long-term memory (LTM) is significantly impaired.

171 trials in the formation of long-term memory (LTM) is widely appreciated, surprisingly little is known

172 Forming long-term memory (LTM) often requires repetitive experience spread over ti

173 tion of aversive olfactory long-term memory (LTM) requires multiple training sessions pairing odor an

174 Creating long-term memory (LTM) requires new protein synthesis to stabilize learnin

175 The formation of spatial long-term memory (LTM) requires the de novo synthesis of distinct sets of

176 mporoparietal junction and long-term memory (LTM) retrieval processes are localized to the left later

177 buted to the recovery of a long-term memory (LTM) signal.

178 itial learning defect, but long-term memory (LTM) specifically is abolished under these training cond

179 tophosphorylation mediates long-term memory (LTM) storage.

180 Short-term memory (STM) or long-term memory (LTM) was evaluated in rutabaga (rut) and dunce (dnc) mut

181 grate information coded in long-term memory (LTM) with ongoing perceptual processing remain unknown.

182 eshold learning event into long-term memory (LTM), and hSyn-HM4D completely impaired LTM formation.

183 LTP), a cellular model for long-term memory (LTM), requires de novo protein synthesis.

184 erm potentiation (LTP) and long-term memory (LTM).

185 , synaptic plasticity, and long-term memory (LTM).

186 (LTEE), two correlates of long-term memory (LTM).

187 hly proficient in auditory long-term memory (LTM).

188 tures for the formation of long-term memory (LTM).

189 nts that possess defective long-term memory (LTM).

190 t role in the formation of long-term memory (LTM).

191 tization, a simple form of long-term memory (LTM).

192 ntial for the formation of long-term memory (LTM).

193 lity of C. elegans to form long-term memory (LTM).

194 stent memory identified as long-term memory (LTM).

195 etry (MTC) and laser tracking microrheology (LTM) are described.

196 Latent linear trajectory modeling (LTM) was applied to identify patients with a similar tra

197 Long Term Video-EEG Monitoring (LTM) is the gold standard for diagnosis.

198 Long-term monitoring (LTM) of groundwater remedial projects is costly and time

199 d with I(h) and I(h) density for all non-MSA LTMs, and for Adelta-nociceptors.

200 Look-through mutagenesis (LTM) is a multidimensional mutagenesis method that simul

201 ansmission of food preference (STFP), but no LTM 24 h post training.

202 Importantly, PDE11A KO mice show normal LTM for nonsocial odor recognition.

203 l hippocampus impairs LTM formation, but not LTM maintenance, suggesting that CaMKII activity is not

204 hich induces short-term memory (STM) but not LTM, can be consolidated into LTM by exposing animals to

205 exposure to IMD and TMX affected STM but not LTM.

206 Compared to NTM, LTM reduced area under the curve (AUC) of FPD lesion sco

207 to some extent, the temporary activation of LTM.

208 might be important for repetitive aspects of LTM formation, such as memory consolidation.

209 shortly afterwards, blocks consolidation of LTM and prevents its subsequent induction by truncated t

210 Thus, the consolidation of LTM depends on two functionally distinct phases of prote

211 n of genes regulated during consolidation of LTM.

212 Here, we explore how the contents of LTM optimize perception by modulating anticipatory brain

213 g, we first demonstrate that the contents of LTM sharpen perceptual sensitivity for targets presented

214 n visual cortex according to the contents of LTM.

215 transgene failed to show any enhancement of LTM.

216 on is necessary for the normal expression of LTM.

217 of sleep did not result in the formation of LTM after massed training.

218 ication of DOX might impair the formation of LTM via the p38 MAPK pathway.

219 f the Arc/Arg3.1 ODN showed an impairment of LTM (tested approximately 24 later), but no deficit in S

220 We also found a comparable impairment of LTM in dTORC2-deficient flies, highlighting the evolutio

221 e expression and the behavioral induction of LTM.

222 e regulation is mediated in the induction of LTM.

223 Both the consolidation and maintenance of LTM depend on DNA methylation.

224 anism that contributes to the persistence of LTM.

225 olateral prefrontal cortex was predictive of LTM for words studied on both reorder and rehearse trial

226 e supported by the temporary reactivation of LTM representations.

227 ng protein (CREB), an essential regulator of LTM formation.

228 ies in Drosophila suggest aversive olfactory LTM is optimal after spaced training, multiple trials of

229 xtended neural network involved in olfactory LTM: (i) inhibiting protein synthesis in MB-V3 neurons i

230 ffective for enhancing the effects of PRT on LTM and muscle strength and reducing circulating IL-6 co

231 nd observe whether training regimens (FTM or LTM) can induce durable changes in the parameters of loc

232 istinct connections is associated with WM or LTM benefits.

233 est of postreactivation long-term memory (PR-LTM).

234 reactivation (PR)-STM are intact, whereas PR-LTM is significantly impaired.

235 g-term mindfulness meditation practitioners (LTMs, n = 31) and a matched group of non-meditators (Con

236 ormance, FFA connectivity with MFG predicted LTM improvements.

237 thesis: an early phase that appears to prime LTM; and a later phase whose successful completion is ne

238 ing on-line processing, and this may promote LTM for associations between items.

239 growth factor signaling systems that promote LTM formation.

240 lded premature habituation and depressed PSD-LTM.

241 the consolidation of ARM, it eliminated PSD-LTM.

242 ly active ROCK enhanced ARM and impaired PSD-LTM, while decreasing ROCK activity rescued the enhanced

243 enhanced ARM consolidation and impaired PSD-LTM.

244 The formation of ARM inhibits PSD-LTM but the underlying molecular processes that mediate

245 r store protein synthesis-dependent LTM (PSD-LTM) as well as protein synthesis-independent, anesthesi

246 in synthesis-dependent long-term memory (PSD-LTM), but not anesthesia-resistant memory.

247 consolidation, allowing the formation of PSD-LTM.

248 n of ARM, which permits the formation of PSD-LTM.

249 gest remote LTM can be decoupled from recent LTM, which may have relevance for cognitive deficits ass

250 TFP) despite eliminating or silencing recent LTM for those same social events.

251 ivation (i.e., Arc mRNA) suggests the recent LTM deficits observed in Pde11 knockout mice correspond

252 ingle training trial, possibly by regulating LTM consolidation-specific transcription.

253 cortex of Pde11a knockout mice during remote LTM retrieval may be related to an upregulation of the N

254 In contrast, the enhanced remote LTM observed in Pde11a knockout mice corresponds with in

255 ale mice, deletion of PDE11A enhances remote LTM for social odor recognition and social transmission

256 and more dependent on the cortex for remote LTM.

257 Together, our findings suggest remote LTM can be decoupled from recent LTM, which may have rel

258 ssion in RIM neurons is sufficient to rescue LTM defects of creb1/crh-1-null mutants.

259 aled a deficit in LTM compared to the robust LTM observed in control flies.

260 and precocious doming of the vegetative SAM LTM encodes a kelch domain-containing protein, with no l

261 as a potential mechanism involved in spatial LTM formation.

262 set of MB neurons is converted into a stable LTM through protein synthesis in dendrites of MB-V3 neur

263 emory in the MB are consolidated into stable LTM at a few postsynaptic MBONs through sequential ORB-r

264 in alphaCaMKII autophosphorylation can store LTM after a massed training protocol, but cannot form LT

265 reorder trials was predictive of subsequent LTM.

266 a more general role in promoting successful LTM formation.

267 tal cortex (VLPFC) contributes to successful LTM formation, whereas the dorsolateral prefrontal corte

268 ional repressor, and the crammer and tequila LTM-specific mutations.

269 and tested their short (STM) and long-term (LTM) olfactory memories.

270 e significantly greater for nociceptive than LTM units in all CV groups.

271 could reflect increased fluency rather than LTM retrieval per se.

272 significant improvement would indicate that LTM training maximizes the contribution of spinal locomo

273 Here, we report that LTM can be induced by partial training after disruption

274 We now report that LTM can be induced with only two spaced training trials

275 Biochemical analysis reveals that LTM-inducing training regimens generate repetitive waves

276 Here, we show that LTM storage and synaptic change can be dissociated.

277 ng was partially suppressed, suggesting that LTM functions to suppress SP in the vegetative SAM In ag

278 ing training for LTM formation abolishes the LTM of the animal.

279 ts) in the same enclosure on the FTM and the LTM, the changes in averaged locomotor characteristics m

280 vCA1 alone is sufficient to rescue both the LTM phenotypes and upregulation of NR1 exhibited by Pde1

281 ory-specific patterns of activity during the LTM task, these patterns were not reinstated in PFC duri

282 o acids K247 and K266 as responsible for the LTM related functions of CREB1/CRH-1 while being dispens

283 memory trace was defective in all 26 of the LTM mutants.

284 ) to regularly train cats for 6 weeks on the LTM to determine whether such regular training improves

285 emispinalized and trained for 6 weeks on the LTM, whereas the 3 other cats were hemispinalized and tr

286 In addition, we find evidence that the LTM for sensitization persists covertly after its appare

287 We reasoned that the LTM-trained classifier would be able to decode delay-per

288 bservations elevate the significance of this LTM trace given that 26 independent mutants all exhibit

289 Thus, this LTM/combinatorial beneficial mutagenesis strategy genera

290 rt the view that the DLPFC may contribute to LTM through its role in active processing of relationshi

291 pothesized that the DLPFC does contribute to LTM, but under specific circumstances.

292 pport the view that the DLPFC contributes to LTM formation through its role in organization of inform

293 ian oscillation, both of which are linked to LTM formation.

294 s on the rungs of a moving ladder treadmill (LTM); (2) to assess the capability of cats after a unila

295 paper introduces a method (ladder treadmill [LTM]) to study the locomotor ability of cats with an int

296 vide a narrow molecular window for two-trial LTM formation.

297 row permissive training window for two-trial LTM is accompanied by an equally narrow window of transi

298 We report the novel finding that, under LTM-guided attention, both RH and LH IPS0-2 exhibit bila

299 long-term synaptic plasticity that underlies LTM.

300 system Lymnaea, we investigate here whether LTM formation is associated with specific changes in the