ライフサイエンスコーパス: critical period

1 the pattern of afferent activity during this critical period.

2 ened sensory experience during an early-life critical period.

3 aling is precocious, it induces a precocious critical period.

4 canonical model of plasticity confined to a critical period.

5 xpression during the disease state early-use critical period.

6 blocked by monocular deprivation during the critical period.

7 from long-term MD started at the peak of the critical period.

8 dulation, with impairments restricted to the critical period.

9 be restored to the nervous system after the critical period.

10 tion of leptin is limited to a developmental critical period.

11 by monocular deprivation spanning the entire critical period.

12 coustic influences during an early postnatal critical period.

13 plasticity to the genetic regulation of the critical period.

14 s (P10, P15, and P20) spanning the tonotopic critical period.

15 ystems that are still developing during this critical period.

16 cuits that disappear after the somatosensory critical period.

17 f dendritic segment number during the visual critical period.

18 y and essential step in OD plasticity to the critical period.

19 (SSNs) that disappears by the end of the L4 critical period.

20 , these manipulations are able to reopen the critical period.

21 sine kinase erbB4 regulate the timing of the critical period.

22 ptor 1 (ngr1/rtn4r) is required to close the critical period.

23 ic program of gene expression determines the critical period.

24 y before or as early as possible within this critical period.

25 erience-driven tuning during the post-vision critical period.

26 is progressively lifting the curtain on this critical period.

27 a result of sensory manipulation during the critical period.

28 orrect formation of circuits during cortical critical periods.

29 ting heightened sensitivity to change during critical periods.

30 uits throughout development during specified critical periods.

31 nct phases of postnatal development known as critical periods.

32 marks of cortical plasticity during juvenile critical periods.

33 te, to modulate plasticity levels during the critical period?

34 wing the closure of one eye during a defined critical period [a process referred to as ocular dominan

35 After a critical period, a state of chronic denervation develops

36 period delay by total sensory deprivation or critical period acceleration by deletion of MeCP2, the c

37 o prevailing views of the termination of the critical period, active maintenance of strong excitation

38 Critical period activity modulation via odorant stimuli,

39 These findings suggest a critical period after bleeding events when patients are

40 respond to monocular deprivation during the critical period, altering their morphology, motility and

41 sion (monocular deprivation [MD]) during the critical period alters ocular dominance (OD) by shifting

42 t NRG1/ErbB4 signaling is implicated in both critical period and adult visual cortical plasticity.

43 oids to the developing offspring during this critical period and alters postnatal neurodevelopment.

44 tone-reared mice (7 kHz pips) during the 3-d critical period and collected A1 at P15 and P20.

45 between adolescence and early adulthood as a critical period and the populations that could benefit f

46 of presynaptic boutons increased during the critical period and then declined.

47 l structural remodeling during developmental critical periods and in response to alteration in sensor

48 in L2/3, L5, or L6, prevented closure of the critical period, and adult mice remained sensitive to br

49 resh evidence that mechanisms for regulating critical periods are broadly conserved across evolution.

50 al neuronal functions.SIGNIFICANCE STATEMENT Critical periods are developmental windows of opportunit

51 Critical periods are temporary windows of heightened neu

52 Critical periods are windows of development when the env

53 mice retain plasticity characteristic of the critical period as adults, and that ngr1 operates within

54 ecline, which appears to accelerate during a critical period at 48 to 72 months of age, suggesting in

55 t innervation to inner hair cells during the critical period before the onset of hearing is involved

56 tained transmission, particularly during the critical period before they are detected via clinical or

57 ar response thresholds when treated during a critical period between postnatal day 1 and 5, respectiv

58 bited ocular dominance plasticity during the critical period but rescued plasticity in transgenics wi

59 CS accumulates in PNNs at the critical period, but its function in earlier life is unc

60 ate whether disinhibition is confined to the critical period by ngr1 We demonstrate that ngr1 mutant

61 mon inducers of both onset and offset of the critical period by promoting PV-cell function throughout

62 e mice designed with the goal of identifying critical periods by which exercise may have a lasting im

63 cal control of closure mechanisms during the critical period can potentially impart evolutionarily ad

64 rkness imposed near the trailing edge of the critical period can restore a heightened susceptibility

65 e removing the olfactory stimulus during the critical period can reverse the connectivity changes.

66 We find that TrkB activation during a critical period can substitute for visual experience in

67 ting binocular vision during a developmental critical period can yield enduring changes to ocular dom

68 Abnormal experience during these critical periods can yield enduring maladaptive changes

69 Monocular deprivation (MD) during the visual critical period causes shifts in ocular preference, or d

70 ry input was removed, we determined that the critical period closes around postnatal day 14.

71 Critical period closure is marked by the condensation of

72 Loss of this modulation may contribute to critical period closure.

73 During the visual critical period, closure of one eye elicits changes in t

74 ortical plasticity after closure of juvenile critical period consolidates neural circuits and behavio

75 If accurate, reopening the critical period could make the adult susceptible to path

76 ts that rapid telomere attrition during this critical period could reflect the improved growth in the

77 posed in adulthood or beyond the peak of the critical period could rejuvenate the ability of MD to re

78 e maturation of synapses and circuits during critical period (CP) development in the somatosensory co

79 Experience-dependent critical period (CP) plasticity has been extensively stu

80 implicated in both the onset and closure of critical period (CP) plasticity.

81 rly phase of enhanced sensitivity called the critical period (CP), monocular deprivation causes a shi

82 s of the adult nervous systems develop in a "critical period" (CP), during which high levels of plast

83 ing visual experience during auditory cortex critical periods (CPs) by assessing the influence of ear

84 ensory experience during early developmental critical periods (CPs) has profound and long-lasting eff

85 changes to sensory information occur across Critical Periods (CPs).

86 g normal development and under conditions of critical period delay by total sensory deprivation or cr

87 dulate calcium signaling, activity-dependent critical period development, and the excitation-inhibiti

88 unctional refinement of cortical circuits in critical period development.

89 ugged from hearing onset throughout auditory critical periods displayed impaired behavioral gap detec

90 clinical relevance for the understanding of critical periods disruption in autism spectrum disorder

91 When it is deficient, the critical period does not start.

92 that brief monocular deprivation during the critical period downregulates neuregulin-1(NRG1)/ErbB4 s

93 ctory sensory experience during an early-use critical period drives loss of OSN innervation of antenn

94 h between faces and nonfaces is subject to a critical period during development.

95 Recent studies have begun to define a critical period during early development in which disrup

96 ed expression in developing gonads after the critical period during which sex is determined by incuba

97 t infantile amnesia reflects a developmental critical period during which the learning system is lear

98 These results uncover critical period dysregulation as a novel mechanism in th

99 These results provide the first evidence for critical period dysregulation in NF1 and suggest that tr

100 mportantly, beta1-integrins operate during a critical period equivalent to early adolescence in human

101 At an adult critical period, experience increases fiber number and b

102 nction training, while after closure of this critical period, extinction training only temporarily an

103 al circuit maturation and timing of cortical critical period, features that may be disrupted in neuro

104 nt did not disrupt segregation, indicating a critical period for activity-dependent shaping of patter

105 We find that at the peak of the critical period for binocular plasticity, acetylcholine

106 re still plastic, in line with findings on a critical period for binocular vision development.

107 Early childhood is a critical period for development, and early life stress m

108 Adolescence is a critical period for emotional maturation and is a time w

109 ole of GABAergic signaling in establishing a critical period for experience in visual cortex is well

110 nes may trigger the opening of an adolescent critical period for experience-dependent rewiring of cir

111 mice at gestational day 7.75, targeting the critical period for HPE.

112 an from 600-400 ka (thousand years ago) is a critical period for human evolution in East Asia.

113 arly exposure to AASDs suggest this may be a critical period for inducing long-term functional conseq

114 To temporally delineate closure of this critical period for leptin-stimulated growth, we treated

115 Thus, a critical period for long-term olfactory habituation in D

116 ol and young enough to be within the classic critical period for neuroplasticity [7, 8].

117 sponsible for the opening and closing of the critical period for ocular dominance and how changes in

118 al acuity, inhibition, and regulation of the critical period for ocular dominance plasticity (Hanover

119 y circuits is necessary for the onset of the critical period for ocular dominance plasticity (ODP) in

120 hich closes early in adulthood can, like the critical period for ocular dominance plasticity in mamma

121 terns during early cortical development, the critical period for ocular dominance plasticity is short

122 cible in adults after the termination of the critical period for ocular dominance plasticity, and can

123 plicated in the control of the timing of the critical period for ocular dominance plasticity.

124 that ngr1 limits disinhibition to close the critical period for OD plasticity and that a decrease in

125 ing environmental conditions accelerates the critical period for plasticity in the primary visual cor

126 vioral plasticity.SIGNIFICANCE STATEMENT The critical period for plasticity represents a stage of lif

127 amine signaling cascade is required during a critical period for promotion of social-context-dependen

128 Exposure during early gestation, a critical period for reproductive development, is of part

129 th fundus photography and OCT to determine a critical period for retinal intervention.

130 amined the role of TrkB signaling during the critical period for RF refinement in SC.

131 hylendioxymethamphetamine (MDMA) reopens the critical period for social reward learning and leads to

132 sion) in the nucleus accumbens establishes a critical period for social reward learning.

133 ral folds at gestational day 8.25 during the critical period for subsequent forebrain division.

134 successfully bridged the animals through the critical period for survival after acute liver failure,

135 peeding of NMDA receptor kinetics during the critical period for TC plasticity, despite no reduction

136 ies to defective channel function during the critical period for thalamic network stabilization in im

137 mary auditory cortex (A1) of mice exhibits a critical period for thalamocortical connectivity between

138 haly also indicate prenatal development as a critical period for this condition.

139 netic tolerance induction studies revealed a critical period for TLR2 involvement in adoptive transfe

140 during development around the time that the critical periods for developmental plasticity end and ar

141 n localization in the lower urinary tract at critical periods for forebrain division and urogenital d

142 sex, timing and type of stress exposure, and critical periods for intervention in various brain syste

143 and pod-fill periods were identified as the critical periods for irrigations and affected the nutrit

144 st cancer risk, younger ages may be the more critical periods for lifestyle modifications aimed at br

145 Further observations show that critical periods for plasticity can be regulated by spat

146 cted mechanisms, potentially allowing varied critical periods for plasticity to stimuli of different

147 ture stages, adult-born neurons pass through critical periods for survival and plasticity.

148 irst postnatal month, corresponding to known critical periods for synapse and neuron formation in mou

149 d the importance of visual experience during critical periods for the development of normal sensory-e

150 A critical period governs memory performance during the fi

151 identification of manipulations that reopen critical periods has been a priority for translational n

152 Mechanistic characterization of critical periods has revealed an important role for exub

153 nocular deprivation during the developmental critical period impairs binocular integration in mouse p

154 ht a novel regulatory pathway that creates a critical period in brain development vulnerable to dysre

155 how that depriving one eye of input during a critical period in development chronically impairs binoc

156 During a critical period in development, spontaneous and evoked r

157 al system, normal visual experience during a critical period in early life drives the matching of ind

158 ientation preference is established during a critical period in early life, but the underlying circui

159 During a critical period in early life, neurons in the primary vi

160 nce plasticity is easily observed during the critical period in early postnatal life.

161 ansion of commensal ecology after birth is a critical period in human immune development.

162 bipolar disorder (BD), with adolescence as a critical period in its development.

163 he host and microbial factors governing this critical period in Pseudomonas aeruginosa pulmonary path

164 s, we have discovered a narrowly constrained critical period in Purkinje neuron development subject t

165 We have identified a critical period in rat development during the second wee

166 Reopening the critical period in the adult restores vulnerability to s

167 Long-lasting imprinted aversion has a critical period in the first larval stage and is specifi

168 Alzheimer's disease or related dementia is a critical period in the process of transitioning into car

169 nding patterns of network development during critical periods in at-risk children may inform strategi

170 Identifying and understanding critical periods in brain development is essential to de

171 New research on plasticity and critical periods in development, increasing understandin

172 es, can impair ability to autoresuscitate at critical periods in postnatal development and that basel

173 ial signals by emphasizing the occurrence of critical periods in the development of its sensory gatin

174 through mechanisms typical of developmental critical periods, including the expression switch of the

175 er-expression of Toll-2 and wek at the adult critical period increased brain size.

176 ain of function and neuronal activity at the critical period increased cell number.

177 ge of isotonic intravenous saline during the critical period increased from 57% to 90% in adult patie

178 A critical period is a developmental epoch during which th

179 The formation of imprinted memories during a critical period is crucial for vital behaviors, includin

180 aling in PV-INs during and shortly after the critical period is necessary for the expression of LTP a

181 fferentiated across cortical regions in this critical period is unknown.

182 and the concomitant impact on plasticity and critical periods, is hypothesized to be disrupted in neu

183 amplitudes; but when administered after the critical period, it only restored GABA(B) receptor-media

184 mice, we demonstrate that 14 d MD during the critical period leads to a chronic loss of binocular dLG

185 oval of the odorant stimulus only during the critical period leads to OSN reinnervation, demonstratin

186 PTPsigma-CSPG complex.SIGNIFICANCE STATEMENT Critical period-like plasticity can be reactivated in th

187 n to promote TRKB phosphorylation and reopen critical period-like plasticity in the adult brain, disr

188 ropose that both chABC and fluoxetine reopen critical period-like plasticity in the adult visual cort

189 uding visual deprivation, are able to induce critical period-like plasticity in the visual cortex of

190 In disease states, closure of critical periods limits the ability of the brain to adap

191 Understanding how plasticity is confined to critical periods may provide clues how to better treat a

192 Our data demonstrate that critical-period MD produces long-lasting disruptions in

193 Following the critical period NMDA receptor function was unaffected by

194 tical layer (L) a gene required to close the critical period, nogo-66 receptor (ngr1).

195 splanted neurons reach the age of the normal critical period of activity-dependent ocular dominance (

196 visual cortex, such neurons induce a second critical period of activity-dependent plasticity when th

197 tone promote microglia phagocytosis during a critical period of amygdala development.

198 e a mild, reversible hearing loss during the critical period of auditory cortex development.

199 effects in one amygdala hemisphere during a critical period of brain development could guide further

200 If such violations occur during a critical period of brain development, the detrimental ef

201 rly pharmacological treatment to target this critical period of brain development.

202 er (MDD) often emerges during adolescence, a critical period of brain development.

203 The disease occurs during a critical period of brain vascular development, is charac

204 ity of interneurons in Fmr1 KO mice during a critical period of cortical development.

205 Puberty is a critical period of development marked by sexual, immune,

206 e incubation temperature of the egg during a critical period of development.

207 , including: (1) a vulnerable neonate; (2) a critical period of development; (3) evidence of hypoxia;

208 tion and atmospheric oxygenation during this critical period of Earth history.

209 understanding of vertebrate phylogeny over a critical period of evolutionary expansion.

210 that ancestral exposure to vinclozolin at a critical period of gestation induces the epigenetic tran

211 We define the critical period of GR intervention as the first 1-week p

212 rom the dam for three hours per day during a critical period of hippocampal development (PNDs 2-14).

213 napses and raise the possibility of an early critical period of hippocampal plasticity that may ultim

214 inadequacy of oral iron in late pregnancy, a critical period of iron need for normal foetal brain dev

215 Exposure to UFPs during a critical period of lung development was linked to the on

216 naptic connectivity during the developmental critical period of neural circuit optimization for senso

217 ulated when energy depletion occurs during a critical period of neuronal maturation.

218 of valproate (VPA), which can re-instate the critical period of plasticity via histone deacetylase (H

219 During the critical period of postnatal development, neuronal prope

220 striatal synaptic plasticity during an early critical period of postnatal development, which suggests

221 mmature motor systems that develop through a critical period of postnatal development.

222 males exposed to excessive androgen during a critical period of prenatal development.

223 within proliferating blastema cells during a critical period of regeneration.

224 ce supporting the idea that adolescence is a critical period of the development that is vulnerable to

225 s improved nutrition among women during this critical period of the life course.

226 various postnatal timepoints and identify a critical period of vulnerability to GALC ablation betwee

227 re easily be breached by inflammation during critical periods of brain development.

228 e of timing and timescales in plasticity and critical periods of brain development; epigenetics and t

229 Exposure to distinct stimuli during critical periods of development can affect behavior long

230 Exposure to stress during critical periods of development can have adverse effects

231 endocrine-disrupting chemicals (EDCs) during critical periods of development can result in altered br

232 Unregulated stress during critical periods of development is proposed to drive def

233 oreover, ELS may further accelerate or delay critical periods of development, which reflect GABA circ

234 re to multiple industrial carcinogens during critical periods of development.

235 are shaped by incoming sensory inputs during critical periods of development.

236 f cardiac myocytes induced by hypoxia during critical periods of development.

237 ral circuits are shaped by experience during critical periods of development.

238 emodeling of primary sensory cortices during critical periods of development.

239 of experimentation, the mechanisms by which critical periods of enhanced synaptic plasticity are ini

240 Suboptimal vitamin D levels during critical periods of immune development have emerged as a

241 nvironmental exposures simultaneously during critical periods of life.

242 ribute to the acute defense potential during critical periods of migration-based DC absence.

243 which compromises fetal brain development at critical periods of pregnancy and might be causally link

244 , such as introducing a means of identifying critical periods of risk for mental state deterioration.

245 turation is associated with the end of early critical periods of synaptogenesis.

246 regarding cumulative impacts during specific critical periods of the life course.

247 been considered as a glacial refugium during critical periods of the Neanderthal timeline and might t

248 s are thought to play a key role during the "critical period" of brain development, the nature and ti

249 dismantling the binocular circuit present at critical period onset and building it anew.

250 st binocular neurons present in layer 2/3 at critical period onset are poorly tuned and are rendered

251 g confirmed GABA circuit function determines critical period onset, while Nogo receptor signaling is

252 Critical periods open with the onset of sensory experien

253 have examined adult-born neurons beyond the critical period or directly compared them to neurons bor

254 lasting deficits attributed to MD during the critical period originate in the thalamus.

255 Activating TrkB receptors during the critical period (P33-P40) in dark reared subjects produc

256 nrg1 and nrg3 decreases in PV neurons at the critical period peak, postnatal day 28 (P28) after monoc

257 citation onto FS INs is a key determinant of critical period plasticity and is maintained at high lev

258 In the visual system, critical period plasticity drives the establishment of b

259 This yields the first precise time course of critical period plasticity for an inhibitory circuit.

260 ation through dark exposure (DE) reactivates critical period plasticity in adults.

261 ffers from more commonly studied examples of critical period plasticity in visual pathways in that it

262 ovel mechanisms involved in both induced and critical period plasticity.

263 ting MET signaling leads to early closure of critical period plasticity.

264 al conditions experienced during a short but critical period play a central role in the demography of

265 SGRI treatment during the critical period prevented the hearing loss-induced reduc

266 ly, suppressing SST cell activity during the critical period prevents the normal development of binoc

267 cular deprivation (MD) during the adolescent critical period produces marked enhancement of GABAergic

268 many of these interneurons at the end of the critical periods reduces their plasticity and sets their

269 hibition is increased during development and critical period regulation is disturbed.

270 d schizophrenia, are linked to disruption of critical period remodeling.

271 MDMA-induced reopening of this critical period requires activation of oxytocin receptor

272 ce in early postnatal life, during so-called critical periods, restructures neural circuitry to enhan

273 Experiences during the critical period sculpt the circuitry within the neocorte

274 ng of brain neural circuitry in an early-use critical period.SIGNIFICANCE STATEMENT Neurodevelopmenta

275 However, the molecular mechanisms underlying critical period synaptic plasticity are unclear.

276 tion of the brain occurs during a restricted critical period that begins in utero and overlaps with t

277 the consequences of MD likewise adheres to a critical period that ends by about 3 months of age, afte

278 e visual system is restricted to a so-called critical period that, for cats, peaks at about one postn

279 vely and qualitatively similar to the normal critical period; that is, short-term occlusion of either

280 During a developmental critical period, the most dramatic consequence of occlud

281 In mice before the critical period, the thalamic input is already slightly

282 Despite the recognition of this critical period, there have been few evaluations of the

283 the receptor tyrosine kinase erbB4 determine critical period timing by controlling the strength of ex

284 at the hippocampus undergoes a developmental critical period to become functionally competent.

285 rcome the challenges encountered during this critical period to ensure optimal care.

286 dent plasticity observed during the juvenile critical period: to rapidly reduce the activity of parva

287 ce during a discrete developmental time, the critical period, trigger robust changes in the visual co

288 f NRG1/ErbB4 in regulating the initiation of critical period visual cortical plasticity.

289 Taken together, our results suggest that critical period visual experience induces global changes

290 sual deprivation, we examined the effects of critical period visual experience on the development of

291 l knock-in of wild-type ephrin-B3 during the critical period when axon targeting and fear responses a

292 stereopsis emerges during an early postnatal critical period when binocular neurons in the primary vi

293 Early childhood has emerged as a critical period when these factors have a dramatic impac

294 is relationship may help clinicians identify critical periods when patients are at highest risk.

295 synaptic remodeling occurs during early-use critical periods, when naive juveniles experience sensor

296 a brief interval of plasticity, termed the "critical period," when the circuitry of primary visual c

297 ce-dependent remodeling during an early-life critical period, which requires olfactory reception, OSN

298 former is responsible for the opening of the critical period, while the latter limits the plasticity

299 inance plasticity during the normal cortical critical period; while ablating MET signaling leads to e

300 s a "lower PV network configuration" in both critical-period wild-type mice and adult ngr1(-/-) mice.