ライフサイエンスコーパス: critical period

1 canonical model of plasticity confined to a critical period.

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

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

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

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

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

7 ic program of gene expression determines the critical period.

8 tic environment during the auditory cortical critical period.

9 s facilitated in part by experience during a critical period.

10 enriched genes that are prominent during the critical period.

11 ulates the initiation and termination of the critical period.

12 dulation, with impairments restricted to the critical period.

13 plastic even beyond the peak of its natural critical period.

14 nt during a time commonly referred to as the critical period.

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

16 g from excessive anticoagulation during this critical period.

17 bout inhibitory neurotransmission during the critical period.

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

19 rticularly when recovering vision during the critical period.

20 when visual deprivation persists beyond the critical period.

21 es only after the completion of the thalamic critical period.

22 ehavioral and cognitive deficits during this critical period.

23 dependent mechanisms only operate during the critical period.

24 units from neonatal to adult form around the critical period.

25 sensitive to the cue is often described as a critical period.

26 by monocular deprivation spanning the entire critical period.

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

28 coustic influences during an early postnatal critical period.

29 blocked by monocular deprivation during the critical period.

30 plasticity to the genetic regulation of the critical period.

31 ystems that are still developing during this critical period.

32 cuits that disappear after the somatosensory critical period.

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

34 nct phases of postnatal development known as critical periods.

35 hibition determines the onset and closure of critical periods.

36 en after early blindness that extends beyond critical periods.

37 n a mechanistic continuum with developmental critical periods.

38 ntrol of brain plasticity and the closure of critical periods.

39 orrect formation of circuits during cortical critical periods.

40 pes A1 binaural selectivity during two early critical periods.

41 ting heightened sensitivity to change during critical periods.

42 uits throughout development during specified critical periods.

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

44 em that is maximal early in life, within the critical period [1-3].

45 and to modulate the onset and offset of the critical period [4, 5].

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

47 Critical period activity modulation via odorant stimuli,

48 patient has the closest relationships in the critical period after a cancer diagnosis--is in a unique

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

50 of EGFR-expressing progenitor cells during a critical period after brain injury, and promotes cellula

51 at address parental mental health during the critical period after the child's autism diagnosis when

52 f hyperstimulation, providing evidence for a critical period after which proper microvascular pattern

53 During critical periods, all cortical neural circuits are refin

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

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

56 lated with a precocious onset and closure of critical period and deficient binocular visual function

57 or the development of depression during this critical period and thus may provide clues as to etiolog

58 se findings suggest that current accounts of critical periods and experience-dependent development sh

59 On the other hand, the "critical period" and newly emerged "biomarkers window" h

60 Critical periods are developmental time windows during w

61 Critical periods are developmental windows during which

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

63 Critical periods are temporary windows of heightened neu

64 During nervous system development, critical periods are usually defined as early periods du

65 rected by applying exogenous strain during a critical period around gastrulation.

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

67 This form of plasticity is restricted to a critical period before the developmental change in GABAe

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

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

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

71 cular dominance column plasticity during the critical period, but later research has suggested otherw

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

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

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

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

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

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

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

79 An early OT treatment in this critical period could be a novel therapeutic approach fo

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

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

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

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

84 asticity occurs on the cusp of the canonical critical period (CP).

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

86 ge acquisition research is whether there are critical periods (CPs) in development during which the s

87 ing windows of heightened plasticity termed "critical periods" (CPs).

88 asses exhibit distinctive activity-dependent critical period dendritic remodeling.

89 was used to explore the relationship between critical period dendritic spine abnormalities, cortical

90 sculpting dendritic arbors during early-use, critical period development of learning and memory circu

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

92 hannelrhodopsin-driven depolarization during critical period development, but are reduced by halorhod

93 unctional refinement of cortical circuits in critical period development.

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

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

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

97 These data also suggest that critical-period duration links synapse maturation rates

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

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

100 s and suggest that early postnatal life is a critical period during which nutrition can affect hypoth

101 that early and mid-adolescence constitute a critical period during which repeated CB1 receptor stimu

102 r results suggest that P11-P23 encompasses a critical period during which sensory deprivation disrupt

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

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

105 o the mouse bulbar circuitry and highlight a critical period during which the principal cells' activi

106 pression of SK2 channels, we identified the "critical period" during which spiking activity influence

107 rience-dependent functional optimization and critical periods end.

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

109 nty-four children in grade 3 (ages 8-9 y), a critical period for acquisition of basic mathematical sk

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

111 is highly expressed at axon tips during the critical period for axon development.

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

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

114 e in a brain state-dependent manner during a critical period for experience-dependent plasticity.

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

116 Midlife may be a critical period for initiating treatments to lower perip

117 Dusk is a critical period for interactions amongst species in this

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

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

120 al cortical principal neurons terminates the critical period for ocular dominance plasticity but also

121 was sufficient to govern the duration of the critical period for ocular dominance plasticity in the v

122 PV) INs plays a central role in enabling the critical period for ocular dominance plasticity.

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 er monocular lid suture is restricted to the critical period for ODP and appears to be necessary for

126 ction of PV cell firing rates can extend the critical period for ODP.

127 One critical period for optimizing human language mapping is

128 ptic circuits defines the time window of the critical period for plasticity in sensory cortices.

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

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

131 The critical period for relevant recovery of renal function

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

133 This defines a previously undocumented critical period for SGN survival.

134 Adolescence is a critical period for suboptimal behavioral choices and th

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

136 lso reveal that adult-generated neurons in a critical period for survival use GABA signaling to rapid

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

138 ars in life are increasingly recognized as a critical period for the development of diet-related beha

139 significantly, demonstrating that there is a critical period for the regeneration of cochlear support

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

141 We show the presence of distinct critical periods for Atoh1 in each of these functions, s

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

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

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

145 We then go on to discuss how the critical periods for these genetic deficits will shape t

146 rator-VEGF-C double-transgenic mice during a critical period from embryonic day 15.5 to postnatal day

147 A critical period governs memory performance during the fi

148 nt animal and human studies now support the "critical period" hypothesis for E2 neuroprotection where

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

150 none have demonstrated the creation of a new critical period in adulthood.

151 ightened expression of GlyRalpha1 around the critical period in all respiratory-related nuclear group

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

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

154 Epidemiological data point toward a critical period in early life during which environmental

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

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

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

158 n induce pulmonary lymphangiectasia during a critical period in perinatal development.

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

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

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

162 ircuits in juvenile visual cortex triggers a critical period in the development of the visual system.

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

164 pressing specific odorant receptors during a critical period in the formation of the olfactory sensor

165 The school years are known to be a critical period in the life course for shaping attitudes

166 ity induced by pure tone exposure during the critical period in the primary auditory cortex.

167 xamine neurochemistry in children during the critical period in which the neurocircuits that support

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

169 issions (DPOAEs), and to further clarify the critical periods in development where cochlear status ma

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

171 Experience shapes neural circuits during critical periods in early life.

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

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

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

175 is study, their accumulation relative to the critical period indicates that they may contribute to th

176 properties in cortical regions that underlie critical periods influence the onset and duration of win

177 lasticity and synaptic refinement during the critical period is altered in the cortex of fragile X mi

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

179 racteristic of bs seizure models, during the critical period is sufficient to suppress seizure.

180 The timing of critical periods is regulated by both genetics and the e

181 t evidence to suggest that learning during a critical period may be important for how animals respond

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

183 Following the critical period NMDA receptor function was unaffected by

184 ns of inhibition can alter the timing of the critical period, none have demonstrated the creation of

185 KO mice undergo accelerated death during the critical period of 2-3 wk around their birth and exhibit

186 nal WldS expression postaxotomy, we reveal a critical period of 4-5 h postinjury during which the cou

187 During the critical period of a few weeks after birth when newborn

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

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

190 l exposure to solvents before first birth, a critical period of breast tissue differentiation, may re

191 We identify a critical period of cellular developmental during which n

192 During the critical period of commitment around 24 to 30 h poststar

193 lated proteolysis both before and during the critical period of commitment to sporulation.

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

195 nces that lead to hospitalization-during the critical period of development of the first 2 years of l

196 AeYA is a critical period of development, and cancer during this p

197 itatory afferent input for survival during a critical period of development.

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

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

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

201 In this study we describe a critical period of embryonic development in Drosophila d

202 ulation (stage 8-12.5) was identified as the critical period of exposure leading to left-right (LR) p

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

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

205 xpression and function is altered during the critical period of hippocampal development.

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

207 death and, in particular, the existence of a critical period of increased risk.

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

209 Here, we identify a critical period of olfactory sensory axon targeting duri

210 y impacts the thyrotrope population during a critical period of pituitary development and may have lo

211 mouse visual cortex before the onset of the critical period of plasticity [postnatal day 5 (P5)], at

212 ggest that ongoing mGluR5 signaling during a critical period of postnatal development establishes the

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

214 A critical period of respiratory development occurs in rat

215 and MCs exhibit correlated activity during a critical period of retinal maturation that is enabled by

216 r LTP and silent synapse activation during a critical period of synapse development.

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

218 Indeed, there is a critical period of time when all communications are lost

219 nement of neural circuit connectivity during critical periods of brain development is essential for o

220 n development, coinciding with the ending of critical periods of brain development.

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

222 to play an important role in the opening of critical periods of brain plasticity.

223 ese findings support the idea that disrupted critical periods of dendritic growth and spine plasticit

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

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

226 Is visual input during critical periods of development crucial for the emergenc

227 During critical periods of development early in life, excessive

228 Drug exposure during critical periods of development is known to have lasting

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

230 osed to potentially harmful chemicals during critical periods of development.

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

232 inhibitory synapse protein expression during critical periods of early postnatal development that cou

233 on and other environmental influences during critical periods of embryonic, fetal, and early postnata

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

235 ing inhibitory interneurons normally defines critical periods of experience-dependent cortical plasti

236 intrauterine perfluorocarbon exposure during critical periods of fetal development is urgently needed

237 nal circuits are shaped by experience during critical periods of heightened plasticity.

238 ain injury survivors, by taking advantage of critical periods of high plasticity during childhood, sh

239 no longer result in reward, but only during critical periods of learning.

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

241 Visual plasticity peaks during early critical periods of normal visual development.

242 Synaptic rearrangements during critical periods of postnatal brain development rely on

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

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

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

246 Hjort (1914) famously attributed this "critical period" of low survival to the larvae's inabili

247 presentations during an early developmental "critical period" of plasticity.

248 tributed to everyday L2 use, irrespective of critical periods or the length of L2 learning.

249 We derive a behavioral model that reveals a critical period over which information about the food en

250 delayed circuit maturation with a prolonged critical period permissive for giant depolarizing potent

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

252 yonic inhibitory interneurons can reactivate critical period plasticity and reverse amblyopia in the

253 ns in the mouse primary visual cortex, where critical period plasticity drives binocular matching of

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

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

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

257 rs independently from NE, NE is required for critical period plasticity in auditory cortex.

258 loped a transplantation method to reactivate critical period plasticity in the adult visual cortex.

259 t circadian clock genes control the onset of critical period plasticity in the neocortex.

260 n the visual system, the normal unfolding of critical period plasticity is strongly dependent on the

261 in-positive cells and examined the impact on critical period plasticity using the visual system as a

262 ortex led us to re-examine the role of NE in critical period plasticity.

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

264 ynapse maturation influences the duration of critical-period plasticity windows.

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

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

267 Disruption of experience during a critical period produces neurons that lack specificity f

268 hanisms that shape synapse development alter critical-period properties.

269 n the visual cortex after the closure of the critical period reinstated silent synapses, resulting in

270 At the end of cortical critical period, response properties of GABA transform i

271 ynapses, and its absence before the onset of critical periods resulted in lifelong juvenile ocular do

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

273 ession rescued the precocious opening of the critical period, suggesting its major role in MECP2-medi

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

275 Here, we describe, in mice, a developmental critical period that affects plasticity itself.

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

277 that the resolution phase of infection is a critical period that influences the quality and function

278 nhibitory cell transplantation creates a new critical period that restores visual perception after ch

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

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 impaired by deprivation during the juvenile critical period, transplantation also recovers both visu

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

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

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

289 This early critical period was revealed by the temporally controlle

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

291 Infancy may be a critical period when environmental factors exert a lasti

292 f the rat around postnatal days (P) 12-13, a critical period when the hypoxic ventilatory response is

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

294 disruption of these events, during specific critical periods when they exert maximal influence, may

295 Early life may be a "critical period" when appetite and regulation of energy

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

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

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

299 life beginning shortly after the peak of the critical period, with the highest levels measured in adu

300 Plasticity and recovery are induced when the critical period would have occurred in the donor animal.