ライフサイエンスコーパス: postnatal week

1 solated from rodents at the end of the first postnatal week.

2 s detectable paternal Ube3a beyond the first postnatal week.

3 a similar length toward the end of the first postnatal week.

4 antly increase in the heart during the first postnatal week.

5 s calcium action potentials during the first postnatal week.

6 the developing cortical plate in the second postnatal week.

7 ression levels were highest during the first postnatal week.

8 - 0.14 cell/40-mum section during the second postnatal week.

9 ion and myelination recover during the first postnatal week.

10 ype levels in the brain beginning the second postnatal week.

11 irth and are fully established by the second postnatal week.

12 nd continuing to do so well after the eighth postnatal week.

13 tinguish gamma-from alpha-MNs into the third postnatal week.

14 ed, GDNF-independent signal during the first postnatal week.

15 creased in the Ts65Dn mice during the second postnatal week.

16 e SO in vestibular hair cells over the first postnatal week.

17 l cortex becomes prominent during the second postnatal week.

18 e patterns by the end of the third or fourth postnatal week.

19 ge-matched controls at the end of the second postnatal week.

20 rent input and begin to die during the first postnatal week.

21 icotinic acetylcholine currents in the third postnatal week.

22 these synapses between the first and second postnatal week.

23 del-COMP triggers apoptosis during the first postnatal week.

24 recovery in beta2-/- mice during the second postnatal week.

25 1) to the SC is established during the first postnatal week.

26 ath of these animals near the end of the 2nd postnatal week.

27 rtical activity only by the end of the first postnatal week.

28 g a short window during the second and third postnatal week.

29 g and excitability decreasing into the third postnatal week.

30 icantly increased in diameter over the first postnatal week.

31 l coupling was decreasing, during the second postnatal week.

32 downregulate its expression during the first postnatal week.

33 and die because of seizures during the third postnatal week.

34 nscript and protein occurs during the second postnatal week.

35 postnatal week, but return during the second postnatal week.

36 by BAX-dependent apoptosis during the first postnatal week.

37 mature in the outer retina during the second postnatal week.

38 thood, with peak expression during the first postnatal week.

39 he AS-related theta rhythm during the second postnatal week.

40 frequency range (30-80 Hz) during the fourth postnatal week.

41 inputs relative to controls after the first postnatal week.

42 synaptic development beginning in the first postnatal week.

43 y 13, reaching maximal enrichment by the 3rd postnatal week.

44 activation and for survival beyond the first postnatal week.

45 eaching adult levels at the end of the third postnatal week.

46 he rest of embryogenesis and into the second postnatal week.

47 e neurological deficits and die in the third postnatal week.

48 occur significantly later, during the first postnatal week.

49 diated inputs to D1 SPNs, both in the second postnatal week.

50 d currents compared to wildtype in the third postnatal week.

51 , tonic NMDA current at the end of the first postnatal week.

52 ring development, until the end of the third postnatal week.

53 erent strata of CA3 in rats during the third postnatal week.

54 Pcdh19 and Ncdh expression during the first postnatal week.

55 rred mostly between the second and the third postnatal week.

56 ons and inhibitory interneurons in the first postnatal week.

57 of the deep cortical layers until the first postnatal week.

58 m thalamocortical afferents during the first postnatal week.

59 obtain adult-like features until the fourth postnatal week.

60 e apparent at embryonic day 18 and the first postnatal week.

61 olarizing potentials (GDPs) during the first postnatal week.

62 ons and inhibitory interneurons in the first postnatal week.

63 hat specifically targets L4 during the first postnatal week.

64 ntiate from retinal progenitors in the first postnatal week.

65 DSGCs at the beginning and end of the second postnatal week.

66 epithelia of ILDR1 null mice after the first postnatal week.

67 nditioning begins to emerge during the third postnatal week.

68 air cells degenerate rapidly after the first postnatal week.

69 tivity-dependent refinement during the first postnatal weeks.

70 ion of protein malnutrition during the first postnatal weeks.

71 elected brain regions during the first three postnatal weeks.

72 effect was smaller and confined to the first postnatal weeks.

73 s place almost entirely in the first several postnatal weeks.

74 rk activity, especially during the first two postnatal weeks.

75 lly during development, but die in the early postnatal weeks.

76 fiber inputs mature gradually over the first postnatal weeks.

77 but markedly increased during the first 2-3 postnatal weeks.

78 rain amoeboid microglia during the first two postnatal weeks.

79 in barrel cortex during the third and fourth postnatal weeks.

80 pment, and are active only for the first few postnatal weeks.

81 ly isolated from rats during the first three postnatal weeks.

82 xcitatory to inhibitory during the first two postnatal weeks.

83 and density of SMI-32(+) neurons around 2-5 postnatal weeks.

84 development, peaking in the first to second postnatal weeks.

85 re anatomical features until approximately 8 postnatal weeks.

86 cy and amplitude increase during the first 3 postnatal weeks.

87 l ganglion cells (RGCs) during the first two postnatal weeks.

88 s is transient, being limited to the first 3 postnatal weeks.

89 transiently express syt 2 during the first 2 postnatal weeks.

90 ses progressively increased over the first 2 postnatal weeks.

91 ity within neural circuits, during the first postnatal weeks.

92 Aergic to glycinergic within the first three postnatal weeks.

93 liculus does not change across the first two postnatal weeks.

94 ciceptive spinal activity in the first three postnatal weeks.

95 ses muscle calcium levels during the first 2 postnatal weeks.

96 etion was induced in OPCs during the first 2 postnatal weeks.

97 eased muscle calcium only during the first 2 postnatal weeks.

98 each their ventral destinations during first postnatal weeks.

99 ing in developing mouse cardiomyocytes after postnatal week 1, a time when the cells are no longer di

100 on in mature spermatids observed as early as postnatal week 1.

101 were returned to a non-obesiogenic diet from postnatal week 11 onwards.

102 g1 mice but falls below control levels after postnatal week 12, approximately correlating with the on

103 protocols administered to 30 monkeys between postnatal weeks 17 and 27.

104 nonstress control condition (NS; n = 9) from postnatal weeks 17 to 27.

105 in the photoreceptor outer nuclear layer at postnatal week 2 and highly disorganized outer segments

106 orn: selective block of afferent C fibers in postnatal week 2, using perisciatic injections of the ca

107 on: developmental upregulation of CDF during postnatal week 2.

108 rojections using anterograde tracers between postnatal week 3 (PW3) and PW16.

109 mentally regulated and is undetectable after postnatal week 3.

110 sistent, location-depicting ensembles during postnatal week 3.

111 rs at postnatal day 10, followed by death at postnatal week 3.

112 At postnatal week 35, each mother-offspring dyad underwent

113 was noted at 5 months of age and as early as postnatal week 4 in the eyes of four BBS mouse model str

114 us preconfigured sequences only during early postnatal week 4.

115 In contrast, depletion of BRAG2 during postnatal weeks 4 and 5 reduced the number of AMPAR mini

116 2 and highly disorganized outer segments by postnatal weeks 4 to 6 was observed in all four strains.

117 ring the establishment of emmetropia between postnatal weeks 4-6.

118 ivity unilaterally during a critical period [postnatal week 5 (PW5) to PW7] produces permanent contra

119 ats before and after interneuron maturation [postnatal week 5 (PW5) to PW7].

120 velopment and neurological morphology before postnatal week 5.

121 tivated M1 by muscimol microinfusion between postnatal weeks 5 and 7 to examine activity-dependent in

122 ed motor cortex by muscimol infusion between postnatal weeks 5 and 7.

123 We first inactivated M1 unilaterally between postnatal weeks 5-7.

124 mRNA in thoracic aortas (gestational day 20, postnatal week 7 and 16).

125 collected from embryonic day 12.5 (E12.5) to postnatal week 8 (W8), encompassing major developmental

126 ntrollable movements, and premature death by postnatal week 9-10.

127 In mice, this ability is lost in the first postnatal week, a period physiologically similar to thyr

128 inal development during the second and third postnatal weeks, a period that corresponds to human embr

129 ration of these tissues over the first three postnatal weeks, a time when the normal cortex expands a

130 ironment, becomes more evident with age (> 7 postnatal weeks), activity and stress, is gender specifi

131 postnatal week (juvenile ELE, P21-27), 6(th) postnatal week (adolescent ELE, P35-41), or 4(th)-6(th)

132 t expressed by interneurons until the second postnatal week after reaching the cortex, suggesting tha

133 Arbor remodeling begins during the second postnatal week, after migration to and dispersion within

134 nock-out mice, we show that during the first postnatal week, alpha-syn is not required for synapse fo

135 e and retarded growth starting at the second postnatal week and died on approximately postnatal day 2

136 NS in developing hepatocytes from the first postnatal week and increased DNA damage and hepatocellul

137 letion in hippocampal CA1 cells in the third postnatal week and later throughout the neocortex, brain

138 ssion profile present only during the second postnatal week and not the first or third weeks.

139 pressed in some VBN neurons during the first postnatal week and sharply declined over the second week

140 cortical inputs to SPNs emerge in the second postnatal week and that SPNs that receive superficial co

141 blished in the inner retina during the first postnatal week and that these systems subsequently matur

142 te that mouse microglia mature by the second postnatal week and to predict novel microglial functions

143 es of BG microglia emerged during the second postnatal week and were re-established following genetic

144 ed the retinal vasculogenesis in the first 2 postnatal weeks and impaired the angiogenesis triggered

145 dergoes profound regulation over the first 4 postnatal weeks and that these changes are correlated wi

146 y had achieved their adult-like anatomy by 4 postnatal weeks and were in a position to influence the

147 ) mitochondria become abnormal by the second postnatal week, and a majority of PNs die in the fourth

148 Resonance was absent during the first postnatal week, and emerged during the second week.

149 AVPV fibers reached the PVH during the first postnatal week, and fibers targeting the BSTp and LSv we

150 atal histaminergic innervation by the second postnatal week, and qRT-PCR shows transcripts for H(1),

151 in inner hair cells (IHCs) during the first postnatal week, and the pattern differs along the cochle

152 red CH formation and growth during the first postnatal week, and the phenotypes were exacerbated by f

153 n between VBN relay neurons during the first postnatal week, and then declined sharply during the sec

154 eous activity in the retina during the first postnatal week are disrupted genetically.

155 nsequences of inflammation during the second postnatal week are stunted dendrites of the cerebellum's

156 ed hippocampal gamma rhythm during the first postnatal week, as well as the emergence of the AS-relat

157 dendritic spine dynamics during the first 2 postnatal weeks, as immature filopodia are replaced by m

158 ha10-mediated transmission beyond the second postnatal week associated with abnormally persistent cho

159 ells decreases between the second and fourth postnatal week, at a time when PV cell synapse numbers i

160 ot altered in fmr1 KO mice until the 3rd-4th postnatal week, beyond this age it failed to develop fur

161 hose PNS myelination is delayed in the first postnatal week but eventually resumes.

162 Neuronal number decreased during the first postnatal week but increased 2.5-fold over the next 3 we

163 of heightened arousal during the first three postnatal weeks but comes under inhibitory control in ra

164 dx1(Fl) mice were euglycemic for the first 2 postnatal weeks but showed moderate hyperglycemia from 3

165 ent LTP via H(3) receptors during the second postnatal week, but inhibits synaptic plasticity at late

166 ed retinal waves are absent during the first postnatal week, but return during the second postnatal w

167 itors significantly declines after the early postnatal weeks, but Foxj1-derived neurons in the OB per

168 e majority of PNs die in the fourth to fifth postnatal weeks, but the responsible molecules are unkno

169 clined almost eightfold during the first two postnatal weeks, but there were offsetting increases in

170 cerebellum occur primarily during the third postnatal week by both FISH and immunocytochemistry.

171 life exercise, specifically during the 4(th) postnatal week, can enable hippocampal memory, synaptic

172 mPFC neuron excitability during the first 2 postnatal weeks caused a premature differentiation of ol

173 Before the second postnatal week, clearance of synaptically released gluta

174 at PVFSIs upregulate GluA4 during the second postnatal week coincident with increases in the AMPAR cl

175 gic inhibitory control emerges in the second postnatal week, coinciding with an expression switch fro

176 ces from immature rats (i.e. second to third postnatal weeks), compared to CA3 slices from adult rats

177 Cardiac cells mature in the first postnatal week, concurrent with altered extracellular me

178 l period, in particular, prior to the fourth postnatal week, corresponding to stages in which VEGF in

179 nocular deprivation is started in the fourth postnatal week (CP).

180 showed previously that the end of the second postnatal week (days P11-15) represents a period of deve

181 chronized state is absent during the first 2 postnatal weeks, despite behavioral wakefulness.

182 sensorimotor reflex development in the first postnatal week followed by a degeneration of motor funct

183 showed a substantial increase until the 4th postnatal week followed by a further but moderate increa

184 V(E) ) significantly increased in the second postnatal week, followed by a progressive increase in V(

185 l and temporal cortices during the first two postnatal weeks following three episodes of status-epile

186 retinal waves are necessary during the first postnatal week for both proper distribution and eye-spec

187 d apical neurons obtained during the first 2 postnatal weeks from CBA/CaJ mice.

188 inner nuclear layer at the end of the first postnatal week, from postnatal day (P) 5 to P9, after th

189 After the second postnatal week, GluN2B(DeltaGAD67) mice developed hippoc

190 In Long Evans rats during the first postnatal week, GluR2-lacking AMPARs were expressed pred

191 ion blocker, carbenoxolone, during the first postnatal week greatly diminished the functional similar

192 t chronic nicotine exposure during the first postnatal week has sex-specific long-term effects.

193 ernal separation (MS15) during the first 1-2 postnatal weeks has been shown to increase active matern

194 associated with male gender, older age (> 7 postnatal weeks), higher locomotor activity, daytime rec

195 Second, during the first postnatal week, immunoreactivity for markers of TC termi

196 integrity, increased at the end of the third postnatal week in association with increases in AMPAR re

197 sue anisotropy was measured during the first postnatal week in cortical regions, reflecting the under

198 This event occurs at the end of the first postnatal week in mice.

199 t the tonotopic map emerged during the third postnatal week in normal mice.

200 roglia was observed at the end of the second postnatal week in Npc1(nmf164) mice.

201 birth in humans and by the end of the second postnatal week in rats and mice.

202 of human pregnancy is equivalent to the 1st postnatal week in rodents; both are periods of active br

203 arameters remain unchanged through the first postnatal week in the absence of retinal waves, but quic

204 e excess inhibition at the end of the second postnatal week in Ts65Dn mice is not due to increases in

205 e was first detectable at the end of the 2nd postnatal week in wild-type mice.

206 C) at birth, but develop over the first four postnatal weeks in different temporal patterns and also

207 e was functionally mature during the first 3 postnatal weeks in mice.

208 els gradually increased over the first three postnatal weeks in the hippocampus, and remained stable

209 ial and neuronal subtypes during the first 3 postnatal weeks in the Long Evans and Sprague Dawley rat

210 rring cell death occurs during the first two postnatal weeks in the rat cortex and hippocampus.

211 tiated cells are eliminated in the first two postnatal weeks in these mice, resulting in a modest inc

212 erneurons received broad inputs in the first postnatal week, including inputs from CR cells.

213 already established by the first and second postnatal weeks, including different electrophysiologica

214 ion, axonal tracing in vivo during the first postnatal week indicates that immature mossy fibers exte

215 both inputs after the beginning of the third postnatal week, indicating that both types of inputs dis

216 , silent synapses persist through the second postnatal week, indicating that the maintenance of AMPA

217 eurons decreases between the third and fifth postnatal weeks, indicating a period of connection pruni

218 the developing spinal cord during the first postnatal week inhibited myelination.

219 strongly suggests that the end of the second postnatal week is a critical period of development for b

220 erning of the barrel cortex during the first postnatal week is a frequently assessed feature of roden

221 of the anti-phase pattern during the second postnatal week is accompanied by increased diurnal wakef

222 te that Fth synthesis during the first three postnatal weeks is important for an appropriate oligoden

223 d at higher levels in the embryo and earlier postnatal weeks, it is also expressed in the adult rat b

224 el during three postnatal periods: the 4(th) postnatal week (juvenile ELE, P21-27), 6(th) postnatal w

225 eek (adolescent ELE, P35-41), or 4(th)-6(th) postnatal weeks (juvenile-adolescent ELE, P21-41).

226 V2 connectivity were in place as early as 2 postnatal weeks, labeled cells in V1 and V2 became more

227 that mediate retinal waves during the first postnatal week leads to the generation of "recovered" wa

228 tically enhance sensory inputs in the second postnatal week led to a significant increase in spine de

229 x accessory proteins at the end of the third postnatal week likely "turns on" the hippocampus by incr

230 At the end of the second postnatal week, neocortical networks undergo a transitio

231 In the first postnatal weeks, neuronal protein synthesis and proteaso

232 This asymmetry emerges during the second postnatal week of development, but its basis remains unk

233 eye opening occurs at the end of the second postnatal week of development.

234 rus development and persisted into the first postnatal week of life.

235 During the first postnatal week of mouse development, the MET currents am

236 RNF34 is not expressed until the 2nd postnatal week of rat brain development, being highly ex

237 in a layer-specific pattern from one to four postnatal weeks of age.

238 op spontaneous seizures during the first six postnatal weeks of life and brain slices show neuronal h

239 ells beyond ependymal cells during the first postnatal weeks of the rat.

240 unctional histamine receptors from the first postnatal week onwards, with histamine having diverse ef

241 stamine receptors in striatum from the first postnatal week onwards, with pronounced developmental in

242 triatal synaptic transmission from the first postnatal week onwards.

243 During the first postnatal week (postnatal days P4-P7), V1 was not visual

244 average across genotypes early in the first postnatal week [postnatal day 3 (P3) to P4] and, interes

245 rly deprived for 2 d at the end of the third postnatal week (pre-CP), whereas potentiation is induced

246 in (TARP) expression at the end of the third postnatal week provide a molecular explanation for the i

247 n between the CS systems on each side during postnatal weeks (PW) 3-7.

248 SGCs were of equal strength during the first postnatal week, regardless of whether the SAC was locate

249 m, primarily the cerebellum, the first three postnatal weeks represent a period of significant sensit

250 ed from newborn and adult mice (2nd and 12th postnatal weeks, respectively), were seeded at low (5 ce

251 were not observed until the second and third postnatal weeks, respectively.

252 tion shape spike-timing, VGNs from the first postnatal week respond to synaptic-noise-like current in

253 However, beginning in the second postnatal week, retinal activity does not drive V1 as st

254 ked ventral root potentials until the second postnatal week, revealing a late role for spindle-derive

255 spherules begin to retract during the second postnatal week, rod bipolar cells initially show no sign

256 In the third postnatal week, several amyloid-beta peptides were above

257 igodendrocytes during the first or the third postnatal week significantly reduces oligodendrocyte iro

258 Starting from about 4 postnatal weeks, SOD1-G93A and wild-type (WT) mice were

259 d no defects in the retina before the second postnatal week, suggesting that miRNAs are not required

260 lover excitation persisted beyond the second postnatal week, suggesting that this mechanism may play

261 already established by the first and second postnatal weeks, suggesting guidance through intrinsic d

262 During the second postnatal week the quantal frequency but not the quantal

263 At the fifth postnatal week, the P50 response was suppressed in more

264 se proteins were KO in vivo during the first postnatal week, the sciatic nerve of all 3 conditional K

265 However, by the end of the second postnatal week, the strength of the synapses made from S

266 ation was present throughout the first three postnatal weeks, the size of input maps was developmenta

267 ittermates at the end of the first and third postnatal weeks, the Ts65Dn animals showed significantly

268 subplate neurons, whereas, during the second postnatal week, these AMPARs were highly expressed on co

269 icited in some NG2(+) cells during the first postnatal week, they were not capable of generating acti

270 dense time course sampling between 4 and 20 postnatal weeks to characterize early transcriptomic, mo

271 of mouse auditory cortex during the first 2 postnatal weeks to study the spatial origin of silent sy

272 vocal sequences, we found that in the first postnatal week, twins had more similar vocal sequences t

273 , Rem2 mRNA and protein expression peaked at postnatal week two, which corresponds to the period of r

274 curring for both D1 and D2 SPNs in the first postnatal weeks using in vitro whole-cell patch-clamp el

275 th acutely and longer-term, during the first postnatal weeks, using patch-clamp and field recordings

276 4 somatosensory barrel cortex in the second postnatal week via two distinct mechanisms.

277 Daily administration of OT in the first postnatal week was sufficient to prevent deficits in soc

278 ty, which is normally lost during the second postnatal week, was maintained and synaptic competition

279 CNS myelin, normally occurring in the second postnatal week, was strongly inhibited.

280 During the first postnatal week we observed a reduction of ATP-dependent

281 n the DG and OB born at the end of the first postnatal week were generated from GFAP+ cells.

282 t in CHL1 (lacking CHL1 only after the third postnatal week) were tested relative to littermate contr

283 B-containing NMDARs prevail until the second postnatal week when GluN2A subunits are progressively ad

284 in the rodent hippocampus during the second postnatal week when most synapses become established and

285 in Norway rats around the end of the second postnatal week when nocturnal wakefulness and the in-pha

286 and proliferation in TBCs during the first 3 postnatal weeks, when the number of TBCs decreases.

287 cesses that occur primarily during the first postnatal week, whereas neurogenesis and migration showe

288 within a narrow range during the first three postnatal weeks, whereas glycinergic ones exhibited age-

289 edforward inhibition at the end of the first postnatal week, which has profound effects on circuit fu

290 During the second postnatal week, which is before the onset of hearing in

291 -deficient horizontal cells during the first postnatal weeks, which dropped off abruptly by P30.

292 ication of zinc sulfate during the first two postnatal weeks, which interferes with their ability to

293 Bergmann glia are generated up to first the postnatal weeks, which was proposed to be neurogenic.

294 quantal amplitudes increase during the first postnatal week while the prevalence of silent synapses d

295 poglycemia, and weight loss after the second postnatal week with death by week 4.

296 This period ceases in the second postnatal week with the maturation of C-fiber spinal inp

297 ty begins to decline by the end of the first postnatal week, with approximately 25% of SGNs ultimatel

298 owed a gentle plateau throughout the first 3 postnatal weeks, with only a slight decline of BDNF expr

299 and gradually decreased over the first three postnatal weeks within the hippocampus, amygdala, striat

300 discrete cell clusters emerge over the first postnatal week, yielding an identifiable modular network