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1 ronal and glial maturation (second and third postnatal weeks).
2 ons and inhibitory interneurons in the first postnatal week.
3 tinguish gamma-from alpha-MNs into the third postnatal week.
4 ed, GDNF-independent signal during the first postnatal week.
5 creased in the Ts65Dn mice during the second postnatal week.
6 e SO in vestibular hair cells over the first postnatal week.
7 e patterns by the end of the third or fourth postnatal week.
8 ge-matched controls at the end of the second postnatal week.
9 rent input and begin to die during the first postnatal week.
10 icotinic acetylcholine currents in the third postnatal week.
11 these synapses between the first and second postnatal week.
12 del-COMP triggers apoptosis during the first postnatal week.
13 recovery in beta2-/- mice during the second postnatal week.
14 1) to the SC is established during the first postnatal week.
15 ath of these animals near the end of the 2nd postnatal week.
16 rtical activity only by the end of the first postnatal week.
17 g a short window during the second and third postnatal week.
18 icantly increased in diameter over the first postnatal week.
19 l coupling was decreasing, during the second postnatal week.
20 downregulate its expression during the first postnatal week.
21 and die because of seizures during the third postnatal week.
22 m thalamocortical afferents during the first postnatal week.
23 nscript and protein occurs during the second postnatal week.
24 postnatal week, but return during the second postnatal week.
25 mature in the outer retina during the second postnatal week.
26 thood, with peak expression during the first postnatal week.
27 he AS-related theta rhythm during the second postnatal week.
28 inputs relative to controls after the first postnatal week.
29 ring development, until the end of the third postnatal week.
30 synaptic development beginning in the first postnatal week.
31 y 13, reaching maximal enrichment by the 3rd postnatal week.
32 activation and for survival beyond the first postnatal week.
33 eaching adult levels at the end of the third postnatal week.
34 he rest of embryogenesis and into the second postnatal week.
35 obtain adult-like features until the fourth postnatal week.
36 e neurological deficits and die in the third postnatal week.
37 occur significantly later, during the first postnatal week.
38 when the experience occurs during the third postnatal week.
39 yperpolarization commencing during the third postnatal week.
40 ells (OHCs) from the beginning of the second postnatal week.
41 AII amacrine cells occurred during the third postnatal week.
42 xon terminals appeared only during the third postnatal week.
43 open their eyes until the end of the second postnatal week.
44 increased in size up to the end of the first postnatal week.
45 ccumbs to massive apoptosis after the fourth postnatal week.
46 s induced before HVS regression in the first postnatal week.
47 ectrotonic and dye coupling during the first postnatal week.
48 econdary onset of hydrocephaly in the second postnatal week.
49 atally, nearing adult levels after the third postnatal week.
50 s distributed to dendrites during the second postnatal week.
51 e apparent at embryonic day 18 and the first postnatal week.
52 olarizing potentials (GDPs) during the first postnatal week.
53 ons and inhibitory interneurons in the first postnatal week.
54 hat specifically targets L4 during the first postnatal week.
55 erent strata of CA3 in rats during the third postnatal week.
56 ntiate from retinal progenitors in the first postnatal week.
57 DSGCs at the beginning and end of the second postnatal week.
58 epithelia of ILDR1 null mice after the first postnatal week.
59 nditioning begins to emerge during the third postnatal week.
60 air cells degenerate rapidly after the first postnatal week.
61 solated from rodents at the end of the first postnatal week.
62 s detectable paternal Ube3a beyond the first postnatal week.
63 a similar length toward the end of the first postnatal week.
64 antly increase in the heart during the first postnatal week.
65 s calcium action potentials during the first postnatal week.
66 the developing cortical plate in the second postnatal week.
67 ression levels were highest during the first postnatal week.
68 - 0.14 cell/40-mum section during the second postnatal week.
69 ion and myelination recover during the first postnatal week.
70 Pcdh19 and Ncdh expression during the first postnatal week.
71 ype levels in the brain beginning the second postnatal week.
72 irth and are fully established by the second postnatal week.
73 rred mostly between the second and the third postnatal week.
74 nd continuing to do so well after the eighth postnatal week.
75 ciceptive spinal activity in the first three postnatal weeks.
76 but markedly increased during the first 2-3 postnatal weeks.
77 rain amoeboid microglia during the first two postnatal weeks.
78 in barrel cortex during the third and fourth postnatal weeks.
79 pment, and are active only for the first few postnatal weeks.
80 ly isolated from rats during the first three postnatal weeks.
81 ses muscle calcium levels during the first 2 postnatal weeks.
82 xcitatory to inhibitory during the first two postnatal weeks.
83 development, peaking in the first to second postnatal weeks.
84 re anatomical features until approximately 8 postnatal weeks.
85 cy and amplitude increase during the first 3 postnatal weeks.
86 etion was induced in OPCs during the first 2 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 eased muscle calcium only during the first 2 postnatal weeks.
90 transiently express syt 2 during the first 2 postnatal weeks.
91 ses progressively increased over the first 2 postnatal weeks.
92 y in layers V and II/III, during the first 2 postnatal weeks.
93 cited easily in vitro during the first three postnatal weeks.
94 formation is completed during the first two postnatal weeks.
95 their bulbar distribution during the first 3 postnatal weeks.
96 express brevican during the second and third postnatal weeks.
97 tivity-dependent refinement during the first postnatal weeks.
98 ion of protein malnutrition during the first postnatal weeks.
99 elected brain regions during the first three postnatal weeks.
100 effect was smaller and confined to the first postnatal weeks.
101 s place almost entirely in the first several postnatal weeks.
102 rk activity, especially during the first two postnatal weeks.
103 lly during development, but die in the early postnatal weeks.
104 fiber inputs mature gradually over the first postnatal weeks.
106 ing in developing mouse cardiomyocytes after postnatal week 1, a time when the cells are no longer di
109 g1 mice but falls below control levels after postnatal week 12, approximately correlating with the on
112 in the photoreceptor outer nuclear layer at postnatal week 2 and highly disorganized outer segments
113 orn: selective block of afferent C fibers in postnatal week 2, using perisciatic injections of the ca
121 was noted at 5 months of age and as early as postnatal week 4 in the eyes of four BBS mouse model str
123 2 and highly disorganized outer segments by postnatal weeks 4 to 6 was observed in all four strains.
124 ivity unilaterally during a critical period [postnatal week 5 (PW5) to PW7] produces permanent contra
127 tivated M1 by muscimol microinfusion between postnatal weeks 5 and 7 to examine activity-dependent in
131 wever, animals lacking both connexins die by postnatal week 6 from profound abnormalities in central
134 inal development during the second and third postnatal weeks, a period that corresponds to human embr
135 ration of these tissues over the first three postnatal weeks, a time when the normal cortex expands a
136 ironment, becomes more evident with age (> 7 postnatal weeks), activity and stress, is gender specifi
137 t expressed by interneurons until the second postnatal week after reaching the cortex, suggesting tha
138 nock-out mice, we show that during the first postnatal week, alpha-syn is not required for synapse fo
139 e and retarded growth starting at the second postnatal week and died on approximately postnatal day 2
140 NS in developing hepatocytes from the first postnatal week and increased DNA damage and hepatocellul
141 letion in hippocampal CA1 cells in the third postnatal week and later throughout the neocortex, brain
143 pressed in some VBN neurons during the first postnatal week and sharply declined over the second week
144 cortical inputs to SPNs emerge in the second postnatal week and that SPNs that receive superficial co
145 blished in the inner retina during the first postnatal week and that these systems subsequently matur
146 te that mouse microglia mature by the second postnatal week and to predict novel microglial functions
147 es of BG microglia emerged during the second postnatal week and were re-established following genetic
148 ed the retinal vasculogenesis in the first 2 postnatal weeks and impaired the angiogenesis triggered
149 dergoes profound regulation over the first 4 postnatal weeks and that these changes are correlated wi
150 y had achieved their adult-like anatomy by 4 postnatal weeks and were in a position to influence the
151 ) mitochondria become abnormal by the second postnatal week, and a majority of PNs die in the fourth
153 AVPV fibers reached the PVH during the first postnatal week, and fibers targeting the BSTp and LSv we
154 in inner hair cells (IHCs) during the first postnatal week, and the pattern differs along the cochle
155 red CH formation and growth during the first postnatal week, and the phenotypes were exacerbated by f
156 n between VBN relay neurons during the first postnatal week, and then declined sharply during the sec
157 h, remained relatively high during the first postnatal week, and then steadily decreased to adult lev
159 )R-mediated depolarizations during the first postnatal week are likely to be important for the matura
160 nsequences of inflammation during the second postnatal week are stunted dendrites of the cerebellum's
161 ed hippocampal gamma rhythm during the first postnatal week, as well as the emergence of the AS-relat
162 dendritic spine dynamics during the first 2 postnatal weeks, as immature filopodia are replaced by m
165 ot altered in fmr1 KO mice until the 3rd-4th postnatal week, beyond this age it failed to develop fur
167 Neuronal number decreased during the first postnatal week but increased 2.5-fold over the next 3 we
168 of heightened arousal during the first three postnatal weeks but comes under inhibitory control in ra
169 dx1(Fl) mice were euglycemic for the first 2 postnatal weeks but showed moderate hyperglycemia from 3
170 le in lens epithelial cells during the first postnatal week, but increased as the capillaries of the
171 thalamic reticular nucleus during the second postnatal week, but it extends to other thalamic nuclei
172 ed retinal waves are absent during the first postnatal week, but return during the second postnatal w
173 beta2(-/-) mice lack waves during the first postnatal week, but RGCs have high levels of uncorrelate
174 itors significantly declines after the early postnatal weeks, but Foxj1-derived neurons in the OB per
175 e majority of PNs die in the fourth to fifth postnatal weeks, but the responsible molecules are unkno
176 clined almost eightfold during the first two postnatal weeks, but there were offsetting increases in
177 cerebellum occur primarily during the third postnatal week by both FISH and immunocytochemistry.
178 h levels of brain serotonin during the first postnatal week, causing an exuberant outgrowth of thalam
180 at PVFSIs upregulate GluA4 during the second postnatal week coincident with increases in the AMPAR cl
181 gic inhibitory control emerges in the second postnatal week, coinciding with an expression switch fro
182 ained from cerebella of animals in the first postnatal week, coinciding with the observed in vivo pea
183 ces from immature rats (i.e. second to third postnatal weeks), compared to CA3 slices from adult rats
185 l period, in particular, prior to the fourth postnatal week, corresponding to stages in which VEGF in
186 Maturation of DA axons during the third postnatal week corresponds to the period of onset of vis
188 showed previously that the end of the second postnatal week (days P11-15) represents a period of deve
191 showed a substantial increase until the 4th postnatal week followed by a further but moderate increa
192 V(E) ) significantly increased in the second postnatal week, followed by a progressive increase in V(
193 l and temporal cortices during the first two postnatal weeks following three episodes of status-epile
194 retinal waves are necessary during the first postnatal week for both proper distribution and eye-spec
196 inner nuclear layer at the end of the first postnatal week, from postnatal day (P) 5 to P9, after th
199 ion blocker, carbenoxolone, during the first postnatal week greatly diminished the functional similar
201 ernal separation (MS15) during the first 1-2 postnatal weeks has been shown to increase active matern
202 associated with male gender, older age (> 7 postnatal weeks), higher locomotor activity, daytime rec
204 ivation during the third, but not the fifth, postnatal week, implicating an important role for sensor
205 integrity, increased at the end of the third postnatal week in association with increases in AMPAR re
206 sue anisotropy was measured during the first postnatal week in cortical regions, reflecting the under
210 of human pregnancy is equivalent to the 1st postnatal week in rodents; both are periods of active br
211 arameters remain unchanged through the first postnatal week in the absence of retinal waves, but quic
212 e excess inhibition at the end of the second postnatal week in Ts65Dn mice is not due to increases in
214 C) at birth, but develop over the first four postnatal weeks in different temporal patterns and also
216 els gradually increased over the first three postnatal weeks in the hippocampus, and remained stable
217 ial and neuronal subtypes during the first 3 postnatal weeks in the Long Evans and Sprague Dawley rat
219 tiated cells are eliminated in the first two postnatal weeks in these mice, resulting in a modest inc
221 ion, axonal tracing in vivo during the first postnatal week indicates that immature mossy fibers exte
222 both inputs after the beginning of the third postnatal week, indicating that both types of inputs dis
223 , silent synapses persist through the second postnatal week, indicating that the maintenance of AMPA
224 eurons decreases between the third and fifth postnatal weeks, indicating a period of connection pruni
226 strongly suggests that the end of the second postnatal week is a critical period of development for b
227 erning of the barrel cortex during the first postnatal week is a frequently assessed feature of roden
228 of the anti-phase pattern during the second postnatal week is accompanied by increased diurnal wakef
229 V2 connectivity were in place as early as 2 postnatal weeks, labeled cells in V1 and V2 became more
230 that mediate retinal waves during the first postnatal week leads to the generation of "recovered" wa
231 x accessory proteins at the end of the third postnatal week likely "turns on" the hippocampus by incr
232 be induced in hippocampal slices from first postnatal week mice, in Mg2+-free solution with GABA(A)
235 This asymmetry emerges during the second postnatal week of development, but its basis remains unk
240 op spontaneous seizures during the first six postnatal weeks of life and brain slices show neuronal h
243 dergo programmed cell death during the first postnatal weeks, others relocate within hippocampal lami
245 average across genotypes early in the first postnatal week [postnatal day 3 (P3) to P4] and, interes
246 rly deprived for 2 d at the end of the third postnatal week (pre-CP), whereas potentiation is induced
247 in (TARP) expression at the end of the third postnatal week provide a molecular explanation for the i
249 SGCs were of equal strength during the first postnatal week, regardless of whether the SAC was locate
250 m, primarily the cerebellum, the first three postnatal weeks represent a period of significant sensit
251 ed from newborn and adult mice (2nd and 12th postnatal weeks, respectively), were seeded at low (5 ce
253 ked ventral root potentials until the second postnatal week, revealing a late role for spindle-derive
254 spherules begin to retract during the second postnatal week, rod bipolar cells initially show no sign
256 tic circuitry develops rapidly in the second postnatal week, simultaneous with experience-dependent t
257 at P15 but changed during the third to sixth postnatal weeks so that, by P36-42, FF inputs preferred
258 birth, and gradually declines over the first postnatal week, suboptimal SC acidification at birth can
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
265 ation was present throughout the first three postnatal weeks, the size of input maps was developmenta
266 ittermates at the end of the first and third postnatal weeks, the Ts65Dn animals showed significantly
267 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
275 Daily administration of OT in the first postnatal week was sufficient to prevent deficits in soc
276 ty, which is normally lost during the second postnatal week, was maintained and synaptic competition
279 nd motility change dramatically in the first postnatal weeks, we analyzed these properties in mutant
281 t in CHL1 (lacking CHL1 only after the third postnatal week) were tested relative to littermate contr
282 B-containing NMDARs prevail until the second postnatal week when GluN2A subunits are progressively ad
283 in the rodent hippocampus during the second postnatal week when most synapses become established and
284 in Norway rats around the end of the second postnatal week when nocturnal wakefulness and the in-pha
285 with age, reaching a peak during the second postnatal week, when beta-galactosidase reactivity is vi
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
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
297 ampus to compare acute slices from the third postnatal week with various stages of organotypic slices
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
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