ライフサイエンスコーパス: VIP

1 VIP and SST neurons have complementary contrast tuning.

2 VIP interneuron activity increases in the open arms and

3 VIP interneurons, themselves regulated by neuromodulator

4 VIP neurons are activated by non-sensory inputs, disinhi

5 VIP neurons are glutamatergic stellate cells with sustai

6 VIP then stimulates CD4(+) and resident innate lymphoid

7 VIP-1 amacrine cells are bistratified, wide-field cells

8 VIP-ires-Cre amacrine cells form a neuropeptide-expressi

9 VIP-tdTomato and -Confetti (Brainbow2.1) mouse lines wer

10 VIP/VPAC1 may serve as potential prognostic markers and

11 testing) and discriminant [pcorr (1) > 0.3, VIP > 1.5] analyses showed that >2000 mass spectral feat

12 eld cells that ramify in strata 1, 4, and 5, VIP-2A and 2B amacrine cells are medium-field cells that

13 .1) mouse lines were generated by crossing a VIP-ires-Cre line with either a Cre-dependent tdTomato o

14 gy, neurochemistry and major cell types of a VIP-ires-Cre amacrine cell population.

15 es were considered discriminatory based on a VIP score >=2.5 in the training dataset with some overla

16 P(+) cell activity, we found that activating VIP(+) cells elicited a stronger network response to sti

17 tively immunized adult zebra finches against VIP conjugated to KLH and compared neuronal recruitment

18 demonstrate that active immunization against VIP reduces neuronal recruitment, inhibits reproduction,

19 functions regulated by cholinergic agonists, VIP, and purinergic receptors are decreased in TSP1(-/-)

20 Although VIP neuron activity in the primary visual cortex (V1) of

21 WanFang (2012-2017), SinoMed (2012-2017) and VIP (2012-2017) to retrieve relevant articles published

22 ls that mainly ramify in strata 3 and 4, and VIP-3 displaced amacrine cells are medium-field cells th

23 intracellular chloride regulation in AVP and VIP-expressing SCN neurons and found evidence suggesting

24 etanide had differential effects on AVP+ and VIP+ neurons, while blocking the KCCs with VU0240551 had

25 is differentially regulated between AVP+ and VIP+ neurons-a low concentration of the loop diuretic bu

26 e day than during the night in both AVP+ and VIP+ neurons.

27 o the molecular basis of PACAP27 binding and VIP receptor activation.

28 The PLS-DA, OPLS-DA and VIP analysis demonstrate guttiferone E, guttiferone B, l

29 Here we investigated how excitatory and VIP inhibitory cells in layer 2/3 of mouse visual cortex

30 s of increased translocation include MCs and VIP.

31 The results of metabolomics and VIP analysis outlined molecules such as 3-methylcatechol

32 Conversely, the total numbers of NPY- and VIP-immunoreactive neurons were reduced by 55% and 30%,

33 interneurons and pyramidal cells in PFC and VIP.

34 Both PV and VIP BCs contributed to the increased sIPSC frequency in

35 mor tissue was investigated for secretin and VIP.

36 tion, the expression levels of secretin, and VIP were measured.

37 Compared with barrel cortex, SOM and VIP cells were much less active in entorhinal cortex dur

38 was more sensitive, with PV(+), SOM(+), and VIP(+) interneurons balancing inhibition and disinhibiti

39 ression and splicing across EXC, PV, SST and VIP neurons from male and female mouse brains.

40 tio of neurons expressing Calbindin, TH, and VIP is selectively decreased while, for instance, 5-HT(+

41 s in the SCN: AVP (arginine vasopressin) and VIP (vasoactive intestinal polypeptide).

42 nd Bland and Altman plots of the VIPs-FS and VIPs-DS versus the SF-12, PVC Metra, BISS and DLQI asses

43 electrode in the ventral intraparietal area (VIP) and the lateral prefrontal cortex (PFC) of rhesus m

44 s, including the ventral intraparietal area (VIP), medial superior temporal area, parieto-insular ves

45 During arousal, VIP cells rapidly and directly inhibit pyramidal neurons

46 r neuropeptide signaling mechanisms, such as VIP-VPAC2 signaling, can lead to desynchronization of SC

47 The average VIP-tdTomato fluorescent cell density in the INL and GCL

48 VPAC1 activation by VIP markedly induced TRPV4-mediated Ca(2+) entry, and ev

49 This effect was overcome by VIP treatment of the early pregnant mice.

50 iking (IS), but not continuous adapting (CA) VIP-INs, in Scn1a(+/-) mice.

51 alpha5-GABA(A)R in mice with inactivated CA1 VIP input could still improve spatial learning and was n

52 ns that received cholinergic input from ChAT-VIP interneurons also received GABAergic input from thes

53 L2/3 and L6 receive direct inputs from ChAT-VIP neurons mediated by fast cholinergic transmission.

54 n contrast to regular VIP interneurons, ChAT-VIP neurons did not disinhibit pyramidal neurons.

55 class of vasoactive intestinal peptide (ChAT-VIP) neurons of which circuit and behavioural function a

56 Here, we show that ChAT-VIP neurons directly excite neighbouring neurons in seve

57 Thus, ChAT-VIP neurons are a local source of cortical ACh that dire

58 na National Knowledge Infrastructure [CNKI], VIP, Wanfang) databases for population-based studies com

59 uorescent cells in the INL and GCL contained VIP-immunoreactivity.

60 fibers containing CGRP and fibers containing VIP but not CGRP.

61 o pinpoint a new target for seizure control: VIP interneurons.

62 ur findings further suggest that in cortical VIP neurons, experience-dependent gene transcription reg

63 ACh release depolarized VIP BCs whereas PV BCs depolarized, hyperpolarized or pr

64 1 to a stationary scene, 2) that depolarized VIP cells enhance V1 responses to moving objects by redu

65 However, when stimulus and surround differ, VIP neurons are active, inhibiting SOM neurons, which le

66 Moreover, via this lateral disinhibition, VIP cells in vivo make local and transient "holes" in th

67 The region on the floor of the IPS (i.e., VIP) projects predominantly to dorsal stream areas.

68 to clusters of ILC3 that selectively express VIP receptor type 2 (VIPR2; also known as VPAC2).

69 Number of MCs and MCs that express VIP or VIP receptors were quantified by immunofluorescen

70 th vasoactive intestinal peptide-expressing (VIP) and parvalbumin-expressing (PV) basket cells (BCs)

71 Vasoactive intestinal peptide-expressing (VIP) interneurons in the cortex regulate feedback inhibi

72 at vasoactive intestinal peptide-expressing (VIP) interneurons may play a critical role in the proper

73 asoactive intestinal polypeptide-expressing (VIP(+)), disinhibitory INs in hippocampal area CA1 form

74 asoactive intestinal polypeptide-expressing (VIP) interneurons.

75 asoactive intestinal polypeptide-expressing (VIP+) GABAergic interneurons express Cre recombinase.

76 er of fibers containing immunoreactivity for VIP, CGRP, SP, or nNOS were found.

77 Our data support a key role for VIP interneurons in cortical circuit development and sug

78 iderably, with increasing heterogeneity from VIP to PFC.

79 ErbB4 removal from VIP interneurons during development leads to changes in

80 we find that loss of MeCP2 specifically from VIP interneurons replicates key neural and behavioral ph

81 st VIP is critical for trophoblast function: VIP gene haploinsufficiency results in lower matrix meta

82 On the other hand, VIP+ input onto VIP- neurons became less inhibitory at n

83 To explore how VIP interneurons affect the local circuits, we use two-p

84 This shows how VIP interneurons enable cortical circuits to integrate s

85 some ASD risk genes (NLGN1, STAG1, HSD11B1, VIP, and UBA6) were regulated by an up-regulated circRNA

86 Having identified VIP-independent functions of LHX1, we mapped the VIP-ind

87 markedly between novel and familiar images: VIP cells were stimulus-driven by novel images but were

88 thors report that choice-related activity in VIP neurons is not predictable from their stimulus tunin

89 ate that IGF1 functions cell-autonomously in VIP neurons to increase inhibitory synaptic input onto t

90 This prominent change in VIP activity suggests that these cells may adopt differe

91 he response gain of heading tuning curves in VIP neurons.

92 s-Cre amacrine cell types were identified in VIP-Brainbow2.1 retinas or by intracellular labeling in

93 w2.1 retinas or by intracellular labeling in VIP-tdTomato retinas.

94 e postsynaptic target neuron is reflected in VIP(+)/ChAT(+) interneuron pre-synaptic terminals, as qu

95 as choice-related signals dominate tuning in VIP neurons.

96 t the representation of rotation velocity in VIP is multimodal, driven by both visual and extraretina

97 Other higher-level motion areas including VIP showed weaker to no activation in active dodges.

98 ajor peptidergic cells of the SCN, including VIP, GRP, and arginine vasopressin (AVP) neurons, with e

99 urons and, reciprocally, SST neurons inhibit VIP neurons.

100 Indeed, inhibiting VIP interneurons disrupts network-level representations

101 Optogenetically inhibiting VIP interneurons consistently increased seizure threshol

102 to their laminar differences in local input, VIP+ neurons received inputs predominantly from deep lay

103 intestinal peptide-expressing interneurons (VIPs) disinhibit cortical pyramidal cells through inhibi

104 we provide detailed mechanistic insight into VIP signal transduction in the SCN at the level of genes

105 eurons in the macaque ventral intraparietal (VIP) area are known to represent heading (the direction

106 r temporal (MSTd) and ventral intraparietal (VIP) areas of monkeys during perception of self-motion.

107 etermined by expression of KCNQ channels; IS VIP-INs switched to tonic firing with both pharmacologic

108 t-term memory network, and activation of its VIP neurons improves memory retention.

109 ieved primarily through L1 neuron- and L2/L3 VIP-cell-mediated inhibitory and disinhibitory circuits.

110 Male VIPs were younger (83 +/- 5 vs. 84 +/- 5; p < 0.001), le

111 n the paired analysis, the mortality in male VIPs was higher (mean difference 3.34% 95%CI 0.92-5.76%;

112 We aimed to compare female versus male VIPs in a large, multinational collective of VIPs with r

113 ack-knife confidence intervals, metabolites' VIP values, and univariate statistics.

114 an image-based whole-body adult male model (VIP-Man) to simulate radiation transport and energy depo

115 In darkness, while most VIP and PV neurons remained locomotion responsive, SST a

116 criptomically identified population of mouse VIP+ SCN neurons is active at the "wrong" time of day-ni

117 near RGS16, P=7.0 x 10(-18); rs9479402 near VIP, P=3.9 x 10(-11); rs55694368 near PER2, P=2.6 x 10(-

118 idly and directly inhibit pyramidal neurons; VIP cells also indirectly excite these pyramidal neurons

119 dentify a separate, sparse population of non-VIP ChAT(+) neurons in the medial prefrontal cortex with

120 that circadian function in AVP neurons, not VIP neurons, is essential for autonomous network synchro

121 ntrainment of the SCN; and in the absence of VIP, or its cognate receptor VPAC2, circadian behavior i

122 We show that optogenetic activation of VIP(+) cells results in a shift in network preference to

123 Importantly, the choice-related activity of VIP neurons is not predictable from their stimulus tunin

124 ike and wave discharges, whereas blockade of VIP receptors almost completely abolished this form of e

125 and persists in the presence of blockers of VIP, GABA or neuronal firing.

126 , including VPAC2-expressing target cells of VIP, are, however, not understood.

127 n rhythmicity, the specific contributions of VIP cell output to physiological control remains uncerta

128 Strikingly, the temporal dynamics of VIP activity differed markedly between novel and familia

129 ctively eliminated the stimulatory effect of VIP on p38 and ERK phosphorylation, c-Fos mRNA expressio

130 ncy of sIPSCs that result from excitation of VIP or PV BCs primarily occurred within the low gamma fr

131 Moreover, high expression of VIP and VPAC1, advanced tumor stage and distant metastas

132 chrony at E15.5 appears before expression of VIP or its receptor and persists in the presence of bloc

133 The increased expression of VIP/VPAC1 in gastric cancer correlated positively with i

134 Here, we found that higher expression of VIP/VPAC1 was observed in gastric cancer compared to the

135 otaxis regularity depends on the function of VIP proteins, components of the RNA polymerase II-associ

136 on of surround suppression, the functions of VIP cell depolarization are not fully understood.

137 odel to elucidate the potential functions of VIP cell depolarization during locomotion.

138 Third, we show that roughly one-half of VIP neurons jointly represent heading and rotation veloc

139 Levels of VIP and tryptase were measured in plasma and biopsy lysa

140 from patients with IBS had higher levels of VIP than plasma samples from controls.

141 s, a subset of SST neurons and a majority of VIP neurons.

142 ium imaging and optogenetic manipulations of VIP(+) cell activity, we found that activating VIP(+) ce

143 Optogenetic manipulations of VIP(+) INs and computational modeling further showed tha

144 Two populations of VIP-containing fibers were identified: fibers containing

145 Projections of VIP-producing neurons (VIPergic neurons) in the lamina p

146 e proximal vagina and reduced proportions of VIP, CGRP, and SP containing nerve fibers in the distal

147 However, little is known about the role of VIP interneurons in Rett Syndrome.

148 urn enhanced the expression and secretion of VIP in gastric cancer cells, enforcing a positive feedba

149 1, CGRP, and IB4 binding and upregulation of VIP in the corresponding dorsal root ganglia (DRG) and t

150 VIPs in a large, multinational collective of VIPs with regards to outcome and predictors of mortality

151 iminant Raman modes were identified based on VIP (variables importance in projection) scores.

152 e KCCs with VU0240551 had a larger effect on VIP+ neurons compared to AVP+ neurons.

153 tical and thalamic inputs were greatest onto VIP+ interneurons and smallest onto SST+ neurons.

154 On the other hand, VIP+ input onto VIP- neurons became less inhibitory at night suggesting

155 Acetylcholine released onto VIP interneurons that innervate pyramidal neuron perisom

156 Antagonists of GABA or VIP signaling or action potentials did not disrupt circa

157 neurons and optogenetic suppression of PV or VIP BCs inhibited sIPSCs occurring in the gamma range.

158 Firing of a few SOM or VIP INs recruits additional members within the cell type

159 Somatostatin or VIP neuron activation also impaired or enhanced performa

160 Number of MCs and MCs that express VIP or VIP receptors were quantified by immunofluorescence.

161 sparsely onto layer 1 interneurons and other VIP(+)/ChAT(+) interneurons.

162 In isolated islets, carbachol and PACAP/VIP synergistically promote beta-cell proliferation thro

163 le and male very elderly intensive patients (VIPs) might differ in characteristics and outcomes.

164 contains both vasoactive intestinal peptide (VIP) and somatostatin (SST) neurons.

165 nd its ligand vasoactive intestinal peptide (VIP) are important in gastrointestinal physiology, their

166 Vasoactive intestinal peptide (VIP) has been widely accepted as the main mediator of WD

167 opulations of vasoactive-intestinal peptide (VIP) interneurons expressing the synaptic reporter SyGCa

168 urons and the vasoactive intestinal peptide (VIP) interneurons that suppress activation of other inte

169 could be the vasoactive intestinal peptide (VIP) interneurons, which disinhibit other interneurons.

170 Vasoactive intestinal peptide (VIP) is a pleiotropic neuropeptide synthetized in tropho

171 neuropeptide vasoactive intestinal peptide (VIP) mediate retinal entrainment of the SCN; and in the

172 Vasoactive intestinal peptide (VIP) mediates a broad range of biological responses by a

173 ve identified vasoactive intestinal peptide (VIP) neurons as a novel class of IC principal neurons.

174 nses of L2/L3 vasoactive intestinal peptide (VIP) neurons were suppressed by sound, both preferential

175 ecombinase in vasoactive intestinal peptide (VIP) or parvalbumin (PV) interneurons using whole cell p

176 in (SST), and vasoactive intestinal peptide (VIP) show cell-type-specific connectivity patterns leadi

177 that express vasoactive intestinal peptide (VIP)(4).

178 gic agonists, vasoactive intestinal peptide (VIP), and the purinergic agonists ATP and UTP.

179 atin (SOM) or vasoactive intestinal peptide (VIP), are active as populations rather than individually

180 e activity of vasoactive intestinal peptide (VIP), somatostatin (SST) and parvalbumin (PV)-positive i

181 es, including vasoactive intestinal peptide (VIP), which drives light entrainment, synchrony, and amp

182 s made by the vasoactive intestinal peptide (VIP)- and calretinin-positive terminals onto dendrites o

183 consisting of vasoactive intestinal peptide (VIP)-expressing and somatostatin (SOM)-expressing inhibi

184 min (PV)- and Vasoactive intestinal peptide (VIP)-expressing INs exhibit skewed distributions towards

185 in (SOM)- and vasoactive intestinal peptide (VIP)-expressing INs led to an increase of the N+ activit

186 d the role of vasoactive intestinal peptide (VIP)-expressing interneurons in the postnatal maturation

187 m in cortical vasoactive intestinal peptide (VIP)-expressing neurons that is markedly distinct from t

188 t, activating vasoactive intestinal peptide (VIP)-positive interneurons enhanced behavioral performan

189 s and release vasoactive intestinal peptide (VIP).

190 acid peptide, vasoactive intestinal peptide (VIP).

191 he release of vasoactive intestinal peptide (VIP).

192 e presence of vasoactive intestinal peptide (VIP).

193 ns expressing vasoactive intestinal peptide (VIP+ neurons).

194 and MD drives vasoactive intestinal peptide (VIP+) cells in L1b.

195 se expressing vasoactive intestinal peptide (VIP-IN) -is unknown.

196 n (SOM), and vasoactive intestinal peptitde (VIP)-expressing interneurons, whereas excitatory neurons

197 develop a vapor induced intermediate phase (VIP) strategy to manipulate the morphology of perovskite

198 urrent study, a new viral imprinted polymer (VIP)-based biosensor was designed and fabricated for the

199 inding behavior at virus-imprinted polymers (VIPs) via stimulated emission depletion (STED) microscop

200 xpressing vasoactive intestinal polypeptide (VIP(+)) play a causal role in regulating the spatial fre

201 xpressing vasoactive intestinal polypeptide (VIP(+)) regulate the spatial frequency (SF) tuning of py

202 xpressing vasoactive intestinal polypeptide (VIP) are known to disinhibit cortical neurons.

203 or ligand vasoactive intestinal polypeptide (VIP) had no effect on plasma corticosterone levels even

204 (MCs) and vasoactive intestinal polypeptide (VIP) in barrier regulation in IBS and healthy individual

205 tivity of vasoactive intestinal polypeptide (VIP) interneurons resulted in an increased somatostatin

206 mammals, vasoactive intestinal polypeptide (VIP) is known to have many neuroprotective properties, b

207 xpressing vasoactive intestinal polypeptide (VIP) or its cognate receptor, VPAC2, are neurochemically

208 ar, while vasoactive intestinal polypeptide (VIP) signalling is essential for SCN function and whole

209 rikingly, vasoactive intestinal polypeptide (VIP), a neuropeptide critical for synchrony in the adult

210 (NPY) and vasoactive intestinal polypeptide (VIP), and the numerical density of the nLOT cholinergic

211 peptides vasoactive intestinal polypeptide (VIP), calcitonin-gene related peptide (CGRP), substance

212 eptin and vasoactive intestinal polypeptide (VIP), positive regulators of GnRH neurons.

213 inates in vasoactive intestinal polypeptide (VIP)-expressing interneurons.

214 that only vasoactive intestinal polypeptide (VIP)/gastrin-releasing peptide (GRP) cells located ventr

215 t to vasoactive intestinal peptide-positive (VIP+) neurons than to somatostatin-positive (SST+) neuro

216 , or vasoactive intestinal peptide-positive (VIP+) neurons, to map the brain-wide input to the three

217 vasoactive intestinal polypeptide positive (VIP) interneuron depolarization can account for the redu

218 set of SCN neurons unrelated to postsynaptic VIP expression.

219 ess this, we examined the role of prefrontal VIP interneurons in a widely studied mouse behavior: dec

220 me and T2-weighted volume-intensity product (VIP) by using a black-blood T2-weighted radial fast spin

221 through the variable importance projection (VIP) values, allowed to identify ten volatiles as potent

222 es with a variable importance in projection (VIP) score >=2.5 were tested for predictability in the "

223 based on variable importance in projection (VIP) scores was achieved for all lipids that were detect

224 lized variable importance in the projection (VIP) and regression vector statistics of partial least s

225 heir variables importance in the projection (VIP) values, since they contribute mainly to the discrim

226 In human MST and putative VIP, multivoxel pattern analysis permitted classificatio

227 sponses by activating two related receptors, VIP receptor 1 and 2 (VIPR1 and VIPR2).

228 We recorded VIP-INs in brain slices from Scn1a(+/-)mice and wild-typ

229 In contrast to regular VIP interneurons, ChAT-VIP neurons did not disinhibit py

230 omotion, the relevance of locomotion-related VIP neuron activity to visual coding is not known.

231 Revealing VIP+ cell morphologies, receptive fields and synaptic co

232 one secretion, collectively establishing SCN VIP cells as influential regulators of physiological tim

233 Here we reveal a key role for SCN VIP cells in central clock output.

234 tional, di-synaptic connectivity between SCN(VIP) neurons and dorsomedial hypothalamic neurons, provi

235 ether, our work establishes necessity of SCN(VIP) neurons for the LMA circadian rhythm, elucidates or

236 e intestinal polypeptide-expressing SCN (SCN(VIP)) neurons, including their molecular clock, in gener

237 suggests distinct functions for specific SCN(VIP) subtypes.

238 ngle-nuclei RNA-sequencing revealed that SCN(VIP) neurons comprise two transcriptionally distinct sub

239 ian outflow from and modulatory input to SCN(VIP) cells, and demonstrates a subpopulation-level molec

240 , providing a circuit substrate by which SCN(VIP) neurons may regulate LMA rhythms.

241 In vivo photometry revealed that while SCN(VIP) neurons are acutely responsive to light, their acti

242 on, based on a method of variable selection, VIP (variable importance in projection) and the results

243 k downstream of LHX1 and a largely separable VIP-dependent transcriptional network.

244 reduced from stage 0 through 4, and (2) SGII(VIP) was markedly reduced from stage 1 to 2.

245 tidergic vasoactive intestinal peptide (SGII[VIP]), and cutaneous amyloid index.

246 d transcriptional network and by significant VIP-directed plasticity in the internal phasing of the c

247 When stimulus and surround are similar, VIP neurons are inactive, and activity of SOM neurons le

248 By optogenetically activating single VIPs in live mice while recording the activity of nearby

249 , and do not typically express somatostatin, VIP, or the muscarinic acetylcholine receptor M2.

250 ical ChAT(+) neurons in mice are specialized VIP(+) interneurons that release GABA strongly onto othe

251 o stimuli of higher SFs, whereas suppressing VIP(+) cells resulted in a network response shift toward

252 ort the relevance of trophoblast-synthesized VIP as a critical factor in vivo for trophoblast-cell fu

253 We find that VIP interneurons have narrow axons and inhibit nearby so

254 g optogenetic circuit mapping, we found that VIP neurons integrate input from the contralateral IC an

255 We tested the hypothesis that VIP neurons simultaneously represent both heading and ho

256 Network modeling indicates that VIP-SST mutual antagonism regulates the gain of the cort

257 Here we show that VIP neurons in mouse V1 respond strongly to low contrast

258 and optogenetic manipulations, we show that VIP neurons provide coordinated daily waves of GABAergic

259 These results show that VIP-INs express Nav1.1 and are dysfunctional in DS, whic

260 d computational modeling further showed that VIP(+) disinhibition is necessary for goal-directed lear

261 Several studies have shown that VIP(+) cells are sensitive to neuromodulation and increa

262 Thus, our observations suggest that VIP has a direct positive role in neuronal recruitment a

263 the activity of nearby neurons, we find that VIPs break open a hole in blanket inhibition with an eff

264 The VIP-independent network does not affect core clock ampli

265 The VIP-ires-Cre amacrine cell types were identified in VIP-

266 The VIP/VPAC2 cellular axis is therefore a neurochemically a

267 opsies were exposed to agents that block the VIP receptors (VPAC1 and VPAC2) or MCs.

268 ubunit is targeted to synapses formed by the VIP- and calretinin-expressing inputs, and plays a speci

269 ed inositol hexakisphosphate kinase from the VIP family that pyrophosphorylates phytic acid (InsP6) t

270 decoupled stimulus and choice signals in the VIP area, and challenge our understanding of choice sign

271 independent functions of LHX1, we mapped the VIP-independent transcriptional network downstream of LH

272 regulator DUSP4 are critical elements of the VIP-directed circadian re-programming.

273 re clock amplitude and synchrony, unlike the VIP-dependent network.

274 ng subgroup increased in number, whereas the VIP-containing subgroup decreased.

275 efficients and Bland and Altman plots of the VIPs-FS and VIPs-DS versus the SF-12, PVC Metra, BISS an

276 Here, we ask whether this VIP-SST circuit enhances plasticity directly, independen

277 e target virus (AdV5) were observed at those VIPs, even in competitive binding experiments with minut

278 Thus, VIP cells regulate surround suppression to allow pyramid

279 Thus, VIP interneurons effectively gate the ability of hippoca

280 Thus, VIP neurons are well-positioned to influence auditory co

281 nucleus also drove feedforward inhibition to VIP neurons, indicating that inhibitory circuits within

282 stained circuit-level circadian responses to VIP that are mediated at a cell-autonomous level.

283 ctivity-regulated genes that are specific to VIP neurons, and demonstrate that IGF1 functions cell-au

284 eurons was strongly biased toward Go trials, VIP neurons were similarly active in Go and No-Go trials

285 Trophoblast VIP deficiency entails immune homeostasis loss and adver

286 cells, here we demonstrate that trophoblast VIP is critical for trophoblast function: VIP gene haplo

287 uggests that disinhibition of the cortex via VIP+ cells, which inhibit SST+ cells, might be a general

288 pha5-GABA(A)R-mediated phasic inhibition via VIP input to interneurons plays a predominant role in th

289 traditional submerged cultures without VIP, VIP-assisted ALI culture significantly boosted the numbe

290 ignal-intensity volume (HSV) and T2-weighted VIP independently, and the average score was chosen as c

291 ge, 0.1%-17%), respectively, and T2-weighted VIP was equal to 0 msec and 303 msec (range, 39-1012 mse

292 ease in both T2-weighted HSV and T2-weighted VIP was observed (P = .03).

293 ants with CF, T2-weighted HSV or T2-weighted VIP were associated with forced expiratory volume in 1 s

294 dominantly found in the tumor tissue whereas VIP and its mRNA were scarce.

295 onomous and circuit-level mechanisms whereby VIP synchronises the SCN are poorly understood.

296 ing adolescence, and mature animals in which VIP interneurons lack ErbB4 exhibit reduced cortical res

297 pregnancy in normal maternal background with VIP-deficient trophoblast cells, here we demonstrate tha

298 Also, the perovskite solar cells with VIP processing shows less hysteresis behavior and a stab

299 e increase in intracellular [Ca(2+)](I) with VIP and UTP was significantly smaller in MECs from TSP1(

300 with traditional submerged cultures without VIP, VIP-assisted ALI culture significantly boosted the