ライフサイエンスコーパス: VIP

1 VIP did not increase the phosphorylation of the EGFR.

2 VIP does not activate with EGFR.

3 VIP increased delayed rectifier K+ current and L-type ca

4 VIP interneurons, themselves regulated by neuromodulator

5 VIP is also shown to prolong the duration of acetylcholi

6 VIP is expressed, in a circadian manner, in interneurons

7 VIP stimulated an increase in ciliary beat frequency (EC

8 VIP stimulates a cAMP-dependent increase in [Ca(2+)]i an

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

10 VIP vector-transduced mice exhibited long-lived mAb expr

11 VIP- and VPAC-specific agonists increased [Ca(2+)]i and

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

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

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

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

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

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

18 results demonstrate that administration of a VIP antagonist after allo-BMT is a promising safely ther

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

20 E but was antagonized by pretreatment with a VIP antagonist.

21 punishment) strongly and uniformly activated VIP neurons in auditory cortex, and in turn VIP recruitm

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

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

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

25 Cell migration against VIP was sensitive to protein kinase C (PKC) and protein

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

27 n index (SGII) for PGP 9.5 (SGIIPGP 9.5) and VIP (SGIIVIP).

28 nterior to the angular gyrus such as AIP and VIP are less medially displaced relative to macaque monk

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

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

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

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

33 harge, Beta peptide design, NCBB design, and VIP redesign.

34 very of both local and systemic insulin- and VIP-like neuropeptides, sculpt the growth of specific tr

35 Of SOM-IR, SP-IR, and VIP-IR varicosities that lacked VAChT-immunoreactivity,

36 s of increased translocation include MCs and VIP.

37 rea V6 is interconnected with areas MSTd and VIP, allowing for the possibility that V6 also integrate

38 Similar to areas MSTd and VIP, the population of V6 neurons was best able to discr

39 However, unlike areas MSTd and VIP, V6 neurons are almost universally unresponsive to i

40 d by cholinergic, adrenergic, nitrergic, and VIP-positive terminals.

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

42 interneurons and pyramidal cells in PFC and VIP.

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

44 mor tissue was investigated for secretin and VIP.

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

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

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

48 anglionic eminences and had fewer SST(+) and VIP(+) interneurons.

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

50 ergic conditions in the IAS of wild-type and VIP(-/-) mice.

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

52 ral population, nitrergic subpopulation and (VIP) varicosities were reduced.

53 ral population, nitrergic subpopulation and (VIP) varicosities were reduced.

54 man sinonasal physiology are unknown, as are VIP's interactions with histamine, a major regulator of

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

56 g signals in the ventral intraparietal area (VIP) are represented in body-centered coordinates.

57 ral area (MSTd), ventral intraparietal area (VIP), and visual posterior sylvian area (VPS), that are

58 a (MSTd) and the ventral intraparietal area (VIP), have been shown to integrate visual and vestibular

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

60 n signals in the ventral intraparietal area (VIP), parietoinsular vestibular cortex (PIVC), and dorsa

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

62 ation: An activating coupling agent, such as VIP, must act in-phase with the activity of core-clock p

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

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

65 te the first evidence of association between VIP and CRTH2 in recruiting eosinophils.

66 rong association and co-localization between VIP peptide and CRTH2 molecules.

67 Herein we investigate the effects of both VIP analogues on cell viability, membrane integrity, and

68 redicted that phase tumbling following brief VIP treatment would accelerate entrainment to shifted en

69 ether the left ventricle is also affected by VIP gene deletion is unknown.

70 ent of inhibitory NMT in the IAS mediated by VIP.

71 g, and cycloplegic retinoscopy, performed by VIP-certified optometrists and ophthalmologists who were

72 Through its diverse effects on ion channels, VIP shortens APD with increased APD spatial heterogeneit

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

74 netic experiments showed that, collectively, VIP+ cells made strong connections with OFF delta, ON-OF

75 However, specific details concerning VIP-ergic NMT are limited, largely because of difficulti

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

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

78 In contrast, VIP-positive basket cells provided perisomatic inhibitio

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

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

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

82 1 to a stationary scene, 2) that depolarized VIP cells enhance V1 responses to moving objects by redu

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

84 We examined VIP(-/-)and wild type (WT) mice using Magnetic Resonance

85 the VIP(-/-) mouse and mimicked by exogenous VIP (1-100 nm).

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

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

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

89 ower visual field immediately medial to face VIP.

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

91 ut onto 49% of neurons with a preference for VIP-negative (VIP-) neurons.

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

93 iderably, with increasing heterogeneity from VIP to PFC.

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

95 Further, VIP acts together with GABAA signaling to couple the net

96 d identification of phosphoproteome in gels (VIPing) through coupling specific detection of phosphopr

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

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

99 an LIP paradoxically ends up medial to human VIP.

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

101 In the current study, we examined if VIP knockout mice (VIP(-/-)) develop both right (RV) and

102 We find that synchrony is only possible if VIP (an inducer of Per expression) is released in-phase

103 d the ability of vectored immunoprophylaxis (VIP) to prevent intravenous transmission of HIV in human

104 We have used vectored immunoprophylaxis (VIP), an adeno-associated virus-based technology, to int

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

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

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

108 Hearts were dilated in VIP(-/-) mice, with thinning of LV wall and increase in

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

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

111 apping in LIP and face-centered remapping in VIP, and weaker evidence for hand-centered remapping.

112 Depolarizing responses in VIP or PV BCs resulted in increased amplitudes and frequ

113 e frames of visual and vestibular signals in VIP, and emphasize that frames of reference for neurons

114 resentation of vestibular heading signals in VIP.

115 Vestibular heading tuning in VIP is invariant to changes in both eye and head positio

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

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

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

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

120 inase A (PKA), PKC and calcium all inhibited VIP-induced cAMP formation, whereas calcineurin or calmo

121 Optogenetically inhibiting VIP interneurons consistently increased seizure threshol

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

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

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

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

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

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

128 ole-cell recordings of fluorescently labeled VIP+ cells revealed three predominant types: wide-field

129 h are orthologous to the yeast and mammalian VIP kinases.

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

131 ent study, we examined if VIP knockout mice (VIP(-/-)) develop both right (RV) and left ventricular (

132 histocompatibility complex (MHC)-mismatched VIP-knockout (KO) or wild-type donors, and treated with

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

134 Although the use of native VIP facilitates neuroprotection, clinical application of

135 Consequently, we found that the native VIP is less potent as an antibacterial and fails as a le

136 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(-

137 neurons with a preference for VIP-negative (VIP-) neurons.

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

139 bitory circuit module in which activation of VIP interneurons transiently suppresses primarily somato

140 Optogenetic activation of VIP neurons increased V1 visual responses in stationary

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

142 iated disinhibitory circuit, the activity of VIP interneurons in vivo increased and that of somatosta

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

144 Secondary analysis of VIP data from participants who underwent comprehensive e

145 For most aspects of VIP+ network output, there was no circadian regulation.

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

147 Genetic and pharmacological blockade of VIP-signaling protected allo-BMT recipients from lethal

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

149 fect of locomotion, and photolytic damage of VIP neurons abolished the enhancement of V1 responses by

150 s depended on both the phase and the dose of VIP.

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

152 However, the effects of VIP on human sinonasal physiology are unknown, as are VI

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

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

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

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

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

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

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

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

161 To overcome the metabolic limitations of VIP, we modified the native peptide sequence and generat

162 Presence and localization of VIP receptors (VPAC1 and 2) were determined by RT-PCR, i

163 lular signaling is disrupted through loss of VIP-VPAC2 signaling.

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

165 transcriptional elements and generic mode of VIP-VPAC2R signaling.

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

167 Our results demonstrate the potential of VIP as a path toward the elusive goal of immunization ag

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

169 An up-regulation of VIP in histamine-driven allergic rhinitis would likely e

170 cordings, we examined the functional role of VIP interneurons in awake mice, and investigated the und

171 We found that heading tuning of VIP neurons based on optic flow generally shifted with e

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

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

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

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

176 Acetylcholine released onto VIP interneurons that innervate pyramidal neuron perisom

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

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

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

180 Somatostatin or VIP neuron activation also impaired or enhanced performa

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

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

183 neuropeptide, vasoactive intestinal peptide (VIP) and its canonical receptor, VPAC2R, using the trans

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

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

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

187 Vasoactive intestinal peptide (VIP) is an anti-inflammatory neuropeptide recently ident

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

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

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

191 tance P (SP), vasoactive intestinal peptide (VIP) or vesicular acetylcholine transporter (VAchT), and

192 We show that vasoactive intestinal peptide (VIP) secreted by the innervating ganglia promotes ductal

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

194 pon G-coupled vasoactive intestinal peptide (VIP) signaling.

195 c neurons and vasoactive intestinal peptide (VIP) varicosities.

196 l marker, and vasoactive intestinal peptide (VIP), a sudomotor nerve functional marker, followed by q

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

198 ation between vasoactive intestinal peptide (VIP), CRTH2, and eosinophil recruitment.

199 statin (SOM), vasoactive intestinal peptide (VIP), or neuropeptide Y.

200 14) find that vasoactive intestinal peptide (VIP), secreted by parasympathetic nerves, is a surprisin

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

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

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

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

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

206 t increase in vasoactive intestinal peptide (VIP)-mediated disinhibition.

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

208 ion activates vasoactive intestinal peptide (VIP)-positive neurons in mouse V1 independent of visual

209 he release of vasoactive intestinal peptide (VIP).

210 acid peptide, vasoactive intestinal peptide (VIP).

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

212 s strongly recruited vasointestinal peptide (VIP)-expressing GABAergic interneurons, a subset of sero

213 subcutaneous injections of VIPhyb (peptidic VIP-antagonist) or phosphate-buffered saline (PBS).

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

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

216 Moreover, anti-phasic VIP release suppresses coherent rhythms by moving the ne

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

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

219 press the vasoactive intestinal polypeptide (VIP) and calretinin contact several distinct types of in

220 d by both vasoactive intestinal polypeptide (VIP) and GABAA signaling.

221 ropeptide vasoactive intestinal polypeptide (VIP) and its VPAC2 receptor form a key component of inte

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

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

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

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

226 Vasoactive intestinal polypeptide (VIP) is released from intracardiac neurons during vagal

227 e require vasoactive intestinal polypeptide (VIP) or its receptor VPAC2R.

228 retin and vasoactive intestinal polypeptide (VIP) receptors are responsible for the activation of ade

229 tase, and vasoactive intestinal polypeptide (VIP) to detect neural elements and their transmitter con

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

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

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

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

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

235 +/- 1.3% vasoactive intestinal polypeptide (VIP)-IR varicosities in guinea pig rectal myenteric gang

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

237 d) and vasoactive intestinal polypeptide(+) (VIP) (CGE-derived) neocortical interneurons, but had a n

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

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

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

241 set of SCN neurons unrelated to postsynaptic VIP expression.

242 ch effectively varies the initial potential (VIP) of the system of interest.

243 ty and spontaneous firing of the presynaptic VIP+ neurons were unchanged between day and night, and t

244 with high expression levels of MECOM, PREX2, VIP, MYCT1, and PAWR.

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

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

247 Moreover, animals receiving VIP that expresses a modified VRC07 antibody were comple

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

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

250 5-item of the Vitiligo Impact Patient scale (VIPs) of who 235 were of skin phototype I to III and 66

251 and fluid secretion in response to secretin, VIP and forskolin through cAMP/PKA pathway activation.

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

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

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

255 n the mammalian PVN (CCK, CRH, ENK, NTS, SS, VIP, OXT, AVP), we provide the first 3D arrangement map

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

257 We conclude that VIP below 100 nM synchronizes SCN cells and above 100 nM

258 Here we demonstrate that VIP is capable of protecting humanized mice from intrave

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

260 n within the ventromedial SCN, we found that VIP+ afferents provided input onto 49% of neurons with a

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

262 Together, these results indicate that VIP signaling modulates the output from the OB to mainta

263 Biochemical assays showed that VIP-induced eosinophil chemotaxis from AR patients and E

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

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

266 nsmitted founder HIV strain, suggesting that VIP may be effective in preventing vaginal transmission

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

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

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

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

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

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

273 abolished by VIP6-28 (30 mum), absent in the VIP(-/-) mouse and mimicked by exogenous VIP (1-100 nm).

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

275 The cytotoxicity of the VIP derivatives is specific for pathogens, because they

276 These data suggest that components of the VIP network and its synaptic output up through GABAA-R o

277 challenge were dependent on the dose of the VIP vector.

278 These results indicate that the VIP analogues emerge as attractive alternatives for trea

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

280 The sensitivity and specificity of the VIPing strategy was demonstrated using standard protein

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

282 These VIP interneurons preferentially inhibited somatostatin-e

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

284 Thus, VIP cells regulate surround suppression to allow pyramid

285 application of the hormone is limited due to VIP's rapid metabolism and inability to distinguish betw

286 or calmodulin did not modify the response to VIP.

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

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

289 VIP neurons in auditory cortex, and in turn VIP recruitment increased the gain of a functional subpo

290 We found that the two VIP derivatives kill various non-pathogenic and pathogen

291 However, the ionic mechanisms underlying VIP effects are largely unknown.

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

293 sis of atrial arrhythmias in scenarios where VIP release is increased.

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

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

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

297 -starved for 2 hours before stimulation with VIP, VPAC1-, or VPAC2-specific agonists.

298 lphareg in Eol-1 cells upon stimulation with VIP.

299 ice treated with VIPhyb or transplanted with VIP-KO allografts had significantly lower viral loads, i

300 (3) A cortical sector within VIP processes movement around and toward the face indepe