ライフサイエンスコーパス: substance P

1 sion of preprotachykinin-A (the precursor of substance P).

2 highly correlated to the process elicited by substance P.

3 equency response to exogenous application of substance P.

4 kinin is another tachykinin with homology to substance P.

5 glucagon, glucagon-like peptide 1 (GLP1) and substance P.

6 tes at sites of intestinal inflammation make substance P.

7 by iontophoretic application of serotonin or substance P.

8 ndependent of the major sensory neuropeptide substance P.

9 viors and inhibits stress-induced release of substance P.

10 r myelin, or immunofluorescently labeled for substance P.

11 lucagon, glucagon-like peptide 1 (GLP1), and substance P.

12 r subunit 5 and GABA(A) receptors as well as substance P.

13 -preprotachykinin I), and protein levels for substance P.

14 one that resembled degranulation induced by substance P.

15 alized within 48 hours, including release of substance P.

16 by the striosomally enriched neuromodulator substance P.

17 ptive neuronal markers IB4, TRPV1, CGRP, and substance P.

18 reased number of neurons expressing CGRP and substance P.

19 tes modulatory responses to the neuropeptide substance P.

20 (p = 0.001) and thiobarbituric acid reactive substances (p = 0.001) as well as the mean percent chang

21 as a small and high affinity ligand for the substance P 1-7 (SP(1-7), H-Arg-Pro-Lys-Pro-Gln-Gln-Phe-

22 ollowing TTX application, carbachol (1 muM), substance P (1 muM) and an NKI agonist (GR73632, 100 nM)

23 d to the endothelium-dependent vasodilators, substance P (10(-8) M) and adenosine 5diphosphate (10(-5

24 200, 2 mum) antagonists and mimicked by NK1 (substance P, 100 nm) and NK3 (neurokinin B [NKB], 100 nm

25 on increases in flow evoked by intracoronary substance P (20 pmol/min).

26 In this study, we test the role of substance P, a neuroinflamatory peptide, in RLB-induced

27 Substance P, a peptide derived from the TAC1 gene, media

28 ormed rapid quantification of serum level of substance P, a potential biomarker of acute neuroinflamm

29 in GFAP and IL-1beta after inflammation, and substance P, a prototype neurotransmitter of primary aff

30 nction with capillary LC for the analysis of substance P, a tryptic digest of bovine serum albumin, a

31 Intrathecal injection of Substance P activated this cascade (increased phosphoryl

32 ed brainstem nuclei and the neurotransmitter substance P, among other substrates.

33 Intradermal administration of substance P, an activator of skin mast cells, and challe

34 Neurokinin-1 antagonists compete with substance P, an endogenous ligand with a high density of

35 It has been proposed that substance P and calcitonin gene-related peptide (CGRP) a

36 type 1, the small peptidergic neuron markers substance P and calcitonin gene-related peptide, and the

37 emonstrate that glutamate together with both substance P and CGRP mediate tissue-injury associated pa

38 neurons that expressed either enkephalin or substance P and extended fibers to the globus pallidus.

39 a(2+) transients to KCl, caffeine, nicotine, substance P and GR 64349 (an NK2 agonist), suggesting th

40 Substance P and its truncated receptor exert oncogenic e

41 re-embedding immunoelectron microscopy using substance P and Met-/Leu-enkephalin antibodies to label

42 muscle afferents excite NTS GABA neurons via substance P and microinjection of a substance P-neurokin

43 All mutant receptors were able to bind to substance P and neurokinin A ligand with similar affinit

44 o demonstrate TAC1 (encoding the tachykinins substance P and neurokinin A) to be strongly activated b

45 pocampal and ventral tegmental area neurons, substance P and neurotensin activate a channel complex c

46 These include peptides, such as substance P and neurotensin, as well as acetylcholine an

47 Tandem mass spectra of two other peptides, substance P and oxidized insulin alpha-chain, demonstrat

48 n of mass/charge peak expression levels with substance P and proenkephalin A (218-228).

49 itively correlated with expression levels of substance P and proenkephalin A (amino acids 218-228), r

50 The spatial expression patterns of substance P and proenkephalin, marker neuropeptides of t

51 mmatory-cell infiltration, and the pulmonary substance P and pulmonary Th2 cytokine levels that occur

52 ed levels of the stem cell chemoattractants, substance P and SDF-1, in both the injured cornea and bl

53 V-1 Gp120-induced calcium influx mediated by substance P and significantly decreased the permeability

54 odilators adenosine 5'-diphosphate (ADP) and substance P and the endothelium-independent vasodilator

55 of the tachykinin family of peptides, namely substance P and the newly discovered endokinins A and B

56 functional maturation via angiotensin II and substance P and through the angiotensin II receptor type

57 wn Prep substrates, such as the neuropeptide substance P and thymosin-beta4, the precursor to the bio

58 egulate the transmission of pain messages by substance P and TRPV1-expressing pain fibers.

59 xicant reactions increase skin sensory nerve substance P and, in turn, increase itching responses.

60 Substance-P and hemokinin-1 are proinflammatory neuropep

61 tive for calcitonin gene-related peptide and substance P) and myelinated non-nociceptive fibers (posi

62 nerve-derived dilator neuropeptides CGRP and substance P, and also nNOS-derived NO.

63 that expressed choline acetyltransferase and substance P, and in inhibitory motoneurons and interneur

64 e under resting conditions, independently of substance P, and internalized following activation by DO

65 kers calcitonin gene-related peptide (CGRP), substance P, and isolectin B4.

66 lapse, including the urocortins, nociceptin, substance P, and neuropeptide S.

67 The baseline responses to ADP, substance P, and SNP of arterioles from the UDM patients

68 t from multiple raphe nuclei, (2) serotonin, substance P, and TRH activate RTN chemoreceptors, and (3

69 ive RTN neurons were activated by serotonin, substance P, and TRH.

70 thase (nNOS), vasoactive intestinal peptide, substance P, and tyrosine hydroxylase to quantify nerves

71 , stimulated with carbachol, stimulated with substance P, and, as a test for synergy, stimulated with

72 Together, substance P- and enkephalin-positive terminals represent

73 mining the well-characterized model peptides substance P, angiotensin II, and bradykinin.

74 as not only a critical pharmacophore for the substance P antagonist activities, but as an address reg

75 ifunctional peptides with opioid agonist and substance P antagonist bioactivities were designed with

76 (18)F-Labeled substance P antagonist-receptor quantifier ([(18)F]SPA-R

77 ak clusters in mass spectra of reserpine and substance P are measured using Fourier transform ion cyc

78 uction by the toxin [Sar(9), Met (O(2))(11)]-substance P as the rest of the RTN Phox2b(+)/TH(-) cells

79 [M + 2H](2+) or [M + 3H](3+) charge state of substance P as well as individual trisaccharide isomers

80 ides belonging to the tachykinin family with substance P being the predominant member.

81 iatal matrix, whose axons corelease GABA and substance P, both at synapses with GABAergic neurons in

82 cid (GABA)-ergic striatal neurons expressing substance P, but it is also influenced by indirect basal

83 Gq, Gs, and beta-arrestin when stimulated by substance P, but it lacks any sign of constitutive activ

84 of dynorphin and prodynorphin with CGRP and substance P, but not with isolectin B4.

85 d glycation end-products-in the neuropeptide substance P by ultrahigh-resolution Fourier transform io

86 No apparent differences were observed in substance P, calcitonin gene-related peptide, or neurope

87 1,4,5-trisphosphate-dependent signaling with substance P causes idiosyncratic changes in dynamic Ca(2

88 relationship between central nervous system substance P containing neural circuits and aggression in

89 ts correlated with a significant increase in substance P content of the cutaneous nerves and an accom

90 the authors analyzed brain regional, CCK-8, substance P, corticotropin releasing factor (CRF), and n

91 ay a role in the pathogenesis of IBD include substance P, corticotropin-releasing hormone, neurotensi

92 y activation of the neurokinin-1 receptor by substance P decreases sepsis survival through multiple m

93 IgE-dependent and substance P-dependent activation in vivo also induced di

94 opical corticosteroid, alcohol delamination, substance P-derived peptide and ILGF-I drops, botulinum

95 Topical treatment with the MC trigger substance P does not affect wound healing in MC-deficien

96 Another crucial finding is that substance P does not regulate the production of SDF-1alp

97 ing product-ion spectra of doubly protonated substance P, doubly protonated gramicidin S, doubly prot

98 in striatal mRNAs encoding the neuropeptides substance P, dynorphin, enkephalin and cholecystokinin.

99 te, GABA, thyrotropin releasing hormone, and substance P encoded by the Tachykinin-1 (Tac1) gene.

100 aboratory demonstrated that the neuropeptide substance P enhances the striatal METH-induced productio

101 xons and terminals overlap with cholinergic, substance P-ergic, and glutamatergic markers.

102 confirmed that preBotC neurons responsive to substance P exhibited similar responsiveness to bradykin

103 ally, the majority of neurons that expressed substance P expressed both enzymes but did not bind IB4.

104 these receptors are expressed on polymodal, substance P-expressing neurons.

105 n of Gad65, dopamine receptor D1 (Drd1), and substance P expression at different phases of prenatal d

106 production, while TGF-beta blocks macrophage substance P expression.

107 Siebenharr et al. demonstrate that substance P fibers are increased in early lesions, and t

108 They also suggest that any release of substance P from injured Abeta afferents is unlikely to

109 ted inflammation, suggesting that release of substance P from nerve fibers triggers the inflammatory

110 f HXA(3) correlated with enhanced release of Substance P from primary sensory afferents.

111 n types of nerve injury, and that release of substance P from these afferents contributes to the resu

112 sis, it was found that IL-12 and IL-23 drive substance P gene expression and peptide synthesis in mur

113 nce P-positive neurons in the vlPAG, and the substance P gene, a direct target for DeltaFosB, is down

114 Substance P had bidirectional effects on dopamine releas

115 Tachykinin/Substance P has been implicated in aggression in mammals

116 modulation of aggression, but no studies of substance P have yet been reported with regard to human

117 Substance P, however, does not act as autocrine stimulat

118 escent cells colocalized with enkephalin and substance P immunoreactive medium spiny neurons.

119 ncreased calcitonin gene-related peptide and substance P immunoreactivity.

120 gic and surrounded by terminals with intense substance P immunoreactivity.

121 The high production of substance P in breast cancer cells (BCCs) is caused by t

122 lated peptide but increases the neuropeptide substance P in LPS-treated mice.

123 lts demonstrate the relative contribution of substance P in regulating the clinical severity of HSK l

124 Coexistence of serotonin and substance P in terminals within RTN confirmed that lower

125 and nociceptor activation via the release of substance P in the skin and dorsal root ganglion.

126 horns revealed increased immunoexpression of Substance P in week 8 and neurokinin-1 in weeks 8 and 12

127 P<0.01) but, in contrast to SMTC, inhibited substance P-induced increases in flow (P<0.01).

128 Overall, substance P-induced vasorelaxation corresponded poorly w

129 and without RLB revealed an increase of the substance P-inducible neurokinin 1 receptor (NK1-R) in t

130 A spontaneous IPSCs (sIPSCs), (2) endogenous substance P influence on sIPSC frequency, and (3) sIPSC

131 Exogenous PACAP and substance P initiated a slow depolarization in the neuro

132 uence on the signal intensities of molecular substance P ions.

133 Substance P is a tachykinin that enhances pathways of in

134 with the potential to release both 5-HT and substance P is necessary for normal respiratory dynamics

135 ese results do not support the proposal that substance P is present at significant levels in the term

136 , we show that the neurokinin 1 receptor for substance P is required for SCC-mediated inflammation, s

137 Substance P is the prototype tachykinin peptide and trig

138 Substance P knockout (KO) mice retained their ability to

139 -2, iNOS, and VGSC was investigated by using substance P, l-arginine, and veratrine, respectively, as

140 uch as up-regulation of the NK1 receptor and substance P, lead to antiopioid effects in ascending or

141 Substance P-like immunoreactive free nerve endings were

142 immunoreactive en plaque motor endplates and substance P-like immunoreactive, thin and varicose free

143 Substance P-like immunoreactivity (SPL-IR) was semiquant

144 The cerebrospinal fluid substance P-like immunoreactivity levels were directly c

145 subjects with personality disorder (PD) and substance P-like immunoreactivity was measured and corre

146 complex, the patterns of calbindin-like and substance P-like immunoreactivity, and the organization

147 T2 in the Trpv1-Cre population together with substance P mediate acute cold pain, whereas glutamate t

148 ls and neurokinin receptors are important in substance P-mediated inhibition of ductal bicarbonate se

149 ferent weighting of dopamine transmission by substance P modified the apparent center-surround contra

150 rough the angiotensin II receptor type 1 and substance P neurokinin 1 receptors.

151 rons via substance P and microinjection of a substance P-neurokinin 1 receptor (NK1-R) antagonist int

152 ation of DeltaFosB in the vlPAG desensitizes substance P neurons enriched in this area and opposes be

153 Substance P neuropeptide and its receptor, neurokinin-1

154 data suggest that an interaction between the substance P NK1-R and GABAergic transmission in the NTS

155 uorescence labeling in NTS show an increased substance P NK1-R internalization on GABA neurons.

156 tion channel subfamily V, receptor 1 (TRPV1)-substance P nociceptive signaling pathway.

157 ough TACR1 (a G-protein-coupled receptor for substance P) occurs by means of a unique mechanism: it d

158 in the same region, microinjections of 1 mum substance P or 1 mm nicotine into the pTRG restored rhyt

159 urthermore, by pharmacological inhibition of substance P or calcitonin gene-related peptide (CGRP) si

160 We found no evidence of either substance P or CGRP expression in injured Abeta terminal

161 cient mice, we evaluated the contribution of substance P or CGRP to these sensory modulations, with o

162 ross-sectional area-and some co-labeled with substance P or isolectin B4.

163 id not prevent modulation of RTN activity by Substance P or thyrotropin-releasing hormone, previously

164 d NS309-induced vasodilatation and abolished substance P- or adenosine 5 diphosphate-induced relaxati

165 or Gal, Penk, and Adcyap1, and receptors for substance P, orexin, serotonin, and ATP.

166 e possibility is raised that blocking of the substance P pathway with NK1-R antagonists postocular tr

167 Drift field application frequency scans of substance P peptide ions show that it is possible to sep

168 ures of ions produced by electrospraying the substance P peptide, as well as a mixture of tryptic pep

169 d in an increased labeling of CGRP-, but not substance P-positive cells in the lumbar dorsal root gan

170 in corneal epithelial nerve regeneration and substance P-positive nerve density in both wounded and u

171 Induction of DeltaFosB by IS predominates in substance P-positive neurons in the vlPAG, and the subst

172 treatment also targeted the regeneration of substance P-positive nociceptive axons but had no effect

173 hat proposed for basic neuropeptides such as substance P, possibly involving Mas-related gene 2 (MrgX

174 IL-10 inhibits T-cell substance P production, while TGF-beta blocks macrophage

175 tor beta (TGF-beta) in controlling leukocyte substance P production.

176 effect of SDF-1alpha on hemopoiesis through substance P production.

177 Pro-substance P (ProSP) is a stable surrogate marker for lab

178 a subset of dissociated neurons responded to substance P, putatively corresponding to inspiratory pre

179 cribes an asymmetric synthesis of the potent substance P receptor antagonist (+)-CP-99,994 from 4-phe

180 Administration of a substance P receptor antagonist in mice.

181 anisms responsible for this improvement, the substance P receptor was blocked in mice after traumatic

182 ify NALCN as the cation channel activated by substance P receptor, and suggest that UNC-80 and Src fa

183 We focused on substance P receptor-expressing (NK1R+) projection neuro

184 Activation of substance P receptors, which are coupled to Galpha(q), i

185 not elicit degranulation of human skin MC or substance P release from NT2N cells in vitro.

186 by noxious heat and mechanical stimulations, substance P release was measured in the spinal cord by v

187 te cyclase-activating polypeptide (PACAP) or substance P released during tetanic neural stimulation m

188 stellation pharmacology, we found that these substance P-responsive neurons also responded to histami

189 lood-brain barrier impermeable toxin, stable substance P-saporin (SSP-SAP), which ablates cells expre

190 otrapezoid nucleus region was destroyed with substance P-saporin prior to lentivirus injection into t

191 a neurokinin-1-receptor antagonist to block substance P signaling eliminated the improved survival o

192 des illustrated how many of these, including substance P, somatostatin, and neurotensin have actions

193 x/POU domain protein 3b, Ets variant gene 1, substance P, somatostatin, vasoactive intestinal polypep

194 ions, and 10 chloride and contains a single Substance P (SP) [SP + 3H](3+) ion (SP(3+); amino acid s

195 we investigated the role of the neuropeptide substance P (SP) and cognate neurokinin 1 (NK1) nocicept

196 Substance P (SP) and hemokinin-1 (HK-1) are neuropeptide

197 peptides of the tachykinin family, including substance P (SP) and hemokinin-1 (HK-1), bind the neurok

198 We have shown that substance P (SP) and its neurokinin-1 receptor (NK-1R) r

199 ting evidence suggests that the neuropeptide substance P (SP) and its principal receptor neurokinin 1

200 Substance P (SP) and its receptors are involved in anxie

201 eloped a combination of systemic delivery of substance P (SP) and local release of stromal-derived fa

202 factor, and endogenous pruritogens, such as substance P (SP) and serotonin.

203 The peptide substance P (SP) and the cytokine tumor necrosis factor

204 n-converting enzyme-1 (ECE-1) in controlling substance P (SP) and the neurokinin 1 receptor (NK(1)R)

205 Substance P (SP) and the neurokinin-1 receptor (NK-1R) a

206 We examined the hypothesis that substance P (SP) and the neurokinin-1 receptor (NK-1R),

207 IL-33 augments VEGF release induced by substance P (SP) and tumor necrosis factor (TNF) release

208 Studies have shown that blocking substance P (SP) binding to neurokinin 1 receptor with s

209 e is increasing evidence that the tachykinin substance P (SP) can augment inflammatory immune respons

210 he structural evolution of the undecapeptide substance P (SP) during the final stages of ESI.

211 kephalinergic striatal neurons, and enhanced substance P (SP) expression by SP striatal projection ne

212 Release of substance P (SP) from nociceptive nerve fibers and activ

213 The peptide substance P (SP) has been implicated in inflammatory con

214 othelin-converting enzyme-1 (ECE-1) degrades substance P (SP) in early endosomes of epithelial cells

215 he nasal mucosa and higher concentrations of substance P (SP) in nasal secretions than HCs.

216 nd superresolution microscopy, we found that substance P (SP) induces the association of the neurokin

217 gh some work has suggested that intracranial substance P (SP) infusion reinstates cocaine seeking fol

218 To determine the effects of blocking substance P (SP) interactions with its major receptor (N

219 Substance P (SP) is a neuropeptide that mediates numerou

220 Substance P (SP) is a proinflammatory mediator implicate

221 Substance P (SP) is a prominent neuromodulator, which is

222 Substance P (SP) is also involved in inflammatory diseas

223 Substance P (SP) is an 11-amino acid peptide that belong

224 Substance P (SP) is an undecapeptide present in the CNS

225 Substance P (SP) is involved in wound healing, but its e

226 Substance P (SP) is linked to itch and inflammation thro

227 Substance P (SP) is thought to play a cardinal role in e

228 Substance P (SP) mediates colitis.

229 in part, by inhibiting GABAergic input onto substance P (SP) neurons in the ventral tegmental area (

230 U73,122 did not interfere with the effect of Substance P (SP) on cellular morphology and cellular imp

231 Furthermore, by pharmacologic inhibition of substance P (SP) or calcitonin gene-related peptide (CGR

232 ved cultured mast cells were stimulated with substance P (SP) or IgE/anti-IgE with or without preincu

233 Substance P (SP) plays a critical role in the cutaneous

234 To determine whether substance P (SP) plays a role in LH-induced antinocicept

235 ne PanIN cells that express the neuropeptide substance P (SP) receptor neurokinin 1-R (NK1-R).

236 Substance P (SP) regulates important intestinal function

237 ct, while the delayed phase occurs following substance P (SP) release in the brainstem.

238 Restoration of substance P (SP) signaling in denervated KC-Tie2 skin pr

239 Substance P (SP) specifically triggered intracellular ca

240 d paw edema and the anterograde transport of substance P (SP) that occur following formalin injection

241 The current study examined the effect of substance P (SP) upon intestinal epithelial cells and th

242 The role of substance P (SP) was investigated by pretreating animals

243 GFAP), tyrosine receptor kinase B (TrkB) and substance P (SP) were significantly increased in the col

244 We hypothesized that KARs and Substance P (SP), a modulatory neuropeptide that is used

245 ivery (RMD) technology utilizes a variant of substance P (SP), a neuropeptide that is rapidly interna

246 Substance P (SP), a pleotropic neuropeptide implicated i

247 network via simultaneous release of 5-HT and substance P (SP), acting at 5-HT(2A/2C), 5-HT(4), and/or

248 using production of the major Tac1 peptide, substance P (SP), as readout.

249 Approximately 50% of MSNs corelease substance P (SP), but how this neurotransmitter controls

250 vious evidence of colocalization of EM2 with substance P (SP), calcitonin gene-related peptide (CGRP)

251 Neuropeptides, such as substance P (SP), have long been seen as mediators of wi

252 Substance P (SP), involved in neurogenic inflammation by

253 The tachykinin, substance P (SP), is well known to augment inflammatory

254 ins are a family of neuropeptides, including substance P (SP), neurokinin A (NKA), and neurokinin B (

255 ioid peptide cholecystokinin, pronociceptive Substance P (SP), Neurokinin B, and a late wave of somat

256 ers: calcitonin gene-related peptide (CGRP), substance P (SP), neuronal nitric oxide synthase (nNOS),

257 IP), calcitonin-gene related peptide (CGRP), substance P (SP), neuropeptide tyrosine (NPY), and the n

258 Substance P (SP), one of the most widely expressed pepti

259 Substance P (SP), released by skin nerve fibers, is a po

260 gene's encoded peptide, the neurotransmitter substance P (SP), unless stimulated with the inflammator

261 PY), nitric oxide synthase (NOS), serotonin, substance P (SP), vasoactive intestinal peptide (VIP) or

262 ther calcitonin gene-related peptide (CGRP), substance P (SP), vesicular glutamate transporter 1 (VGl

263 al levels of the antiapoptosis neuropeptide, substance P (SP), were treated with the SP antagonist, S

264 renergic and delta-opioid receptors (DOP) on substance P (SP)-immunoreactive (-ir) varicosities in th

265 o both NA and 5HT, but transient central and Substance P (SP)-insensitive lamina I cells were unaffec

266 noreactive (IR) varicosities; 20 +/- 4.3% of substance P (SP)-IR varicosities and 9 +/- 1.3% vasoacti

267 issue of Blood, Janelsins et al report that substance P (SP)-treated dendritic cells (DCs) efficient

268 s calcitonin gene-related peptide (CGRP) and substance P (SP).

269 mesis model which also vomits in response to substance P (SP).

270 rtebrates is modulated by neuropeptides like Substance P (SP).

271 uch information to the spinal cord expresses substance P (SP).

272 The lower limit of detection was 30pM Substance P (SP, 2pg/50microl), and reproducible respons

273 lcitonin gene-related peptide (CGRP) without substance P (SP; CGRP(+) SP(-) ).

274 The selective NK1R agonist, GR73632, and Substance-P (SP) inhibited NE transport and reduced plas

275 the NK1 receptor agonist [Sar9,Met(O(2))11]-substance P (SSP), and fully blocked by the NK1 receptor

276 Injection of the neurotoxin saporin-substance P (SSP-SAP) into the retrotrapezoid nucleus (R

277 n the NTS while SAP conjugated to stabilized substance P (SSP-SAP) selectively killed neurons with NK

278 in the human coronary vascular bed, whereas substance P-stimulated vasodilatation is eNOS mediated.

279 od antagonist activity in the GPI assay with substance P stimulation ( K e = 26 nM) and good affinity

280 study examined possible mechanisms by which Substance P (Sub P) assumes a pronociceptive role in the

281 This study investigated the ability of substance P (Sub P) to induce dendritic varicosities (DV

282 Intestinal macrophages also produce substance P, subject mostly to IL-23 and TGF-beta regula

283 us secretion by sensory neurons that release substance P (SubP).

284 Laboratory animal studies of substance P suggest a facilitory role for this undecapep

285 Cytokine induction of substance P synthesis both in T cells and in macrophages

286 Certain signals, including substance P, the complement anaphylatoxins C3a and C5a,

287 Substance P, the principal ligand for the neurokinin-1 r

288 The activation by substance P through TACR1 (a G-protein-coupled receptor

289 These data support the postulate that substance P transmits early inflammatory signals from th

290 ers are increased in early lesions, and that substance P treatment induces catagen follicles along wi

291 pendent microvascular relaxation response to Substance P was diminished in HCC swine, which was rescu

292 Substance P was elevated in the cortex over the basal ga

293 Although substance P was not detected in terminals of injured aff

294 cted in bullwhip cells at about E10, whereas substance P was not detected in the bullwhip cells until

295 itonin gene-related peptide (CGRP-alpha) and substance P was significantly increased in ETR compared

296 ferently in striosome-matrix compartments by substance P.We paired detection of evoked dopamine relea

297 The post-CPB relaxation responses to ADP and substance P were significantly decreased in all 3 groups

298 oSP) is a stable surrogate marker for labile substance P, which has pro-inflammatory effects, increas

299 gh traumatic brain injury-induced release of substance P, which improves innate immunity to decrease

300 d RTN neuron activation by the neuropeptide, substance P, without affecting pH-sensitive background K