ライフサイエンスコーパス: CGRP

1 CGRP and VEGF expression was not related to the duration

2 CGRP caused sustained excitation of neurons in slices of

3 CGRP did not alter the passive properties of BNST-AL cel

4 CGRP dilated dural, but not pial, vessels and significan

5 CGRP increases langerin expression, decreases selected i

6 CGRP is also expressed in vestibular efferent neurons as

7 CGRP positive neurons expressed PACAP but not glutamate.

8 CGRP was also expressed by neutrophils and eosinophils a

9 CGRP(+) SP(-) afferent neurons are likely to be non-noci

10 CGRP(+) SP(-) boutons were prevalent in lateral lamina I

11 CGRP(PBN) neurons are also activated in Apc(min/+) mice,

12 CGRP-based agents induce effects at nanomolar concentrat

13 CGRP-containing nerves innervate dermal blood vessels an

14 iography was performed with [(3)H]MK-3207 (a CGRP receptor antagonist).

15 ed the effect of fremanezumab (TEV-48125), a CGRP-mAb, on the activity of second-order trigeminovascu

16 rugs, the 5-HT1B/D agonist sumatriptan and a CGRP-blocking monoclonal antibody, attenuated the periph

17 We examined the binding sites of a CGRP receptor antagonist (MK-3207) and related this to t

18 study, we show that, if given enough time, a CGRP-mAb can prevent the activation and sensitization of

19 he CGRP pathway was shown in skin by using a CGRP receptor antagonist.

20 on at the site of intradermally administered CGRP led to a similar bias in CD4(+) T cells from draini

21 approaches are humanised antibodies against CGRP or the CGRP receptor.

22 l calcitonin gene-related polypeptide-alpha (CGRP) in both the peripheral cortex of the femur and the

23 g-lasting (t(1/2) >/=7 hours) acylated alpha-CGRP analogue (alphaAnalogue) could alleviate and revers

24 alpha-calcitonin gene-related peptide (alpha-CGRP) has been limited because of its peptide nature and

25 Although CGRP has immunomodulatory effects on LC functions, its p

26 Although CGRP-null (-/-) mice demonstrate a significant reduction

27 ohistochemistry, we confirmed that, although CGRP staining was absent in the vestibular end-organs of

28 transient receptor potential vanilloid 1 and CGRP.

29 calcitonin gene-related peptide (CGRP), and CGRP treatment inhibited osteoclastogenesis in vitro.

30 er, these data highlight a novel circuit and CGRP/glutamatergic mechanism through which cisplatin-ind

31 d with CCL17 or various other cytokines, and CGRP expression was measured by using RT-PCR, quantitati

32 le interaction between the glutamatergic and CGRP system.

33 Norepinephrine and CGRP act through the alpha(2)-adrenergic receptor and CG

34 glutamate together with both substance P and CGRP mediate tissue-injury associated pain.

35 through the alpha(2)-adrenergic receptor and CGRP receptor, respectively, because blocking these rece

36 In lesional skin, VEGF and CGRP co-localised to UEA-1+ blood vessels.

37 d elucidated by the CGRP receptor antagonist CGRP(8-37).

38 403, a genetically engineered humanised anti-CGRP antibody, for migraine prevention.

39 proach to migraine treatment, humanized anti-CGRP monoclonal antibodies (CGRP-mAbs) were developed to

40 y, a new class of such drugs, humanized anti-CGRP monoclonal antibodies (CGRP-mAbs), were found to be

41 of two doses of TEV-48125, a monoclonal anti-CGRP antibody, in the preventive treatment of chronic mi

42 and efficacy of TEV-48125, a monoclonal anti-CGRP antibody, in the preventive treatment of high-frequ

43 ven recent clinical trials showing that anti-CGRP monoclonal antibodies can reduce and even prevent m

44 elated peptide (CGRP) monoclonal antibodies (CGRP-mAbs) are capable of preventing migraine.

45 d that humanized CGRP monoclonal antibodies (CGRP-mAbs) prevent activation and sensitization of high-

46 , humanized anti-CGRP monoclonal antibodies (CGRP-mAbs) were developed to reduce the availability of

47 , humanized anti-CGRP monoclonal antibodies (CGRP-mAbs), were found to be effective in reducing the f

48 Moreover, applying CGRP caused taste buds to secrete serotonin (5-HT), a Pr

49 We found that both CGRP(+) and IB4(+) terminals were devoid of GlyR alpha1-

50 L-4, we demonstrated that IL-6 production by CGRP-treated pDMECs was involved in these effects.

51 , IPSP paired-pulse ratios were unchanged by CGRP, and there was no correlation between IPSP potentia

52 that virtually all NTS-->lPBN and lPBN-->CeA CGRP projections coexpress vesicular glutamate transport

53 isolated rat periosteum-derived stem cells, CGRP induces CALCRL- and RAMP1-dependent activation of c

54 As a consequence, CGRP is released, which induces local and systemic vasod

55 penetrating lamina IV/V, 6 +/- 3% contained CGRP (n = 5), and 21 +/- 2% contained VGluT1 (n = 3).

56 ng fibers were identified: fibers containing CGRP and fibers containing VIP but not CGRP.

57 In contrast, CGRP homeostasis is disrupted with age in wild-type mice

58 Cutaneous CGRP(+) SP(-) fibers were numerous within dermal papilla

59 In vivo, HIV-1 infection decreases CGRP plasma levels in both vaginally SHIV-challenged mac

60 To define CGRP receptor binding sites, in vitro autoradiography wa

61 This study demonstrates CGRP receptor binding sites and expression of the CGRP r

62 termine whether CCL17 induces CCR4-dependent CGRP synthesis and secretion by human airway epithelial

63 Actions of nerve-derived CGRP on ECs may have important regulatory effects on the

64 -84 or RAMP2 Glu-101 contacting the distinct CGRP/AM C-terminal residues.

65 RP within taste buds and studied what effect CGRP exerts on taste bud function.

66 K and DBH neurons in the NTS directly engage CGRP(PBN) neurons to promote anorexia.

67 These findings establish CGRP(PBN) neurons as key mediators of cancer-induced app

68 wo separate populations that directly excite CGRP(PBN) neurons.

69 t neurons in the central amygdala expressing CGRP receptors are also critical for establishing a thre

70 hat enhancing the activity of MET-expressing CGRP neurons might be a useful strategy to reduce bowel

71 ay an increased number of neurons expressing CGRP and substance P.

72 n DRG and spinal cord sections colabeled for CGRP and SP.

73 significantly different immunoreactivity for CGRP, SP, nNOS, and TRPV1 (56 +/- 9%, 39 +/- 15%, 17 +/-

74 subpopulations were immunoreactive (IR) for CGRP (30 +/- 3% and 29 +/- 3%, respectively), SP (26 +/-

75 d from C57Bl/6 mice and multiple-labeled for CGRP, SP, and either marker for the sensory neuron subpo

76 The findings are consistent with a role for CGRP as an inhibitory transmitter that shapes peripheral

77 RAMP1/2 alter CLR selectivity for CGRP/AM in part by RAMP1 Trp-84 or RAMP2 Glu-101 contact

78 comparable conditions, CCL17 induced greater CGRP release from BEAS-2B cells than either IL-13, a cyt

79 sCT and AC413 supported a shared non-helical CGRP-like conformation for their TN(T/V)G motif prior to

80 However, CGRP-positive nerves were significantly more superficial

81 ATEMENT Recently, we reported that humanized CGRP monoclonal antibodies (CGRP-mAbs) prevent activatio

82 induced a several thousand-fold increase in CGRP mRNA expression and released peptide product from B

83 regions in the brainstem may be involved in CGRP signaling.

84 No significant differences were observed in CGRP and VEGF expression between non-lesional skin and c

85 vels of the neurochemical SP, a reduction in CGRP fibers and changes in pERK/ERK and pAKT/AKT ratios.

86 n spinal cord nociceptive neurons, increased CGRP release from sciatic nerves and DRGs, and a reducti

87 taglandin (indomethacin) synthesis increased CGRP EC50 in both age groups.

88 ing NO and prostaglandin synthesis increased CGRP EC50 in Young and Old MAs.

89 CCL17-induced CGRP release was inhibited by a specific anti-CCR4 block

90 arrier, which suggests that drugs inhibiting CGRP signaling may not be able to penetrate the central

91 way and the possibility that this injectable CGRP analogue may be effective in cardiac disease.

92 , but was seen after intracerebroventricular CGRP injection.

93 tility changes after intracerebroventricular CGRP.

94 In addition, as with intracerebroventricular CGRP, there was no general increase in anxiety as measur

95 low light was not seen after intraperitoneal CGRP injection, but was seen after intracerebroventricul

96 After intraperitoneal CGRP, motility was decreased in the dark only, similar t

97 in an open-field assay after intraperitoneal CGRP.

98 n is indicated by the ability of intravenous CGRP to trigger migraine in humans and the efficacy of C

99 or-bound structure of the homologous ligands CGRP and AM.

100 Binding of one of the three peptide ligands, CGRP, adrenomedullin (AM), and intermedin/adrenomedullin

101 As the main CGRP-mAb site of action appears to be situated outside t

102 clinical trials with multiple small molecule CGRP receptor antagonists.

103 nal skin in CSU contained significantly more CGRP+ and VEGF+ cells than non-lesional skin.

104 III) taste cells (53%) responded to 0.1 mum CGRP with an increase in intracellular Ca(2+).

105 taste cells rarely (4%) responded to 0.1 mum CGRP.

106 ing inflammation of the hindpaw, myelinated, CGRP-positive neurons projecting to the paw skin display

107 amplified mechanical currents in myelinated, CGRP-negative neurons projecting to muscle.

108 ion decreases production of the neuropeptide CGRP from sensory endings innervating the pancreatic isl

109 rsal horn that co-expressed the neuropeptide CGRP.

110 n of osteoclastogenesis via the neuropeptide CGRP.

111 ed by exogenous addition of the neuropeptide CGRP.

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

113 our findings show that the neurotransmitter CGRP plays a key role in ensuring VOR efficacy.

114 ining CGRP and fibers containing VIP but not CGRP.

115 d further explore the mechanism of action of CGRP-mAbs, we tested the effect of fremanezumab on the c

116 Using pharmacological tools, the actions of CGRP were probed and elucidated by the CGRP receptor ant

117 were developed to reduce the availability of CGRP, and were found effective in reducing the frequency

118 y help to explain the therapeutic benefit of CGRP-mAb in reducing headaches of intracranial origin su

119 pes of noxious stimuli caused a depletion of CGRP from corneal nerves, indicating that all modalities

120 However, the end-to-end distance of CGRP is larger than that of IAPP.

121 Whereas the distribution of CGRP receptor proteins was similar in SMCs, RAMP1 associ

122 The distribution of CGRP-positive nerves did not differ significantly betwee

123 ta show that the reconfiguration dynamics of CGRP is significantly slower than that of human IAPP in

124 With no difference in efficacy, the EC50 of CGRP as a vasodilator was approximately 6-fold greater i

125 We demonstrated that this effect of CGRP was dependent on phospholipase C activation and was

126 rve function and diminished effectiveness of CGRP as a vasodilator is multifaceted and may adversely

127 Thus, we investigated the effects of CGRP on BNST-AL neurons using patch recordings in vitro

128 d the vascular and behavioral the effects of CGRP.

129 igger migraine in humans and the efficacy of CGRP receptor antagonists that evidently do no penetrate

130 -3207) and related this to the expression of CGRP and its receptor in rhesus trigeminal ganglion.

131 Increased expression of CGRP and VEGF in lesional, but not uninvolved, skin indi

132 Immunofluorescence revealed expression of CGRP, CLR and RAMP1 in trigeminal cells.

133 creased airway epithelial cell expression of CGRP, together with increased CCL17 expression, was prev

134 Compelling evidence for the importance of CGRP in migraine has been provided by clinical trials wi

135 We show that pharmacologic inactivation of CGRP receptors in old wild-type animals can restore meta

136 Inactivation of CGRP(PBN) neurons before tumor implantation prevents ano

137 Inactivation of CGRP(PBN) neurons in Apc(min/+) mice permits hyperphagia

138 We also demonstrate that inactivation of CGRP(PBN) neurons prevents lethargy, anxiety and malaise

139 pain sensory receptors or the inhibition of CGRP are associated with increased metabolic health and

140 Peripheral (intraperitoneal) injection of CGRP resulted in light-aversive behavior in wild-type CD

141 therapeutics that inhibit the interaction of CGRP with its receptor in migraineurs.

142 The loss of CGRP in (-/-) mice was associated with a reduction of th

143 e, it is unknown whether and how the loss of CGRP influence vestibular system function.

144 afferents also include a small population of CGRP-expressing myelinated nociceptors that we now ident

145 sed to correlate binding and the presence of CGRP and its receptor components, calcitonin receptor-li

146 ma or IL-4 were decreased by the presence of CGRP-treated pDMECs.

147 To determine central projections of CGRP(+) SP(-) neurons, Neurobiotin (NB) was applied to t

148 There was recovery of CGRP-positive neurons and an increase in corneal sensiti

149 CCL17-induced, CCR4-dependent release of CGRP by human airway epithelial cells represents a novel

150 To address the role of CGRP both within and outside the CNS, we used CGRP-induc

151 Therefore, to elucidate the role of CGRP, it is critical to identify the regions within the

152 Genetic silencing of CGRP neurons blocks pain responses and memory formation,

153 that act peripherally, the relevant sites of CGRP action remain unknown.

154 evious reports on the secondary structure of CGRP, we find that the end-to-end distance of the peptid

155 We report crystal structures of CGRP analog-bound CLR:RAMP1 and AM-bound CLR:RAMP2 extra

156 In this report, we determined the targets of CGRP within taste buds and studied what effect CGRP exer

157 ion via the Trpv1-Cre population, depends on CGRP and gastrin-releasing peptide receptor (GRPR) trans

158 e found that (1) YAP was mainly expressed on CGRP- and IB4-immunoreactive primary afferent nerve term

159 We also noted that TRPM8-IR or CGRP-IR corneal afferent neurons are almost entirely sma

160 evaluated the contribution of substance P or CGRP to these sensory modulations, with or without the p

161 n in Trpv1-Cre afferents together with SP or CGRP is essential for the development of the heat hypera

162 we also evaluated the contribution of SP or CGRP to inflammation-induced hyperalgesia, with or witho

163 Here, we test the hypothesis that PBel CGRP neurons are sufficient and necessary for CTA acquis

164 ogether, these results demonstrate that PBel CGRP neurons mediate a gastrointestinal distress signal

165 forebrain sites under the control of a PBel(CGRP) switch that is necessary to arouse animals from hy

166 mogenetic and optogenetic activation of PBel(CGRP) neurons caused wakefulness, whereas optogenetic in

167 ness, whereas optogenetic inhibition of PBel(CGRP) neurons prevented arousal to CO2, but not to an ac

168 Optogenetic inhibition of PBel(CGRP) terminals identified a network of forebrain sites

169 PBN CGRP neurons become active in response to anorexigenic h

170 ppetite-suppressing effects and activate PBN CGRP neurons.

171 and to decrease activity in anorexigenic PBN CGRP neurons, thereby increasing food intake during home

172 on stimulation reduces Fos expression in PBN CGRP neurons across all conditions.

173 ing chemogenetic-mediated stimulation of PBN CGRP neurons.

174 gene-related protein (CGRP)-expressing PBN (CGRP(PBN)) neurons; however, the molecular identity of t

175 ors for the calcitonin gene-related peptide (CGRP) and adrenomedulin (AM) recently published.

176 he peptides calcitonin gene-related peptide (CGRP) and adrenomedullin (AM) that have diverse function

177 dynamics of calcitonin-gene-related peptide (CGRP) and amylin (islet amyloid polypeptide, IAPP), two

178 aine target calcitonin gene-related peptide (CGRP) and serotonin (5-hydroxytryptamine, 5-HT1F) recept

179 ive agents' calcitonin gene-related peptide (CGRP) and vascular endothelial growth factor (VEGF) are

180 containing calcitonin gene-related peptide (CGRP) and vGluT2.

181 hicken anti-calcitonin gene-related peptide (CGRP) antibody.

182 The calcitonin gene-related peptide (CGRP) family of G protein-coupled receptors (GPCRs) is f

183 he peptides calcitonin gene-related peptide (CGRP) from sensory nerve terminals and insulin from isol

184 phrine, and calcitonin gene-related peptide (CGRP) in denervated kidneys mimicked the fibrotic respon

185 nt role for calcitonin gene-related peptide (CGRP) in migraine pathophysiology.

186 expressing calcitonin gene-related peptide (CGRP) in the parabrachial nucleus are critical for relay

187 Benefits of calcitonin-gene related peptide (CGRP) inhibition have not been established in chronic mi

188 infusion of calcitonin gene-related peptide (CGRP) into BNST was reported to potentiate anxiety while

189 europeptide calcitonin gene-related peptide (CGRP) is a central player in migraine pathogenesis, yet

190 Calcitonin gene-related peptide (CGRP) is a classic molecular marker of peptidergic prima

191 europeptide calcitonin gene-related peptide (CGRP) is a key player in migraine.

192 Calcitonin gene-related peptide (CGRP) is a neuropeptide with well-established immunomodu

193 Calcitonin gene-related peptide (CGRP) is a potent arterial and venous vasodilator.

194 Calcitonin gene-related peptide (CGRP) is a potent neuromodulator and vasodilator.

195 Calcitonin gene-related peptide (CGRP) is a validated target for the treatment of episodi

196 europeptide calcitonin gene-related peptide (CGRP) is associated with activation of the trigeminovasc

197 Calcitonin gene-related peptide (CGRP) is crucial in the pathophysiology of migraine.

198 ive peptide calcitonin-gene related peptide (CGRP) is known to act at efferent synapses and their tar

199 E STATEMENT Calcitonin gene-related peptide (CGRP) monoclonal antibodies (CGRP-mAbs) are capable of p

200 xia made by calcitonin gene-related peptide (CGRP) neurons in the parabrachial nucleus (PBN) that tra

201 The calcitonin gene-related peptide (CGRP) pathway is a promising target for preventive thera

202 The calcitonin gene-related peptide (CGRP) pathway is important in migraine pathophysiology.

203 (lPBN) and calcitonin-gene related peptide (CGRP) projections from the lPBN to the central nucleus o

204 Calcitonin gene-related peptide (CGRP) receptor antagonists have demonstrated anti-migrai

205 ability and calcitonin gene-related peptide (CGRP) release and these effects could be prevented by pe

206 e P (SP) or calcitonin gene-related peptide (CGRP) signaling in Vglut2-deficient mice, we also evalua

207 stance P or calcitonin gene-related peptide (CGRP) signaling in Vglut2-deficient mice, we evaluated t

208 tionship to calcitonin gene-related peptide (CGRP) staining in the dorsal horn.

209 Calcitonin gene-related peptide (CGRP) stimulated CLR endocytosis and activated protein k

210 to release calcitonin gene-related peptide (CGRP) through an unidentified mechanism.

211 ons express calcitonin gene-related peptide (CGRP) without substance P (SP; CGRP(+) SP(-) ).

212 eactive for calcitonin gene-related peptide (CGRP), a marker for polymodal nociceptors, suggesting th

213 ody against calcitonin gene-related peptide (CGRP), a marker of nociceptive sensory nerves.

214 ylin (Amy), calcitonin gene-related peptide (CGRP), and adrenomedullin (AM) peptides.

215 uropeptide, calcitonin gene-related peptide (CGRP), and CGRP treatment inhibited osteoclastogenesis i

216 expressing calcitonin gene-related peptide (CGRP), and in central processes of these cells in the su

217 containing calcitonin gene-related peptide (CGRP), cocaine- and amphetamine-related transcript (CART

218 y targeting calcitonin gene-related peptide (CGRP), is being investigated as a preventive treatment f

219 tide (VIP), calcitonin-gene related peptide (CGRP), substance P (SP), neuropeptide tyrosine (NPY), an

220 Calcitonin gene-related peptide (CGRP), the most abundant neuropeptide in primary afferen

221 CO2 express calcitonin gene-related peptide (CGRP), we hypothesized that CGRP may provide a molecular

222 vasodilator calcitonin gene-related peptide (CGRP), which induces headache in humans.

223 uds contain calcitonin gene-related peptide (CGRP), which may be as an efferent transmitter released

224 et of adult calcitonin gene-related peptide (CGRP)-expressing myenteric neurons produce MET, the rece

225 identified calcitonin gene-related peptide (CGRP)-expressing neurons in the external lateral subdivi

226 n contrast, calcitonin gene-related peptide (CGRP)-expressing neurons in the parabrachial nucleus (PB

227 usively non-calcitonin gene-related peptide (CGRP)-immunoreactive (-IR), medium- to large-sized neuro

228 latation to calcitonin gene-related peptide (CGRP).

229 stained for calcitonin gene-related peptide (CGRP).

230 pression of calcitonin gene-related peptide (CGRP).

231 ivated lPBN calcitonin gene-related peptide (CGRP, a marker for glutamatergic neurons in the lPBN) ne

232 uropeptides calcitonin gene-related peptide (CGRP-alpha) and substance P was significantly increased

233 entified by Calcitonin-Gene-Related-Peptide (CGRP) for peptidergic terminals, and by Isolectin-B4 (IB

234 activity to calcitonin-gene-related-peptide (CGRP).

235 Therefore, GDNF released from peptidergic CGRP/somatostatin+ nociceptors acutely depresses neurona

236 y, endogenous GDNF released from peptidergic CGRP/somatostatin+ nociceptors upon capsaicin stimulatio

237 two separate subpopulations: the peptidergic CGRP/somatostatin+ cells expressing GDNF and the nonpept

238 begin to address the mechanism of peripheral CGRP action, we used transgenic CGRP-sensitized mice tha

239 noclonal antibody, attenuated the peripheral CGRP-induced light aversion and motility behaviors.

240 he regions within the brainstem that process CGRP signaling.

241 sly undefined role of magnesium in promoting CGRP-mediated osteogenic differentiation, which suggests

242 n involving calcitonin gene-related protein (CGRP)-expressing PBN (CGRP(PBN)) neurons; however, the m

243 sensory nerve density was reduced and RAMP1 (CGRP receptor component) associated with nuclear regions

244 conformation of peptides that require RAMPs; CGRP, AM, and amylin.

245 ering RAMPs to CTR enhanced binding of rAmy, CGRP, and the AMY antagonist AC413.

246 d with fewer activated microglia and reduced CGRP expression in the dorsal horn caudal to the lesion.

247 belling revealed reduced density of sensory (CGRP) but not sympathetic (tyrosine hydroxylase) innerva

248 ence of structure-inducing organic solvents) CGRP preferentially populates conformations with short e

249 Additionally, SP-, CGRP-, and VGLUT2-mediated transmission together were fo

250 ated peptide (CGRP) without substance P (SP; CGRP(+) SP(-) ).

251 nd the brain by distinct mechanisms and that CGRP actions may be transmitted to the CNS via indirect

252 related peptide (CGRP), we hypothesized that CGRP may provide a molecular identifier of the CO2 arous

253 These results indicate that CGRP increases ST-evoked GABA-A IPSPs and hyperpolarizes

254 In this study, we report that CGRP can act in both the brain and the periphery of the

255 In the current paper, we report that CGRP-mAbs prevent the activation of Adelta but not C-typ

256 We show that CGRP acts via its receptor expressed by LCs and interfer

257 We show that CGRP(PBN) neurons are activated in mice implanted with L

258 Our data showed that CGRP-evoked 5-HT release reduced taste-evoked ATP secret

259 These results suggest that CGRP can act in both the periphery and the brain by dist

260 Overall, our findings suggest that CGRP potentiates anxiety-like behaviors and increases ne

261 mucosal HIV-1 transmission and suggest that CGRP receptor agonists might be used therapeutically aga

262 peripheral and central targets suggest that CGRP(+) SP(-) neurons are polymodal mechanoceptors.

263 P potentiation and variance, suggesting that CGRP acts postsynaptically.

264 The CGRP innervation of BNST originates in the pontine parab

265 fully human monoclonal antibody against the CGRP receptor, for migraine prevention.

266 fully human monoclonal antibody against the CGRP receptor, in patients with chronic migraine.

267 ns of CGRP were probed and elucidated by the CGRP receptor antagonist CGRP(8-37).

268 this study was to better understand how the CGRP-mAb fremanezumab (TEV-48125) modulates meningeal se

269 sion because pharmacological blockade of the CGRP or GRPR pathway, or genetic ablation of Grpr, led t

270 s indicates the therapeutic potential of the CGRP pathway and the possibility that this injectable CG

271 ical studies have shown that blockade of the CGRP receptor can produce antimigraine efficacy comparab

272 itized mice that have elevated levels of the CGRP receptor hRAMP1 subunit in nervous tissue (nestin/h

273 receptor binding sites and expression of the CGRP receptor in rhesus and rat TG.

274 ize of 473 +/- 14 mum(2) (n = 5); 89% of the CGRP(+) SP(-) neurons expressed NF200 (n = 5), but only

275 Half (50%) of the CGRP-immunoreactive DRG neurons lacked detectable SP and

276 f sensory nerves or knockdown in vivo of the CGRP-receptor-encoding genes Calcrl or Ramp1 substantial

277 are humanised antibodies against CGRP or the CGRP receptor.

278 We show that the CGRP family of receptors displays both ligand- and RAMP-

279 d glutamate were examined and related to the CGRP system.

280 the alphaAnalogue to act selectively via the CGRP pathway was shown in skin by using a CGRP receptor

281 Consistent with this, CGRP hyperpolarized the GABA-A reversal of BNST-AL cells

282 dation reduced the efficacy of dilatation to CGRP by approximately 30% in Old MAs yet increased this

283 othelial denudation attenuated dilatation to CGRP in Old MAs yet enhanced dilatation to CGRP in Young

284 o CGRP in Old MAs yet enhanced dilatation to CGRP in Young MAs while abolishing all dilatations to AC

285 murine dermal microvascular ECs (pDMECs) to CGRP followed by coculture with LCs, responsive CD4(+) T

286 f peripheral CGRP action, we used transgenic CGRP-sensitized mice that have elevated levels of the CG

287 on NO production and activation of HNO-TRPA1-CGRP pathway.

288 e propose that this neuroendocrine HNO-TRPA1-CGRP signalling pathway constitutes an essential element

289 the nociceptive neuronal markers IB4, TRPV1, CGRP, and substance P.

290 GRP both within and outside the CNS, we used CGRP-induced light-aversive behavior in mice as a measur

291 Although migraine can be treated using CGRP antagonists that act peripherally, the relevant sit

292 fibers containing immunoreactivity for VIP, CGRP, SP, or nNOS were found.

293 ximal vagina and reduced proportions of VIP, CGRP, and SP containing nerve fibers in the distal epith

294 jority of spinal afferent nerve endings were CGRP-immunoreactive.

295 tified in the stomach, and most of them were CGRP immunoreactive.

296 ts a type II turn (Gly(28)-Thr(31)), whereas CGRP and AM adopt type I turns.

297 We examined whether CGRP regulates the outcome of Ag presentation by Langerh

298 2 expression nor colocalization of ChR2 with CGRP in the BNST.

299 ese animals, ChR2 partially colocalized with CGRP, and activation generated EPSCs in dorsal anterolat

300 e cold pain, whereas glutamate together with CGRP mediate noxious heat.