ライフサイエンスコーパス: enkephalin

1 rodynorphin) with enkephalin (or Phe-Arg-Met-enkephalin).

2 arasympathetic) neurons and those containing enkephalin.

3 likely interact with nerve fibers containing enkephalin.

4 and specific down-regulation of the DRD2 and enkephalin.

5 otein of the active peptide neurotransmitter enkephalin.

6 stimulation by the opioid peptide methionine enkephalin.

7 mounts of nicotine-induced secretion of (Met)enkephalin.

8 hat cathepsin L in vivo was colocalized with enkephalin.

9 gonist, carboxynitrobenzyl-tyrosine-[Leu(5)]-enkephalin.

10 ntisera against beta-endorphin or methionine-enkephalin.

11 itters gastrin-releasing peptide and leucine-enkephalin.

12 PENK is a stable analyte of labile enkephalins.

13 g with the mu/delta selective opioid [Met(5)]enkephalin (1 mum) decreased spontaneous dopamine transi

14 In contrast, enkephalins (100-1000 nmol) and nociceptin-orphanin FQ (

15 nist, [(3)H][d-Ala(2),N-Me-Phe(4),Gly(5)-ol]-enkephalin ([(3)H]DAMGO).

16 hesis of an azaphenylalanine analogue of Leu-enkephalin 40.

17 Extension to the syntheses of Leu-enkephalin (9) and amyloid-beta (34-42) (10) demonstrate

18 jections coexpress GABA and the neuropeptide enkephalin, a delta and mu opioid receptor (MOR) ligand.

19 nctional, since [D-Ala(2),MePhe(4),Gly-ol(5)]enkephalin, a MOR-selective agonist, and U69,593, a KOR-

20 critical for the hydrolysis of exogenous Leu-enkephalin, a neuropeptide present in the CA3 region of

21 Intra-PFC DAMGO (D-[Ala2,N-MePhe4, Gly-ol]-enkephalin; a mu-opioid agonist) and d-amphetamine were

22 effect associated with administration of the enkephalin alone.

23 totoxicity also exacerbated or prevented the enkephalin alterations.

24 nd limited receptor internalization, whereas enkephalin analogs promote robust trafficking of both be

25 Enkephalin analogues with a 4-anilidopiperidine scaffold

26 Moreover, neurons triple-labeled with c-Fos, enkephalin and 5-HT were noted frequently in the NRP fol

27 duced by EA and examined its relationship to enkephalin and 5-HT.

28 on (LOQ) by analyzing targeted peptides, leu-enkephalin and angiotensin II, spiked in a BSA tryptic d

29 ng the neuropeptides substance P, dynorphin, enkephalin and cholecystokinin.

30 ion of cathepsin L-DsRed fusion protein with enkephalin and chromogranin A neuropeptides that are pre

31 s, including PSD-95, and opioid peptides leu-enkephalin and dynorphin in the hippocampus of young ani

32 age, females showed opposing changes in leu-enkephalin and dynorphin levels in the mossy fiber pathw

33 ird, we examined co-localization of Y1R with enkephalin and dynorphin neurons and the effect of NPY o

34 Both enkephalin and dynorphin partly colocalized with vesicul

35 phase- and gas-phase deuterium uptake of Leu-Enkephalin and Glu-Fibrinopeptide B, confirmed that this

36 we examined how patch output is modulated by enkephalin and identified the underlying circuit mechani

37 c-based solid-phase peptide synthesis of Leu-enkephalin and in microwave-assisted automated synthesis

38 biologically active conformation of leucine enkephalin and its methyl ester in the nonpolar cell mem

39 An equimolar mixture of leucine enkephalin and maltopentaose was studied to verify that

40 agonists [D-Ala(2), N-Me-Phe(4), Gly-ol(5)]-enkephalin and met-enkephalin inhibited both ST-stimulat

41 ase in the pPVN, due to increased endogenous enkephalin and mu-opioid receptor production in brainste

42 s in droplets containing bradykinin, leucine enkephalin and myoglobin, but loss of the heme group fro

43 n V protease for producing the neuropeptides enkephalin and neuropeptide Y (NPY).

44 teolytic conversion of proproteins to active enkephalin and neuropeptides.

45 Whereas CPA6 converts enkephalin and neurotensin into forms known to be inacti

46 in human brain cortex and hippocampus where enkephalin and NPY are produced and is present in purifi

47 Colocalization of cathepsin V with enkephalin and NPY in secretory vesicles of human neurob

48 function of human cathepsin V for producing enkephalin and NPY neuropeptides required for neurotrans

49 the evidence supporting cleavage at proline, enkephalin and peptide A-779, two peptides that do not c

50 2, involved in matrix remodeling, as well as enkephalin and RUNX3, potentially involved in the increa

51 In this study Tyr residues of both leucine enkephalin and salmon calcitonin (sCT) were targeted usi

52 d D3R GFP fluorescent cells colocalized with enkephalin and substance P immunoreactive medium spiny n

53 ta suggest that [D-Ala(2),MePhe(4),Gly-ol(5)]enkephalin and U69,593 divert ES cells from self-renewal

54 g the D1 subtype were immunopositive for met-enkephalin and vesicular glutamate transporter VGLUT2, b

55 These results show that enkephalins and dynorphins are present in different popu

56 oid peptides targeting mu-receptors, such as enkephalins and endorphins, underlying the regulation of

57 erved cell surface protease that inactivates enkephalins and other bioactive peptides.

58 s of the opioid growth factor (OGF, [Met(5)]-enkephalin) and a low dose of the opioid antagonist nalt

59 n opioid peptide ([D-Ala2,N-Me-Phe4,Gly5-ol]-enkephalin) and a selective sodium channel (NaV1.7)-bloc

60 The opioid growth factor (OGF; [Met(5)]-enkephalin) and the OGF receptor (OGFr) form an endogeno

61 s endogenous opioids (beta-endorphin and Met-enkephalin) and uroguanylin in apical compartments close

62 levels of Kcnk5/Gpr4/pre-pro-galanin/pre-pro-enkephalin, and do not respond to hypercapnia.

63 expression of orexigenic peptides, galanin, enkephalin, and dynorphin, in the paraventricular nucleu

64 ion of the striatal dopamine receptor D2 and enkephalin, and improved procedural learning.

65 hin II, [d-Pen(2), d-pen(5)]-enkephalin, met-enkephalin, and SNC-80 ((+)-4-[(alphaR)-alpha-((2S,5R)-4

66 control pain through temporally coordinated enkephalin- and GABA-mediated presynaptic inhibition of

67 be processed by CPA6, including Met- and Leu-enkephalin, angiotensin I, and neurotensin.

68 on microscopy using substance P and Met-/Leu-enkephalin antibodies to label GABAergic terminals from

69 An anti-enkephalin antibody, which recognized Leu-, Met-, and Ph

70 lidal neurons were identified by rabbit anti-enkephalin antibody.In NT mice, PDE10A is equally expres

71 agonist, DAMGO ([d-Ala2, NMe-Phe4, Gly5-ol]-enkephalin), appeared to attenuate this negative incenti

72 the circuit elements in patches regulated by enkephalin are unclear.

73 Enkephalins are cardiodepressive and difficult to measur

74 ar to that of DAMGO, alpha-neoendorphin, Met-enkephalin-Arg-Phe, and the putatively endogenous peptid

75 Using leucine enkephalin as a diagnostic molecule, the fragmentation e

76 ndogenous peptide opioid receptor ligand Leu-enkephalin as a model compound.

77 agonist DAMGO (D-Ala2-N-Me-Phe(4)-glycol(5)-enkephalin), as shown by analysis of downstream targets

78 Met-enkephalin, but not the mu-selective (DAMGO) and delta-s

79 n SK-N-MC cells results in reduction of (Met)enkephalin by more than 80%, illustrating the prominent

80 consistent with the fact that both GABA and enkephalin can exert presynaptic inhibition of the senso

81 A leucine enkephalin-coated surface demonstrated good linearity (R

82 To enhance detection of perikarya containing enkephalin, colchicine (90-100 microg/kg) was administer

83 enhance detection of cell bodies containing enkephalin, colchicine (90-100 mug/kg) was administered

84 dorsal horn homogenates and presynaptic met-enkephalin-containing boutons.

85 alin, resulting from the conversion of PE to enkephalin-containing intermediates of 23, 18-19, 8-9, a

86 in some medullary nuclei (e.g., raphe), only enkephalin-containing neuronal processes were found in t

87 occurs at dibasic residue sites to generate enkephalin-containing peptides and an approximately 24-k

88 orsal horn, probably from a subpopulation of enkephalin-containing presynaptic terminals.

89 eGFP-expressing neurons were associated with enkephalin-containing varicosities, and enkephalin-induc

90 trated that the DOR agonist D-[Pen(2),Pen(5)]enkephalin could induce receptor internalization and ade

91 ts beta-arrestin2, whereas the MOR-selective enkephalin [D-Ala(2),N-Me-Phe(4),Gly(5)-ol]enkephalin (D

92 saturating doses of the hydrolysis-resistant enkephalin [D-Ala2,N-MePhe4,Gly5-ol]enkephalin (DAMGO).

93 ns with the DOR agonist [d-Ala(2), d-Leu(5)]-enkephalin (DADLE) caused a decrease in the membrane abu

94 decreased the potency of [D-Ala(2),D-Leu(5)]-enkephalin (DADLE), and decreased the potency and effica

95 Gly5-ol]-enkephalin (DAMGO), [D-Ala2,D-Leu5]-enkephalin (DADLE), trans-(+/-)-3,4-dichloro-N-methyl-N-

96 the mu-OR agonist, D-Ala2, N-MePhe4, Gly-ol]-enkephalin (DAMGO) (0.25 mug), directly into the AcbSh o

97 The MOR agonist [D-Ala2,N-Me-Phe4,Gly5-ol]-enkephalin (DAMGO) also occluded the ability of DOR agon

98 es of the opioid [d-Ala2, N-MePhe4, Gly5-ol]-enkephalin (DAMGO) and a switch in the functional effect

99 de agonists [d-Ala(2),N-Me-Phe(4),Gly(5)-ol]-enkephalin (DAMGO) and endomorphin-2 activated inwardly

100 MOR with [D-Ala(2), N-Me-Phe(4), Gly(5)-ol]-enkephalin (DAMGO) and morphine and imaged in real time

101 d agonists, [d-Ala(2),N-Me-Phe(4),Gly(5)-ol]-enkephalin (DAMGO) and morphine, to induce mu-opioid rec

102 tor agonist (D-Ala(2),N-Me-Phe(4),Gly-ol(5))-enkephalin (DAMGO) at 1 mum, but not at 1-10 nm, caused

103 ]diprenorphine and [d-Ala2,NMe-Phe4,Gly5-ol]-enkephalin (DAMGO) binding and effect of MTSEA on [3H]di

104 ]diprenorphine and [D-Ala2,NMe-Phe4,Gly5-ol]-enkephalin (DAMGO) binding and effect of MTSEA on [3H]di

105 ne, fentanyl, and [D-Ala2,N-Me-Phe4,Gly5-ol]-enkephalin (DAMGO) induce extensive receptor phosphoryla

106 -opioid agonist [d-Ala2, N-Me-Phe4, Gly5-ol]-enkephalin (DAMGO) markedly increased intake of standard

107 with either MOR [D-Ala, N-Me-Phe, Gly-ol(5)-enkephalin (DAMGO) or morphine] or DOR (D-Pen(5)-enkepha

108 the micro agonist [D-Ala2,N-MePhe4, Gly-ol5]enkephalin (DAMGO) or the alpha2 agonist clonidine inhib

109 eceptor agonist (d-Ala2, N-Me-Phe4, Gly-ol5)-enkephalin (DAMGO) was microinjected into the raphe magn

110 [D-Ala2,Phe4,Gly5-ol]-enkephalin (DAMGO), [D-Ala2,D-Leu5]-enkephalin (DADLE),

111 pplication of [D-Ala(2)-N-Me-Phe(4),Gly5-ol]-Enkephalin (DAMGO), a MOR agonist, that is blocked by D-

112 nfusions of D-Ala(2), NMe-Phe(4), Gly-ol(5)]-enkephalin (DAMGO), a mu-opioid receptor agonist, in the

113 nalizing opiate, and (D-Ala2,MePhe4,Gly-ol5) enkephalin (DAMGO), a potent muOR-internalizing agonist,

114 id agonist [D-Ala(2),methyl-Phe(4),Gly(5)-ol]enkephalin (DAMGO), as demonstrated by both Western blot

115 e mu agonist, Tyr-D-Ala', N-CH, -Phe4, Glyol-Enkephalin (DAMGO), delta opioid agonists, D-pen(2), D-p

116 (Met-Enk), [d-Ala(2), N-MePhe(4), Gly-ol(5)]-enkephalin (DAMGO), endomorphin-2, and morphine in rat a

117 e enkephalin [D-Ala(2),N-Me-Phe(4),Gly(5)-ol]enkephalin (DAMGO), recruits either beta-arrestin.

118 opioid agonist, [d-Ala(2),N-MePhe(4),gly-ol]-enkephalin (DAMGO), to produce tolerance for its inhibit

119 id receptor agonist D-Ala2-N-Me-Phe4-gly5-ol-enkephalin (DAMGO), we demonstrate that orexin signaling

120 electivity of [D-Ala(2),N-MePhe(4),Gly-ol(5)]enkephalin (DAMGO)-related glycopeptides by altering the

121 [d-Ala2,(N-Me)Phe4,Gly5-OH] enkephalin (DAMGO)-stimulated [(35)S]GTPgammaS binding w

122 by morphine and [D-Ala(2),Phe(4),Gly(5)-ol]-enkephalin (DAMGO).

123 esistant enkephalin [D-Ala2,N-MePhe4,Gly5-ol]enkephalin (DAMGO).

124 o the MOR agonist [D-Ala2,N-MePhe4,Gly-ol5] -enkephalin (DAMGO).

125 ffects of the agonist d-Ala2-N-MePhe4-Gly-ol enkephalin (DAMGO).

126 mu-opioid agonist D-[Ala2, N-MePhe4, Gly-ol]-enkephalin (DAMGO, 2.5 mug), then challenged with intra-

127 receptor agonist ([D-Ala2, N-MePhe4, Gly-ol]-enkephalin; DAMGO) generated intense >250% increases in

128 -Phe-Ser-Arg-OH), a human peptide inhibiting enkephalin degradation, was performed.

129 e III (DPP III) is one of the most important enkephalin-degrading enzymes associated with the mammali

130 duced by morphine and RB101 (an inhibitor of enkephalin-degrading enzymes, which increases the synapt

131 or (MOR) selective agonists ([D-Pen2,D-Pen5]-Enkephalin, deltorphin II, SNC80, and DAMGO) and antagon

132 Topical application of [Met(5)]-enkephalin depressed tear secretion from baseline scores

133 be used in RAIC projection neurons, whereas enkephalin distribution was more characteristic of a rol

134 whereas the -selective ligands [D-Pen2,Pen5]-enkephalin (DPDPE) and deltorphin II (1 microM) did not.

135 bolished the ability of [d-Pen(2), d-Pen(5)]-enkephalin (DPDPE) to inhibit forskolin-stimulated intra

136 ), delta opioid agonists, D-pen(2), D-phe(5) enkephalin (DPDPE), and kappa agonist, U50 488, all sign

137 or-BNI) enhanced the potency of [D-Pen(2,5)]-enkephalin (DPDPE), decreased the potency of [D-Ala(2),D

138 od was used to determine met-enkephalin, leu-enkephalin, dynorphin A(1-8), and beta-endorphin in vivo

139 ative peroxidase immunohistochemistry of leu-enkephalin, dynorphin, synaptophysin, and PSD-95.

140 In hAPP mice, enkephalin elevations correlated with the extent of Abet

141 We conclude that enkephalin elevations may contribute to cognitive impair

142 Protecting enkephalins, endogenous opioid peptides released in resp

143 singly, co-injection of naloxone with either enkephalin enhanced the effect associated with administr

144 ibility that the orexigenic peptide systems, enkephalin (ENK) and orexin (OX), which are stimulated b

145 developmentally regulated expression of the enkephalin (ENK) gene, we identified AUF1.

146 male starlings also had significantly higher enkephalin (ENK) immunolabeling densities in the POM tha

147 NT colocalization with the endogenous opioid enkephalin (ENK) in the RVM during thermal hyperalgesia,

148 ing in situ hybridization histochemistry for enkephalin (ENK) mRNA in the ventral striatum.

149 Corticotrophin releasing factor (CRF), enkephalin (ENK), and dynorphin (DYN) mRNAs were colocal

150 only Ucn 3 neurons in the rPFH co-expressed enkephalin (Enk), and Ucn 3/Enk double-labeled nerve fib

151 ergic synapses colocalize the opioid peptide enkephalin (ENK), but the neurons to which they belong a

152 on by gamma-aminobutyric acid (GABA) and met-enkephalin (ENK).

153 opioid peptides [e.g., proopiomelanocortin, enkephalin (ENK)] with the stress-related peptide cortic

154 well as mRNA levels of the endogenous opioid enkephalin (ENK-mRNA).

155 Enkephalins (ENKs) are endogenous opioids that regulate

156 prevented by transfection in vitro with the enkephalin-expressing vector.

157 Met/Leu-enkephalin expression was altered in pathological skin,

158 leus size, loss of dendritic spines, reduced enkephalin expression, diminished nigral dopaminergic pr

159 Here we present SID of leucine enkephalin, fibrinopeptide A, melittin, insulin chain-B,

160 SK-N-MC cells results in production of (Met)enkephalin from proenkephalin.

161 These results suggest that enkephalin gates limbic information flow in dorsal stria

162 Striatal enkephalin gene expression is also downregulated by an i

163 lymer nanoparticles encapsulating leucine(5)-enkephalin hydrochloride (LENK) are able to transport LE

164 ic agonist DAMGO ([D-Ala2,N-Me-Phe4,Gly5-ol]-Enkephalin) hyperpolarizes medially located ITCs (mITCs)

165 Enkephalin immunolabeling was detected within a single m

166 Enkephalin immunoreactivity did not colocalize with the

167 e accurate and precise quantification of Leu-enkephalin in a complex mixture using multiple-reaction

168 gyrus granule cell layer and upregulation of enkephalin in CA1 interneurons, thus reproducing a neuro

169 NL led to increased immunoreactivity for met-enkephalin in dorsal horn homogenates, which was dose-de

170 suggesting a role for the inhibitory peptide enkephalin in responses evoked by glucoprivation.

171 Mass spectroscopy confirmed Leu- and Met-enkephalin in skin.

172 Furthermore, labeling for the opioid met-enkephalin in the medial preoptic nucleus (POM) correlat

173 These data suggest that increased enkephalin in the rVLM induced by repetitive EA contribu

174 study, the authors investigated the role of enkephalins in morphine-induced conditioned place prefer

175 Two series of 22 and 15 atom cyclic enkephalins incorporating a diversely substituted guanid

176 scimol reduced DAMGO (D-Ala2-NMe-Phe4-Glyol5-enkephalin)-induced and baseline food intake, whereas in

177 with enkephalin-containing varicosities, and enkephalin-induced clathrin- and dynamin-mediated endocy

178 treated animals, recovery from acute [Met](5)enkephalin-induced desensitization and receptor recyclin

179 tracellular concentrations and half-lives of enkephalins, inducing potent antinociceptive effects.

180 , N-Me-Phe(4), Gly-ol(5)]-enkephalin and met-enkephalin inhibited both ST-stimulated EPSCs and the fr

181 Neuropeptides dynorphin and met-enkephalin inhibited dopamine neurons, whereas oxytocin

182 one by blocking the enzymatic degradation of enkephalin inhibited GABA neurotransmission in yoked sal

183 ist DAMGO (D-ala(2) -N-Me-Phe(4) -Glycol(5) -enkephalin) into the rostrodorsal part of the accumbens

184 Methionine-enkephalin (M-ENK) and leucine-enkephalin (L-ENK) are small endogenous opioid peptides

185 which recognized Leu-, Met-, and Phe-Arg-Met-enkephalin, labeled the dorsolateral funiculus and numer

186 phalin, which did not recognize Leu- and Met-enkephalin, labeled the same puncta.

187 activatable analogs of two opioids: [Leu(5)]-enkephalin (LE) and the 8 amino acid form of Dynorphin A

188 Within the HF, leu-enkephalin (LENK) is most prominent in the mossy fiber (

189 Leucine(5)-enkephalin (LENK) nanofibres formed from the LENK ester

190 the effect of exposure to exogenous leucine-enkephalin (Leu-Enk), methionine-enkephalin (Met-Enk), a

191 The method was used to determine met-enkephalin, leu-enkephalin, dynorphin A(1-8), and beta-e

192 Met-enkephalin levels in neuronal projections from the entor

193 l, with or without progesterone, altered leu-enkephalin levels in the dentate gyrus and synaptophysin

194 In human AD brains, enkephalin levels in the dentate gyrus were also increas

195 withdrawal from cocaine self-administration enkephalin levels in the VP are elevated and the opioid

196 In Alzheimer's disease (AD), elevated enkephalin levels may reflect compensatory processes or

197 r reserpine was shown previously to increase enkephalin levels severalfold.

198 niques that allow detection of extracellular enkephalin levels.

199 Ligand 16, in which a Dmt-substituted enkephalin-like structure was linked to the N-phenyl-N-p

200 Methionine-enkephalin (M-ENK) and leucine-enkephalin (L-ENK) are sm

201 Taken together, the results suggest that enkephalins may be important for the development of anal

202 tance by submaximal concentrations of Met(5)-enkephalin (ME) and somatostatin (SST; coupling to nativ

203 concentration of the opioid agonist [Met(5)]-enkephalin (ME) caused significantly less desensitizatio

204 afferentation, the opioid agonist methionine-enkephalin (ME) inhibited the amplitude of evoked IPSC (

205 jection of opioid agonists DAMGO or [Met(5) ]enkephalin (ME) into the KF reduced respiratory frequenc

206 Activation of the FLAGMOR with [Met5]enkephalin (ME) produced a hyperpolarization that desens

207 sporine did not reduce the extent of [Met(5)]enkephalin (ME)-induced desensitization but increased th

208 tions of buprenorphine decreased the [Met](5)enkephalin (ME)-induced hyperpolarization or outward cur

209 stimulation of MOR in LC neurons with Met(5)-enkephalin (ME).

210 bition to the mu/delta opioid agonist [Met5] enkephalin (ME; 3 microM).

211 DA) receptor stimulation on enkephalin (Met5-enkephalin; ME) and tachykinin (substance P; SP) systems

212 cysteine protease pathway for producing the enkephalin member of neuropeptides.

213 Numerous met-enkephalin (mENK) and dynorphin-immunoreactive boutons a

214 of such interactions, we exposed methionine-enkephalin (MENK) to PN and identified the major metabol

215 e (ir) for galanin, GABA, TRH, or methionine-enkephalin (mENK) were dense in the ventrocaudal hypotha

216 Met-enkephalin (mENK), an endogenous opioid, and exogenous o

217 ptor-saturating concentrations of methionine-enkephalin (Met-Enk), [d-Ala(2), N-MePhe(4), Gly-ol(5)]-

218 ous leucine-enkephalin (Leu-Enk), methionine-enkephalin (Met-Enk), and the opioid antagonist naloxone

219 nced for deltorphin II, [d-Pen(2), d-pen(5)]-enkephalin, met-enkephalin, and SNC-80 ((+)-4-[(alphaR)-

220 tnatal dopamine (DA) receptor stimulation on enkephalin (Met5-enkephalin; ME) and tachykinin (substan

221 Moreover, Acb enkephalin neurons expressed Y1R and arcuate nucleus NPY

222 2) agonist DAMGO (D-Ala2, N-Me-Phe4, Gly5-ol-enkephalin) of the incorporation of [(35)S]-guanosine 5'

223 1H-imidazole]; the effect of vector-mediated enkephalin on Na(V)1.7 levels was prevented by naltrindo

224 e effect of transgene-mediated expression of enkephalin on pain-related behaviors and their biochemic

225 ioid peptide, opioid growth factor ([Met(5)]-enkephalin), on the onset and progression of EAE.

226 on of cathepsin L for biosynthesis of active enkephalin opioid peptide contrasts with its function in

227 In the hippocampal formation (HF), the enkephalin opioids and estrogen are each known to modula

228 neurons double-labeled with c-Fos and either enkephalin or 5-HT were found more frequently in all thr

229 receptor-deficient or lacking either pre-pro-enkephalin or beta-endorphin.

230 phalin (DAMGO) or morphine] or DOR (D-Pen(5)-enkephalin or SNC80) agonists increased RGS19 and GIPC p

231 c medium spiny neurons that expressed either enkephalin or substance P and extended fibers to the glo

232 ouble-labeled with c-Fos and beta-endorphin, enkephalin or VGLUT3 in the ARC were significantly incre

233 lization of dynorphin (or prodynorphin) with enkephalin (or Phe-Arg-Met-enkephalin).

234 10(-5) M naltrexone (NTX), 10(-5) M [Met(5)]-enkephalin, or sterile vehicle was administered to one e

235 ls and synthesis of the orexigenic peptides, enkephalin, orexin and melanin-concentrating hormone, as

236 be presented for [(eta(6)-Cp*Rh-Tyr(1))-leu-enkephalin](OTf)(2) and [(eta(6)-Cp*Rh-Tyr(3))-octreotid

237 iatum, which expresses the endogenous opioid enkephalin, patches (or striosomes) are limbic-associate

238 protease cathepsin L for producing the (Met)enkephalin peptide neurotransmitter from proenkephalin (

239 YR, and GsYR), to more biologically relevant enkephalin peptides (YGGFL, pYGGFL, and sYGGFL).

240 These results suggest that dynorphin and enkephalin peptides are the predominant endogenous opioi

241 We found that ILC2s produce methionine-enkephalin peptides that can act directly on adipocytes

242 abolic homeostasis in part via production of enkephalin peptides that elicit beiging.

243 In situ Met/Leu-enkephalin peptides were expressed in differentiating ke

244 Enkephalins play a major role in reproductive physiology

245 predominantly expressed in the dendrites of enkephalin-positive gamma-aminobutyric acidergic medium

246 ice, PDE10A content selectively increases in enkephalin-positive striatal neuronal bodies; moreover,

247 Together, substance P- and enkephalin-positive terminals represent 24% of all synap

248 urons containing preprotachykinin and prepro-enkephalin (PPE) mRNAs were also activated, with the non

249 ne expression, leading to an upregulation of enkephalin precursor Penk mRNA and met-enkephalin protei

250 Under these conditions, leucine-enkephalin present at concentrations as low as 125nM was

251 of the presynaptic delta-opioid receptor by enkephalin prevents the increase in neuronal Na(V)1.7 in

252 and related findings, we suggest endogenous enkephalins primarily set a background motivational tone

253 neutral antagonist 6beta-naltrexol; (2) pro-enkephalin, pro-opiomelanocortin, and pro-dynorphin KO m

254 or agonist [D-Ala(2), NMe-Phe(4), Gly-ol(5)]-enkephalin produces paradoxical behavioural responses: e

255 Vector-mediated enkephalin production in vivo prevented the increase in

256 The therapeutic potential of reducing enkephalin production or signaling merits further explor

257 we used viral vectors utilizing dynorphin or enkephalin promoters to drive expression of 5-HT6 recept

258 on of enkephalin precursor Penk mRNA and met-enkephalin protein in sensory neurons.

259 In contrast, the levels of phospholipase A2, enkephalin, PSD-95, synaptophysin, or glutamate NMDA rec

260 method is illustrated by using a set of four enkephalin-related and acetylated peptides to generate 1

261 ype regulates MOR function by modulating met-enkephalin release.

262 olesterol restored [D-Ala2,N-Me-Phe4,Gly5-ol]enkephalin responses back to control values, and were co

263 in highly increased cellular levels of (Met)enkephalin, resulting from the conversion of PE to enkep

264 Immunolabeling for prodynorphin and enkephalin revealed numerous immunopositive cell bodies

265 The enkephalin signaling pathway regulates various neural fu

266 /or efficacy of the orthosteric agonists leu-enkephalin, SNC80 and TAN67, as measured by receptor bin

267 er, desensitization of D-Ala(2)-Met(5)-Glyol-enkephalin-stimulated [(35)S]GTPgammaS binding following

268 emonstrated by reduced D-Ala(2)-Met(5)-Glyol-enkephalin-stimulated [(35)S]GTPgammaS binding to spinal

269 Our initial study on met-enkephalin strongly suggests that even fairly long traje

270 Enkephalin suppresses inhibition onto striatal projectio

271 micro-domain within dorsal neostriatum where enkephalin surges are triggered by the opportunity to co

272 Here, we provide evidence that enkephalin surges in an anteromedial quadrant of dorsal

273 Endogenous >150% enkephalin surges in anterior dorsomedial neostriatum we

274 PENK is a stable surrogate analyte of labile enkephalins that is correlated inversely with renal func

275 GF) is an endogenous opioid peptide ([Met(5)]enkephalin) that interacts with the OGF receptor (OGFr)

276 roach, we have electroosmotically pulled Leu-enkephalin through OHSCs to identify ectopeptidase activ

277 lized with dynorphin, oxytocin, vasopressin, enkephalin, thyrothropin-releasing hormone, and corticot

278 mu-opioid agonist [D-Ala2,N-Me-Phe4,Gly5-ol]enkephalin to acutely inhibit adenylyl cyclase or to cau

279 lthough not affecting the ability of [Met](5)enkephalin to induce desensitization, acutely reversed t

280 is study clearly demonstrates the ability of enkephalins to disrupt insect sexual development and als

281 aine-trained mice, indicating that increased enkephalin tone on presynaptic mu opioid receptors was r

282 Gamma-aminobutyric acid (GABA) and enkephalin tonically inhibit neurons within the RVLM.

283 r prodrug - tyrosinyl(1)palmitate-leucine(5)-enkephalin (TPLENK) were coated with the polymer - N-pal

284 mportant GPCR peptides; namely, [Tyr(1)]-leu-enkephalin, [Tyr(4)]-neurotensin(8-13), and [Tyr(3)]-oct

285 nerve ligation is accompanied by D1R and met-enkephalin upregulation, acquired D1LR-mediated antinoci

286 ory cells that coexpress beta-endorphin, Met-enkephalin, uroguanylin, and Trpm5 exist in mouse duoden

287 Quantitative determination of leu-enkephalin using external calibration was verified by st

288 opioid peptide [d-Ala(2),N-MePhe(4),Gly-ol]-enkephalin was not reversed by ethanol.

289 ally in close proximity to fibers containing enkephalin was noted in the NAmb of EA-treated cats (n=5

290 A standard curve of Leu-enkephalin was performed in the presence of a background

291 erivatization conditions for 1microM leucine-enkephalin were achieved when 10mM cysteine and 200U/ml

292 Axons immunolabeled for enkephalin were also abundant in lamina II/III.

293 While perikarya containing enkephalin were observed in some medullary nuclei (e.g.,

294 ymes, which increases the synaptic levels of enkephalins) were enhanced in BAMBI-KO mice.

295 An antibody against Phe-Arg-Met-enkephalin, which did not recognize Leu- and Met-enkepha

296 In tyrosyl-glycine and Leu-enkephalin, which have N-terminal tyrosines, bicyclic in

297 n of the opioid growth factor (OGF) [Met(5)]-enkephalin with its receptor (OGFr) is a regulator of TC

298 se results indicate increased levels of (Met)enkephalin within secretory vesicles of the regulated se

299 ed in neurons containing the opioid peptide, enkephalin, within the dorsolateral striatum.

300 morphine and DAMGO (D-Ala2-N-Me-Phe4-glycol5-enkephalin) without affecting agonist potency, the onset

301 nated C-terminally methyl esterified leucine enkephalin [YGGFL-OMe+H](+).