ライフサイエンスコーパス: DAMGO

1 DAMGO activation of PKCepsilon and/or ERK was insensitiv

2 DAMGO activation of the receptor promotes MOR ubiquitina

3 DAMGO also produced a postsynaptic inhibition in 233 of

4 DAMGO increased guanosine 5'-O-(3-[(35)S]thio)triphospha

5 DAMGO induced arrestin-2 translocation to the plasma mem

6 DAMGO injection into the CeA also resulted in mu opioid

7 DAMGO microinjection blocked noxious stimulation-evoked

8 DAMGO significantly decreased the frequency of GABA-medi

9 DAMGO similarly stimulated eating behavior in the poster

10 DAMGO-induced LTP was associated with an increase in the

11 DAMGO-induced PPF was diminished after chronic treatment

12 DAMGO-stimulated [(35)S]GTPgammaS and [(3)H]naloxone bin

13 female rats resulted in a suppression of 3H-DAMGO binding in cortical membranes.

14 ed both CCK-8S and JMV-180 suppression of 3H-DAMGO binding.

15 ceptor agonist (CCK-4) failed to suppress 3H-DAMGO binding.

16 l results revealed that CCK-8S suppressed 3H-DAMGO binding in cortical membranes of ovariectomized ra

17 ptor agonist and antagonist followed with 3H-DAMGO.

18 r antagonist or a calcium chelator abolished DAMGO-induced LTP.

19 This result indicates that reversal of AcbSh DAMGO-induced feeding at a 10-fold lower dose was neithe

20 r forebrain sites is necessary for accumbens DAMGO to elicit high-fat intake, and that forebrain MC3/

21 We further show that accumbens DAMGO in the absence of food selectively increases the p

22 tiple phosphorylation was more intense after DAMGO.

23 locks stimulation by the mu(1)/mu(2) agonist DAMGO (D-Ala2, N-Me-Phe4, Gly5-ol-enkephalin) of the inc

24 atment of SH-SY5Y cells with the MOR agonist DAMGO or the DOR agonist DPDPE decreased RGS4 protein by

25 e selective mu-opioid receptor (MOR) agonist DAMGO induced mechanical hyperalgesia and marked prolong

26 tivation by microinjection of the mu agonist DAMGO (0.1 microg) selectively and reversibly enhanced t

27 The selective mu agonist DAMGO (300 nM) also attenuated the nicotine-mediated enh

28 synaptic inhibition caused by the mu agonist DAMGO had an EC(50) of 80 nM, whereas the EC(50) was 350

29 mice, the mu-opioid receptor (muOR) agonist DAMGO slowed burstlet generation.

30 Infusing the mu-opioid agonist DAMGO (300 microM) increased extracellular 5-HT in the D

31 morphine or the selective mu-opioid agonist DAMGO (D-Ala2-N-Me-Phe(4)-glycol(5)-enkephalin), as show

32 The mu opioid agonist DAMGO applied directly into the KF of the in situ arteri

33 wn that application of the mu opioid agonist DAMGO into the basolateral region of the amygdala (BLA)

34 the OFC, we found that the mu-opioid agonist DAMGO produced a concentration-dependent inhibition of G

35 response to application of mu-opioid agonist DAMGO.

36 injection of the mu-opioid receptor agonist DAMGO (D-ala(2) -N-Me-Phe(4) -Glycol(5) -enkephalin) int

37 ways, whereas the mu opioid receptor agonist DAMGO decreased D2-receptor activity only as a result of

38 A(A) IPSCs by the mu-opioid receptor agonist DAMGO is significantly reduced in both high- and low-dri

39 injection of the mu-opioid receptor agonist DAMGO.

40 inhibited by the mu opioid receptor agonist DAMGO.

41 wley rat, the MOP receptor-selective agonist DAMGO (0.5-3 muM) depolarized or increased the firing ra

42 concentrations of the MOR-selective agonist DAMGO induced outward currents in POMC neurons that were

43 oid receptors (MORs) by the specific agonist DAMGO ([D-Ala2,N-Me-Phe4,Gly5-ol]-Enkephalin) hyperpolar

44 reatment with a combination of muOR agonist (DAMGO) and deltaOR antagonist (Tipp(psi)), and this lead

45 The selective MOR agonist, DAMGO (10 pg), completely inhibited LC discharge of male

46 he low dose (0.025 microg) of a MOR agonist, DAMGO, increased cumulative food intake in wild-type and

47 However, the mu agonist, DAMGO ([d-Ala2, NMe-Phe4, Gly5-ol]-enkephalin), appeared

48 Intra-vmPFC infusion of the muOR agonist, DAMGO, provoked Fos expression in the dorsomedial sector

49 treatment with a mu opioid receptor agonist, DAMGO, or a delta opioid receptor agonist, SNC80, did no

50 l inhibition by the higher efficacy agonists DAMGO and morphine.

51 al shell were suppressed by the MOR agonists DAMGO and morphine, which caused a shift in the excitato

52 gi-intact rats, injection of opioid agonists DAMGO or [Met(5) ]enkephalin (ME) into the KF reduced re

53 ns that were inhibited by mu-opioid agonists DAMGO, but not kappa- and delta-opioid agonists.

54 for the chromatophores, the peptide agonists DAMGO and melanotan-II that are specific for the mu-opio

55 AMP signaling by mu-opioid receptor agonists DAMGO and morphine.

56 ted rats were injected with opioid agonists (DAMGO, morphine, dynorphin, U-50488H) followed by the me

57 ession in delta(-/-) neurons without altered DAMGO-induced internalization.

58 however, completely ineffective at altering DAMGO-induced feeding in the anterior dorsal striatum.

59 C DAMGO-induced food intake without altering DAMGO-induced hyperactivity.

60 Although DAMGO (10 pg intra-LC) increased the number of trials to

61 Here we demonstrate that acute U69,593 and DAMGO stimulate ERK phosphorylation by utilization of di

62 s evidenced by studies of opioid binding and DAMGO inhibition of forskolin-stimulated adenylyl cyclas

63 similar affinities for [3H]diprenorphine and DAMGO as the D3.49(164)Y mutant.

64 ation blockage made etorphine, fentanyl, and DAMGO function as morphine in the primary cultures.

65 gative GRK2 enabled etorphine, fentanyl, and DAMGO to activate PKCepsilon.

66 375 to Ala) enabled etorphine, fentanyl, and DAMGO to use the PKCepsilon pathway.

67 mediated inhibition of high-K(+)-induced and DAMGO-induced rises in [Ca(2+)]i.

68 olecystokinin revealed the ability of ME and DAMGO to inhibit IPSC amplitude; this inhibition was pre

69 maximum inhibition of VGCCs by morphine and DAMGO (D-Ala2-N-Me-Phe4-glycol5-enkephalin) without affe

70 and internalizing MOP agonists morphine and DAMGO (Tyr-D-Ala-Gly-N-methyl-Phe-Gly-ol), respectively.

71 Our results show that morphine and DAMGO display different profiles of receptor internaliza

72 Morphine and DAMGO enhanced MOR1 phosphorylation over basal.

73 Our SPR analyses revealed that morphine and DAMGO evoke similar SPR signatures and that Galphai, cAM

74 inity of the mu-opioid agonists morphine and DAMGO in membranes from whole brain, cortex, thalamus, a

75 Similarly, morphine and DAMGO stimulation of G protein, determined using GTPase

76 htward shift in potency of both morphine and DAMGO, whereas the S147C variant displayed a subtle left

77 the spatiotemporal signaling of morphine and DAMGO.

78 nd ERK1/ERK2 have key roles in morphine- and DAMGO-mediated signaling.

79 LC discharge of male but not female rats and DAMGO (30 pg) produced no further inhibition of female L

80 -Pen5]-Enkephalin, deltorphin II, SNC80, and DAMGO) and antagonists (naltriben and CTAP) and determin

81 se three compounds significantly antagonized DAMGO-induced intracellular calcium flux and displayed v

82 Because DAMGO exhibited a similar potency in delta(+/+) and delt

83 t protein kinase A (H89), completely blocked DAMGO-induced RGS19 protein accumulation.

84 Both DAMGO and morphine activated GIRK currents, but the maxi

85 Buffering DAMGO-induced changes in [Ca(2+)]i with BAPTA-AM complet

86 tween mITCs and CeM neurons is attenuated by DAMGO, whereas the glutamatergic transmission on CeM neu

87 mg/kg) depressed the hyperthermia caused by DAMGO (1 micro g/rat, i.c.v.), a selective mu agonist, c

88 restored the inhibition of Ca2+ currents by DAMGO, and abolished receptor coupling.

89 MORs desensitized by DAMGO activation are then readily internalized by an arr

90 Food intake elicited by DAMGO (2 or 5 nmol) injected unilaterally into the VTA w

91 ists prevented decreases in 5-HT elicited by DAMGO in the presence of bicuculline.

92 The enhanced intake elicited by DAMGO injected into the sNAcc was dose-dependently block

93 We also failed to observe an enhancement by DAMGO of morphine-induced desensitization in the electri

94 projected to lamina I were hyperpolarized by DAMGO.

95 urons, we found them to be hyperpolarized by DAMGO.

96 ioned food intake was similarly increased by DAMGO microinjection and decreased by muscimol in CeA.

97 Reduced motility index induced by DAMGO (1.0 nmol) was restored from 48.7+/-3.5% to 88.6+/

98 icrog) attenuated antinociception induced by DAMGO injection, suggesting DAMGO's action on mu recepto

99 tization by morphine but not that induced by DAMGO.

100 rents, GABAergic currents are potentiated by DAMGO after chronic morphine treatment.

101 35)S]GTP gamma S binding can be regulated by DAMGO and EGF by convergent mechanisms and support the h

102 and there was reduced activation of c-Src by DAMGO.

103 was due to decreased maximal stimulation by DAMGO, with no difference in EC(50) values.

104 CeA DAMGO microinjections made rats more vigorously approach

105 In M2 cells DAMGO stimulation of GTPgammaS binding was significantly

106 ar physiological levels (HEK293-MOR1 cells), DAMGO and methadone but not morphine caused rapid MOR in

107 r at the postreceptor level, because chronic DAMGO also reduced GTPgammaS-induced PPF that was indepe

108 In contrast, DAMGO causes a redistribution of the MOR at the plasma m

109 nsitized MOP in A7 cells, i.e., it decreased DAMGO-induced stimulation of GTPgammaS binding.

110 cy for G protein-mediated responses than did DAMGO at native MOPr in mature neurons.

111 desensitization of the K(+) current than did DAMGO.

112 did not significantly increase after either DAMGO, EGF, or H(2)O(2) treatment alone.

113 harin followed by an icv injection of either DAMGO (0.5 microg/1 microl/rat) or an equal volume of sa

114 Prolonged treatment with either DAMGO or clonidine induced a mutual cross-desensitizatio

115 essing primary afferents not only eliminated DAMGO-induced LTP but also prolonged DAMGO-induced inhib

116 administration of EM1, endomorphin-2 (EM2), DAMGO, and morphine in the conscious rat.

117 (D)-Ala(2),N,Me-Phe(4),Gly-ol(5)-enkaphalin (DAMGO), on high-fat consumption and associated locomotor

118 (D-Ala(2),N-Me-Phe(4),Gly-ol(5))-enkephalin (DAMGO) at 1 mum, but not at 1-10 nm, caused an initial d

119 (D-Ala(2),N-Me-Phe(4),Gly-ol(5))-enkephalin (DAMGO) significantly increased the discharge activity of

120 MOR [D-Ala, N-Me-Phe, Gly-ol(5)-enkephalin (DAMGO) or morphine] or DOR (D-Pen(5)-enkephalin or SNC80

121 f [D-Ala(2),N-MePhe(4),Gly-ol(5)]enkephalin (DAMGO)-related glycopeptides by altering the charged res

122 D-Ala(2), NMe-Phe(4), Gly-ol(5)]-enkephalin (DAMGO) in one site and the opioid antagonist naltrexone

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

124 d-Ala(2), N-MePhe(4), Gly-ol(5)]-enkephalin (DAMGO), endomorphin-2, and morphine in rat and mouse loc

125 agonist D-Ala2-N-Me-Phe4-Glycol5-enkephalin (DAMGO) caused increased hedonic "liking" reactions to su

126 s after D-Ala2-N-Me-Phe4-Glycol5-enkephalin (DAMGO) microinjections in rats and compared hedonic incr

127 namely D-Ala2-N-Me-Phe4-Glycol5-enkephalin (DAMGO), cyclic [D-Pen2-D-Pen5]-enkephalin, or trans-3,4-

128 , Tyr-D-Ala', N-CH, -Phe4, Glyol-Enkephalin (DAMGO), delta opioid agonists, D-pen(2), D-phe(5) enkeph

129 d agonist D-Ala2,Nme-Phe4,Glyol5-enkephalin (DAMGO) markedly increases food intake and preferentially

130 u agonist, [D-ala2,mephe4,glyol5]enkephalin (DAMGO), induces a transient stimulation of ERK phosphory

131 [d-Ala2,(N-Me)Phe4,Gly5-OH] enkephalin (DAMGO)-stimulated [(35)S]GTPgammaS binding was then cond

132 e agonist d-Ala2-N-MePhe4-Gly-ol enkephalin (DAMGO).

133 nist Tyr-D-Ala-Gly-MePhe-Gly(ol)-enkephalin (DAMGO) dose-dependently enhances food intake in satiated

134 agonist D-Ala2-N-Me-Phe4-gly5-ol-enkephalin (DAMGO), we demonstrate that orexin signaling in the vent

135 ate, and (D-Ala2,MePhe4,Gly-ol5) enkephalin (DAMGO), a potent muOR-internalizing agonist, on muOR tra

136 ist (d-Ala2, N-Me-Phe4, Gly-ol5)-enkephalin (DAMGO) was microinjected into the raphe magnus, a manipu

137 onist [D-Ala2,N-MePhe4,Gly-ol5] -enkephalin (DAMGO).

138 gonist [D-Ala2,N-MePhe4, Gly-ol5]enkephalin (DAMGO) or the alpha2 agonist clonidine inhibited voltage

139 whereas [D-Ala2,N-MePhe4,Gly-ol5]enkephalin (DAMGO), a high-efficacy agonist, and methadone, an agoni

140 gonist, [D-Ala2,N-MePhe4,Gly-ol5]enkephalin (DAMGO), to test whether strain differences in sensitivit

141 ist [D-Ala2, N-Me-Phe4, Gly-ol5]-enkephalin (DAMGO) (1 microM) and decreased by the delta agonist [D-

142 nist [D-Ala2, N-MePhe4, Gly-ol5]-enkephalin (DAMGO).

143 [D-Ala2, N-Me-Phe4, Gly5-ol] enkephalin (DAMGO, 0.1-10 nmol), a mu-opioid selective agonist, sign

144 or [d-Ala(2),N-MePhe(4), Gly-ol]enkephalin (DAMGO) causes differences in spatiotemporal signaling de

145 D-Ala(2),methyl-Phe(4),Gly(5)-ol]enkephalin (DAMGO), as demonstrated by both Western blot imaging of

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

147 ephalin [D-Ala2,N-MePhe4,Gly5-ol]enkephalin (DAMGO).

148 ecific ([D-Ala2,N-MePhe4,Gly5-ol]enkephalin (DAMGO); 0, 0.21, 0.29, or 0.39 nmol), or kappa-specific

149 onist, D-Ala2, N-MePhe4, Gly-ol]-enkephalin (DAMGO) (0.25 mug), directly into the AcbSh of ad libitum

150 onist [D-Ala2,N-Me-Phe4,Gly5-ol]-enkephalin (DAMGO) also occluded the ability of DOR agonist to stimu

151 ioid [d-Ala2, N-MePhe4, Gly5-ol]-enkephalin (DAMGO) and a switch in the functional effects of mu-opio

152 [d-Ala(2),N-Me-Phe(4),Gly(5)-ol]-enkephalin (DAMGO) and endomorphin-2 activated inwardly rectifying K

153 -Ala(2), N-Me-Phe(4), Gly(5)-ol]-enkephalin (DAMGO) and morphine and imaged in real time single vesic

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

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

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

157 , and [D-Ala2,N-Me-Phe4,Gly5-ol]-enkephalin (DAMGO) induce extensive receptor phosphorylation and use

158 ist [d-Ala2, N-Me-Phe4, Gly5-ol]-enkephalin (DAMGO) markedly increased intake of standard rat chow.

159 nd D-Ala(2), N-MePhe(4), Gly-ol]-enkephalin (DAMGO) nonbiased agonists and to the TRV130 biased agoni

160 [D-Ala2,Phe4,Gly5-ol]-enkephalin (DAMGO), [D-Ala2,D-Leu5]-enkephalin (DADLE), trans-(+/-)-

161 f [D-Ala(2)-N-Me-Phe(4),Gly5-ol]-Enkephalin (DAMGO), a MOR agonist, that is blocked by D-Phe-Cys-Tyr-

162 onist [d-Ala2,N-Me-Phe4,Gly5-ol]-enkephalin (DAMGO), acting via the endogenous mu opioid receptor (MO

163 ns of [D-Ala2,N-Me-Phe4,Gly5-ol]-enkephalin (DAMGO), methadone, or fentanyl, but not morphine, produc

164 st, [d-Ala(2),N-MePhe(4),gly-ol]-enkephalin (DAMGO), to produce tolerance for its inhibition of prost

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

166 onist D-[Ala2, N-MePhe4, Gly-ol]-enkephalin (DAMGO, 2.5 mug), then challenged with intra-Acb shell in

167 nist ([D-Ala2, N-MePhe4, Gly-ol]-enkephalin; DAMGO) generated intense >250% increases in intake of pa

168 Furthermore, DAMGO application and washout induced an initial decreas

169 Furthermore, DAMGO significantly inhibited the peak amplitude of evok

170 t, all regions of the medial shell generated DAMGO-induced robust increases in eating behavior and fo

171 to measure the regional displacement of (3)H-DAMGO binding following cocaine administration.

172 For all studies, (3)H-DAMGO binding to mu opioid receptors was measured in the

173 a time- and dose-dependent reduction in (3)H-DAMGO binding within the nucleus accumbens core and shel

174 exhibited wash resistant inhibition of [(3)H]DAMGO binding at subnanomolar to nanomolar concentration

175 (2),N-Me-Phe(4),Gly(5)-ol]-enkephalin ([(3)H]DAMGO).

176 However, DAMGO had no effect on glutamate-mediated miniature exci

177 In PAG, however, DAMGO E(max) values did not significantly differ between

178 s and that neural projections originating in DAMGO-responsive sites of the nucleus accumbens make clo

179 reduced the expression of cAMP overshoot in DAMGO-dependent cells.

180 ilon), the pronociceptive effects of PGE2 in DAMGO-treated rats demonstrated the following: (1) rapid

181 as gained to implicate CaM and PKCepsilon in DAMGO stimulation of ERK.

182 MGO-induced locomotor activity but increased DAMGO-induced consumption.

183 presence of morphine, but it did not inhibit DAMGO-induced phosphorylation.

184 We also studied the effect of CeA-injected DAMGO on LiCl-induced increases in c-Fos IR in the amygd

185 Consistent with a decreased maximum DAMGO response, MOR protein and mRNA expression were dec

186 cells but by different molecular mechanisms; DAMGO-induced desensitization is GRK2-dependent, whereas

187 Specifically, whereas in naive mice DAMGO inhibits GABA postsynaptic currents, GABAergic cur

188 rmaceutical opioids was studied using micro (DAMGO), kappa (U50488), and Delta (DPDPE) opioid recepto

189 gonist efficacy of ligands selective for mu (DAMGO)-, delta (SNC80)- and kappa (U69593)-opioid recept

190 d receptors via agonist microinjections [mu (DAMGO), delta (DPDPE), or kappa (U50488H)] and construct

191 lkine 30 min before administration of 400 ng DAMGO, 100 ng DPDPE or 20 microg dynorphin significantly

192 omologous, because desensitization by 100 nM DAMGO was blocked by dominant-negative forms of either G

193 significantly reduced by morphine (60 nmol), DAMGO (1 nmol), and DPDPE (100 nmol), but not by the kap

194 Furthermore, PMA-induced, but not DAMGO-induced, HmuOR phosphorylation was partially inhib

195 e GABA(B) receptor agonist baclofen, but not DAMGO.

196 onist CTOP (1 microM) blocked the actions of DAMGO.

197 Bilateral administration of DAMGO (1.2, 2.4 and 4.9 nmol) into the VTA stimulated fe

198 Administration of DAMGO into the CeA increased c-Fos IR levels in the shel

199 Thus, intra-CeA administration of DAMGO may increase feeding, in part, by activating neuro

200 havior following intra-Acb administration of DAMGO, regardless of whether the BLA was inactivated.

201 r data suggest that long-term application of DAMGO initiates heterologous down-regulation of EGFR via

202 itor prior to TF testing with application of DAMGO into the same site.

203 MOR-expressing cells with the combination of DAMGO and EGF completely blocked subsequent DAMGO stimul

204 hanges in the voltage-dependent component of DAMGO action that requires direct interactions between b

205 A subsaturating concentration of DAMGO (100 nM) did not cause receptor internalization bu

206 iments using a half-maximal concentration of DAMGO demonstrate that nor-BNI must be used at concentra

207 upport the theory that low concentrations of DAMGO can increase morphine-induced MOR desensitization

208 In HEK293-MOR1 cells, low concentrations of DAMGO did not convert morphine into a receptor-internali

209 The highest dose of DAMGO (2.5 microg) reduced food intake in the control an

210 The low and middle (0.25 microg) dose of DAMGO significantly increased the amount of high fat die

211 icantly antagonized the inhibitory effect of DAMGO (1.0 nmol).

212 The excitatory effect of DAMGO on seven labeled LC neurons was diminished in the

213 f delta receptors caused reduced efficacy of DAMGO without affecting potency.

214 ibition of TF reflexes following infusion of DAMGO (0.168-0.50 microg), indicating that DAMGO works t

215 proximately 250%, and subsequent infusion of DAMGO decreased 5-HT to approximately 70% above the pre-

216 Repeated intra-Acb shell infusions of DAMGO (2.5 mug) also sensitized intra-Acb shell muscimol

217 Infusions of DAMGO in both regions replicated the effects seen with s

218 pd101 produced almost complete inhibition of DAMGO-induced MOPr phosphorylation at Ser(375), arrestin

219 The incomplete inhibition of DAMGO-stimulated coupling in the MPBN is most likely due

220 of controls at 20 min after icv injection of DAMGO (1.0 nmol).

221 Single injection of DAMGO (2.4 nmol) into the CeA and bilateral injections o

222 As was expected, intra-CeA injection of DAMGO increased food intake of rats over a 4-h period.

223 We also found that intra-CeA injection of DAMGO, prior to LiCl injection, decreased c-Fos IR level

224 ol) into the CeA and bilateral injections of DAMGO (2.4 nmol) into the NAc stimulated feeding (P<0.05

225 ordingly, we confirm a direct interaction of DAMGO with G-protein-coupled mu receptors in the BLA con

226 tle is known about the direct interaction of DAMGO with mu receptors in the amygdala.

227 In the current study, we injected 2 nmol of DAMGO and measured food intake, c-Fos IR levels in vario

228 eta-adrenoceptors, reproduced the profile of DAMGO effects.

229 played signaling profiles similar to that of DAMGO, alpha-neoendorphin, Met-enkephalin-Arg-Phe, and t

230 otemporal signaling profile to mimic that of DAMGO, resulting in a transient increase in nuclear ERK

231 long lasting and not reversed on washout of DAMGO or by application of the mu-opioid receptor antago

232 MOP agonist Tyr-D-Ala-Gly (NMe)-Phe-Gly-ol (DAMGO) or after treatment with the NPFF agonist 1DMe, bu

233 ioid agonist, Tyr-D-Ala-Gly-(me) Phe-Gly-ol (DAMGO), increases food intake in rats when injected into

234 of the G-protein inhibitor had no effect on DAMGO-induced initial inhibition and long-term potentiat

235 MSX-3 had no effect on DAMGO-induced locomotor activity but increased DAMGO-ind

236 intra-BLA muscimol selectively blocked only DAMGO-induced food intake, leaving baseline feeding inta

237 CGS 21680 had no effect on baseline or DAMGO-driven consumption of the high-fat diet.

238 e (CCPA) had no effect on either baseline or DAMGO-induced locomotor or consumption behaviors associa

239 Indeed, morphine (or DAMGO) inhibited prosurvival signaling in neurons.

240 Morphine- or DAMGO-induced muOR endocytosis resulted from direct inte

241 Paradoxically, DAMGO produced facilitatory effects on mEPSCs, which wer

242 at fentanyl and the synthetic opioid peptide DAMGO require M153 to induce beta-arrestin coupling, whi

243 es of morphine and the mu-selective peptide, DAMGO, respectively.

244 Intra-PFC DAMGO (D-[Ala2,N-MePhe4, Gly-ol]-enkephalin; a mu-opioid

245 Conversely, intra-PFC DAMGO engendered 'high-drive-like' effects: enhancement

246 Nlxz infusion prevented DAMGO stimulation of G-protein coupling in LPBNi and mar

247 arrageenan, used to produce priming produced DAMGO tolerance.

248 Prolonged DAMGO exposure induced EGFR internalization/down-regulat

249 minated DAMGO-induced LTP but also prolonged DAMGO-induced inhibition of the miniature and evoked EPS

250 hile the decrease in mobility with prolonged DAMGO exposure corresponded to an increase in colocaliza

251 -induced hyperphagia; 3 ng of amylin reduced DAMGO-mediated feeding by nearly 50%.

252 er, although inactivation of the BLA reduced DAMGO-induced food intake to control levels, this treatm

253 CeA with the GABAA agonist muscimol reduced DAMGO (D-Ala2-NMe-Phe4-Glyol5-enkephalin)-induced and ba

254 Results showed reduced DAMGO-stimulated [(35)S]GTPgammaS binding in the thalamu

255 se (cADPr) signaling that partially relieves DAMGO inhibition of I(Ca) and completely relieves MOR-me

256 ion, whereas either beta-arrestin can rescue DAMGO-induced MOR internalization.

257 phorothioate) triethylammonium both restored DAMGO reward and reversed the DAMGO-mediated potentiatio

258 Amylin dose-dependently reversed DAMGO-induced hyperphagia; 3 ng of amylin reduced DAMGO-

259 ake of the saccharin cue following saccharin-DAMGO pairings.

260 Met-enkephalin, but not the mu-selective (DAMGO) and delta-selective (DPDPE) opioid receptor agoni

261 Similar DAMGO infusions into neighboring areas of lateral orbita

262 Specifically, DAMGO increased premature responses, regressive errors,

263 DAMGO and EGF completely blocked subsequent DAMGO stimulation of [(35)S]GTP gamma S binding membrane

264 ption induced by DAMGO injection, suggesting DAMGO's action on mu receptors in the BLA.

265 nuated the ability of prefeeding to suppress DAMGO-induced food intake, with no effects in non-prefed

266 229U91 directly into the PVH also suppressed DAMGO-induced high-fat intake, but a higher dose was req

267 locked EGFR and ERK activation by short-term DAMGO administration, implicating EGFR transactivation i

268 We found that DAMGO, but not morphine, activates Ras-related C3 botuli

269 This indicates that DAMGO inhibits glutamatergic afferents, which partly off

270 f DAMGO (0.168-0.50 microg), indicating that DAMGO works through G-protein-coupled opioid receptors i

271 The DAMGO-induced increase of food intake following injectio

272 The DAMGO-induced suppression of inhibition was long lasting

273 (GRK2), GRK2-K220R, markedly attenuated the DAMGO-induced desensitization of MOR1, but it had no eff

274 both restored DAMGO reward and reversed the DAMGO-mediated potentiation, thereby reestablishing the

275 In the reverse situation, the DAMGO (2.4 nmol)-induced increase of food intake followi

276 In the reverse situation, the DAMGO-induced increase of food intake following injectio

277 This DAMGO excitation occurs in the presence of GABAA recepto

278 Thus, DAMGO and morphine each induce desensitization of MOR1 s

279 In contrast, 10-minute exposure to DAMGO or morphine increased the fraction of immobile FLA

280 d GIRK currents, but the maximum response to DAMGO was greater than that of morphine, indicating that

281 The responses to DAMGO and morphine desensitized rapidly in the presence

282 112G/G allele exhibited lower sensitivity to DAMGO and morphine compared with major allele carriers (

283 Taken together, we propose that upon DAMGO treatment, MOR activates PKCzeta through a PDK1-de

284 ults suggest a novel mechanism wherein, upon DAMGO binding, CaM is released from the mu receptor and

285 Using DAMGO, CTAP, and Nor-BNI, we demonstrate that the effect

286 Intra-vmPFC DAMGO affected neither water intake nor nonspecific oral

287 Intra-vmPFC DAMGO also elevated the breakpoint for sucrose-reinforce

288 arbohydrate-enriched test diets, intra-vmPFC DAMGO infusions selectively increased carbohydrate intak

289 in the LH-PeF nearly eliminated intra-vmPFC DAMGO-induced food intake without altering DAMGO-induced

290 e in this structure) antagonized intra-vmPFC DAMGO-induced hyperlocomotion but enhanced food intake.

291 When DAMGO (5 nmol) was injected into the sNAcc, the resultin

292 igh-fat diet, but less efficiently than when DAMGO-induced.

293 /- 9.3% vs 24.2% +/- 7.3%; P < .001) whereas DAMGO (10 mumol/L) strongly induced internalization of m

294 ry response (HCVR) only in high doses, while DAMGO and morphine diminished the HCVR in much lower dos

295 several output structures were infused with DAMGO (0, 0.25 microg/0.5 microl) in the accumbens, and

296 and DNQX (300 microM), were co-infused with DAMGO.

297 Activation of FLAG-MORs with DAMGO caused an acute increase in the fraction of mobile

298 ase (GRK) or arrestin, and pretreatment with DAMGO did not affect the Kir3 response to somatostatin r

299 uration-a profile opposite to that seen with DAMGO.

300 After overnight treatment with DAMGO to reduce RGS4 protein, signaling at the Galpha(i/