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 hyperpolarized each of the stellate cells, the spi

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

6 DAMGO induced arrestin-2 translocation to the plasma mem

7 DAMGO injection into the CeA also resulted in mu opioid

8 DAMGO microinjection blocked noxious stimulation-evoked

9 DAMGO significantly decreased the frequency of GABA-medi

10 DAMGO similarly stimulated eating behavior in the poster

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

12 DAMGO-induced PPF was diminished after chronic treatment

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

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

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

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

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

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

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

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

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

22 ase in fat intake induced by intra-accumbens DAMGO at doses of muscimol that did not affect general m

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

24 Acute DAMGO desensitization, however, was not affected by the

25 tiple phosphorylation was more intense after DAMGO.

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

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

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

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

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

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

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

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

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

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

36 response to application of mu-opioid agonist DAMGO.

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

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

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

40 injection of the mu-opioid receptor agonist DAMGO.

41 inhibited by the mu opioid receptor agonist DAMGO.

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

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

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

45 ty and could not be activated by the agonist DAMGO or morphine.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

92 projected to lamina I were hyperpolarized by DAMGO.

93 e III-V; six of these were hyperpolarized by DAMGO.

94 f seven stalked cells 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 The action of ME was mimicked by DAMGO, and blocked by naloxonazine.

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

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

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

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

105 CeA DAMGO microinjections made rats more vigorously approach

106 In M2 cells DAMGO stimulation of GTPgammaS binding was significantly

107 micro and delta receptors (GH3MORDOR cells), DAMGO had an excitatory effect on Ca 2+ signaling that w

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

109 Chronic DAMGO desensitization was heterologous in nature and sig

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

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

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

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

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

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

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

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

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

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

120 (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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

153 [D-Ala(2),N-Me-Phe(4),Gly(5)-ol]-enkephalin (DAMGO) analgesia.

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

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

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

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

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

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

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

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

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

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

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

165 -Ala(2), N-Me-Phe(4), Gly(5)-ol]-enkephalin (DAMGO), and was partially blocked by the mu-selective an

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

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

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

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

170 -Ala(2), N-Me-Phe(4), Gly(5)-ol]-enkephalin (DAMGO; 500 nM) and to address possible downstream conseq

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

172 Furthermore, DAMGO application and washout induced an initial decreas

173 Furthermore, DAMGO significantly inhibited the peak amplitude of evok

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

200 The short-term action of DAMGO resulted in the stimulation of ERK phosphorylation

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

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

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

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

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

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

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

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

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

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

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

212 as been reported that a low concentration of DAMGO, coapplied with morphine, caused morphine to induc

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

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

215 Coapplication of low concentrations of DAMGO did not increase morphine-induced desensitization

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

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

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

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

220 The excitatory effect of DAMGO was also inhibited by pretreatment with pertussis

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

251 arrageenan, used to produce priming produced DAMGO tolerance.

252 Prolonged DAMGO exposure induced EGFR internalization/down-regulat

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

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

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

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

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

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

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

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

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

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

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

264 Similar DAMGO infusions into neighboring areas of lateral orbita

265 Specifically, DAMGO increased premature responses, regressive errors,

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

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

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

269 229U91 directly into the PVH also suppressed DAMGO-induced high-fat intake, but a higher dose was req

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

271 used a lesser degree of desensitization than DAMGO alone.

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

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

274 The DAMGO (2.4 nmol)-induced increase of food intake followi

275 The DAMGO-induced increase of food intake following injectio

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

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

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

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

280 This DAMGO excitation occurs in the presence of GABAA recepto

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

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

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

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

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

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

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

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

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

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

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

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

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

294 /- 9.3% vs 24.2% +/- 7.3%; P < .001) whereas DAMGO (10 mumol/L) strongly induced internalization of m

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

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

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

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/