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1 rodynorphin) with enkephalin (or Phe-Arg-Met-enkephalin).
2 ntisera against beta-endorphin or methionine-enkephalin.
3 itters gastrin-releasing peptide and leucine-enkephalin.
4 arasympathetic) neurons and those containing enkephalin.
5 likely interact with nerve fibers containing enkephalin.
6 and specific down-regulation of the DRD2 and enkephalin.
7 otein of the active peptide neurotransmitter enkephalin.
8 stimulation by the opioid peptide methionine enkephalin.
9 mounts of nicotine-induced secretion of (Met)enkephalin.
10 hat cathepsin L in vivo was colocalized with enkephalin.
11 y residue was proved by the synthesis of Leu-enkephalin.
12 l cord, where multiple peptidases metabolize enkephalin.
13 gonist, carboxynitrobenzyl-tyrosine-[Leu(5)]-enkephalin.
14 PENK is a stable analyte of labile enkephalins.
15 g with the mu/delta selective opioid [Met(5)]enkephalin (1 mum) decreased spontaneous dopamine transi
20 jections coexpress GABA and the neuropeptide enkephalin, a delta and mu opioid receptor (MOR) ligand.
21 critical for the hydrolysis of exogenous Leu-enkephalin, a neuropeptide present in the CA3 region of
22 Intra-PFC DAMGO (D-[Ala2,N-MePhe4, Gly-ol]-enkephalin; a mu-opioid agonist) and d-amphetamine were
23 alated cells of the amygdala as an assay for enkephalin activity, we applied specific peptidase inhib
26 nd limited receptor internalization, whereas enkephalin analogs promote robust trafficking of both be
28 Moreover, neurons triple-labeled with c-Fos, enkephalin and 5-HT were noted frequently in the NRP fol
30 on (LOQ) by analyzing targeted peptides, leu-enkephalin and angiotensin II, spiked in a BSA tryptic d
32 ion of cathepsin L-DsRed fusion protein with enkephalin and chromogranin A neuropeptides that are pre
33 s, including PSD-95, and opioid peptides leu-enkephalin and dynorphin in the hippocampus of young ani
34 age, females showed opposing changes in leu-enkephalin and dynorphin levels in the mossy fiber pathw
35 ird, we examined co-localization of Y1R with enkephalin and dynorphin neurons and the effect of NPY o
37 phase- and gas-phase deuterium uptake of Leu-Enkephalin and Glu-Fibrinopeptide B, confirmed that this
38 we examined how patch output is modulated by enkephalin and identified the underlying circuit mechani
39 c-based solid-phase peptide synthesis of Leu-enkephalin and in microwave-assisted automated synthesis
40 biologically active conformation of leucine enkephalin and its methyl ester in the nonpolar cell mem
42 ase in the pPVN, due to increased endogenous enkephalin and mu-opioid receptor production in brainste
43 s in droplets containing bradykinin, leucine enkephalin and myoglobin, but loss of the heme group fro
47 in human brain cortex and hippocampus where enkephalin and NPY are produced and is present in purifi
49 function of human cathepsin V for producing enkephalin and NPY neuropeptides required for neurotrans
50 the evidence supporting cleavage at proline, enkephalin and peptide A-779, two peptides that do not c
51 2, involved in matrix remodeling, as well as enkephalin and RUNX3, potentially involved in the increa
52 In this study Tyr residues of both leucine enkephalin and salmon calcitonin (sCT) were targeted usi
53 d D3R GFP fluorescent cells colocalized with enkephalin and substance P immunoreactive medium spiny n
54 g the D1 subtype were immunopositive for met-enkephalin and vesicular glutamate transporter VGLUT2, b
56 oid peptides targeting mu-receptors, such as enkephalins and endorphins, underlying the regulation of
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
61 s endogenous opioids (beta-endorphin and Met-enkephalin) and uroguanylin in apical compartments close
63 expression of orexigenic peptides, galanin, enkephalin, and dynorphin, in the paraventricular nucleu
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
68 on microscopy using substance P and Met-/Leu-enkephalin antibodies to label GABAergic terminals from
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
74 ar to that of DAMGO, alpha-neoendorphin, Met-enkephalin-Arg-Phe, and the putatively endogenous peptid
77 agonist DAMGO (D-Ala2-N-Me-Phe(4)-glycol(5)-enkephalin), as shown by analysis of downstream targets
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
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 orexigenic neuropeptide Y, dynorphin and met-enkephalin, consistent with an anorexic role in energy h
86 alin, resulting from the conversion of PE to enkephalin-containing intermediates of 23, 18-19, 8-9, a
87 in some medullary nuclei (e.g., raphe), only enkephalin-containing neuronal processes were found in t
88 occurs at dibasic residue sites to generate enkephalin-containing peptides and an approximately 24-k
90 eGFP-expressing neurons were associated with enkephalin-containing varicosities, and enkephalin-induc
91 trated that the DOR agonist D-[Pen(2),Pen(5)]enkephalin could induce receptor internalization and ade
92 ts beta-arrestin2, whereas the MOR-selective enkephalin [D-Ala(2),N-Me-Phe(4),Gly(5)-ol]enkephalin (D
93 saturating doses of the hydrolysis-resistant enkephalin [D-Ala2,N-MePhe4,Gly5-ol]enkephalin (DAMGO).
94 ns with the DOR agonist [d-Ala(2), d-Leu(5)]-enkephalin (DADLE) caused a decrease in the membrane abu
95 decreased the potency of [D-Ala(2),D-Leu(5)]-enkephalin (DADLE), and decreased the potency and effica
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 tor agonist (D-Ala(2),N-Me-Phe(4),Gly-ol(5))-enkephalin (DAMGO) at 1 mum, but not at 1-10 nm, caused
102 ]diprenorphine and [d-Ala2,NMe-Phe4,Gly5-ol]-enkephalin (DAMGO) binding and effect of MTSEA on [3H]di
103 ]diprenorphine and [D-Ala2,NMe-Phe4,Gly5-ol]-enkephalin (DAMGO) binding and effect of MTSEA on [3H]di
104 by morphine or [d-Ala(2),N-MePhe(4), Gly-ol]enkephalin (DAMGO) causes differences in spatiotemporal
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 e morphine and D-Ala(2), N-MePhe(4), Gly-ol]-enkephalin (DAMGO) nonbiased agonists and to the TRV130
108 with either MOR [D-Ala, N-Me-Phe, Gly-ol(5)-enkephalin (DAMGO) or morphine] or DOR (D-Pen(5)-enkepha
109 the micro agonist [D-Ala2,N-MePhe4, Gly-ol5]enkephalin (DAMGO) or the alpha2 agonist clonidine inhib
110 pplication of [D-Ala(2)-N-Me-Phe(4),Gly5-ol]-Enkephalin (DAMGO), a MOR agonist, that is blocked by D-
111 nfusions of D-Ala(2), NMe-Phe(4), Gly-ol(5)]-enkephalin (DAMGO), a mu-opioid receptor agonist, in the
112 nalizing opiate, and (D-Ala2,MePhe4,Gly-ol5) enkephalin (DAMGO), a potent muOR-internalizing agonist,
113 id agonist [D-Ala(2),methyl-Phe(4),Gly(5)-ol]enkephalin (DAMGO), as demonstrated by both Western blot
114 e mu agonist, Tyr-D-Ala', N-CH, -Phe4, Glyol-Enkephalin (DAMGO), delta opioid agonists, D-pen(2), D-p
115 (Met-Enk), [d-Ala(2), N-MePhe(4), Gly-ol(5)]-enkephalin (DAMGO), endomorphin-2, and morphine in rat a
117 opioid agonist, [d-Ala(2),N-MePhe(4),gly-ol]-enkephalin (DAMGO), to produce tolerance for its inhibit
118 id receptor agonist D-Ala2-N-Me-Phe4-gly5-ol-enkephalin (DAMGO), we demonstrate that orexin signaling
119 electivity of [D-Ala(2),N-MePhe(4),Gly-ol(5)]enkephalin (DAMGO)-related glycopeptides by altering the
124 mu-opioid agonist D-[Ala2, N-MePhe4, Gly-ol]-enkephalin (DAMGO, 2.5 mug), then challenged with intra-
125 receptor agonist ([D-Ala2, N-MePhe4, Gly-ol]-enkephalin; DAMGO) generated intense >250% increases in
127 e III (DPP III) is one of the most important enkephalin-degrading enzymes associated with the mammali
128 duced by morphine and RB101 (an inhibitor of enkephalin-degrading enzymes, which increases the synapt
129 or (MOR) selective agonists ([D-Pen2,D-Pen5]-Enkephalin, deltorphin II, SNC80, and DAMGO) and antagon
131 es CR-triggered hypothermia and that leucine enkephalin directly controls core body temperature when
132 ), delta opioid agonists, D-pen(2), D-phe(5) enkephalin (DPDPE), and kappa agonist, U50 488, all sign
133 or-BNI) enhanced the potency of [D-Pen(2,5)]-enkephalin (DPDPE), decreased the potency of [D-Ala(2),D
134 od was used to determine met-enkephalin, leu-enkephalin, dynorphin A(1-8), and beta-endorphin in vivo
135 exigenic neuromodulators neuropeptide Y, met-enkephalin, dynorphin and the catecholamine dopamine.
141 NK (proenkephalin) is a stable surrogate for enkephalins, endogenous opioid peptides, which exert car
142 singly, co-injection of naloxone with either enkephalin enhanced the effect associated with administr
143 ibility that the orexigenic peptide systems, enkephalin (ENK) and orexin (OX), which are stimulated b
144 male starlings also had significantly higher enkephalin (ENK) immunolabeling densities in the POM tha
145 NT colocalization with the endogenous opioid enkephalin (ENK) in the RVM during thermal hyperalgesia,
147 only Ucn 3 neurons in the rPFH co-expressed enkephalin (Enk), and Ucn 3/Enk double-labeled nerve fib
148 ergic synapses colocalize the opioid peptide enkephalin (ENK), but the neurons to which they belong a
150 opioid peptides [e.g., proopiomelanocortin, enkephalin (ENK)] with the stress-related peptide cortic
155 leus size, loss of dendritic spines, reduced enkephalin expression, diminished nigral dopaminergic pr
160 lymer nanoparticles encapsulating leucine(5)-enkephalin hydrochloride (LENK) are able to transport LE
161 ic agonist DAMGO ([D-Ala2,N-Me-Phe4,Gly5-ol]-Enkephalin) hyperpolarizes medially located ITCs (mITCs)
164 e accurate and precise quantification of Leu-enkephalin in a complex mixture using multiple-reaction
165 NL led to increased immunoreactivity for met-enkephalin in dorsal horn homogenates, which was dose-de
168 Furthermore, labeling for the opioid met-enkephalin in the medial preoptic nucleus (POM) correlat
170 dominant peptidase responsible for degrading enkephalins in the intercalated cells of the amygdala.
172 scimol reduced DAMGO (D-Ala2-NMe-Phe4-Glyol5-enkephalin)-induced and baseline food intake, whereas in
173 with enkephalin-containing varicosities, and enkephalin-induced clathrin- and dynamin-mediated endocy
174 treated animals, recovery from acute [Met](5)enkephalin-induced desensitization and receptor recyclin
175 tracellular concentrations and half-lives of enkephalins, inducing potent antinociceptive effects.
177 one by blocking the enzymatic degradation of enkephalin inhibited GABA neurotransmission in yoked sal
179 ist DAMGO (D-ala(2) -N-Me-Phe(4) -Glycol(5) -enkephalin) into the rostrodorsal part of the accumbens
180 Methionine-enkephalin (M-ENK) and leucine-enkephalin (L-ENK) are small endogenous opioid peptides
181 which recognized Leu-, Met-, and Phe-Arg-Met-enkephalin, labeled the dorsolateral funiculus and numer
183 activatable analogs of two opioids: [Leu(5)]-enkephalin (LE) and the 8 amino acid form of Dynorphin A
186 the effect of exposure to exogenous leucine-enkephalin (Leu-Enk), methionine-enkephalin (Met-Enk), a
188 nimal model of Huntington's disease in which enkephalin levels are reduced in striatum and comorbidit
190 l, with or without progesterone, altered leu-enkephalin levels in the dentate gyrus and synaptophysin
192 wild-type mice, Q175 animals showed reduced enkephalin levels in the NAc and enhanced susceptibility
194 withdrawal from cocaine self-administration enkephalin levels in the VP are elevated and the opioid
201 se in CID sensitivity for protonated leucine enkephalin (m/z 556), and 14x increase of CID sensitivit
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 jection of opioid agonists DAMGO or [Met(5) ]enkephalin (ME) into the KF reduced respiratory frequenc
206 sporine did not reduce the extent of [Met(5)]enkephalin (ME)-induced desensitization but increased th
207 tions of buprenorphine decreased the [Met](5)enkephalin (ME)-induced hyperpolarization or outward cur
211 of such interactions, we exposed methionine-enkephalin (MENK) to PN and identified the major metabol
212 e (ir) for galanin, GABA, TRH, or methionine-enkephalin (mENK) were dense in the ventrocaudal hypotha
214 ptor-saturating concentrations of methionine-enkephalin (Met-Enk), [d-Ala(2), N-MePhe(4), Gly-ol(5)]-
215 ous leucine-enkephalin (Leu-Enk), methionine-enkephalin (Met-Enk), and the opioid antagonist naloxone
216 nced for deltorphin II, [d-Pen(2), d-pen(5)]-enkephalin, met-enkephalin, and SNC-80 ((+)-4-[(alphaR)-
218 2) agonist DAMGO (D-Ala2, N-Me-Phe4, Gly5-ol-enkephalin) of the incorporation of [(35)S]-guanosine 5'
219 1H-imidazole]; the effect of vector-mediated enkephalin on Na(V)1.7 levels was prevented by naltrindo
220 e effect of transgene-mediated expression of enkephalin on pain-related behaviors and their biochemic
222 on of cathepsin L for biosynthesis of active enkephalin opioid peptide contrasts with its function in
224 neurons double-labeled with c-Fos and either enkephalin or 5-HT were found more frequently in all thr
226 phalin (DAMGO) or morphine] or DOR (D-Pen(5)-enkephalin or SNC80) agonists increased RGS19 and GIPC p
227 c medium spiny neurons that expressed either enkephalin or substance P and extended fibers to the glo
228 ouble-labeled with c-Fos and beta-endorphin, enkephalin or VGLUT3 in the ARC were significantly incre
230 10(-5) M naltrexone (NTX), 10(-5) M [Met(5)]-enkephalin, or sterile vehicle was administered to one e
231 ls and synthesis of the orexigenic peptides, enkephalin, orexin and melanin-concentrating hormone, as
232 be presented for [(eta(6)-Cp*Rh-Tyr(1))-leu-enkephalin](OTf)(2) and [(eta(6)-Cp*Rh-Tyr(3))-octreotid
233 iatum, which expresses the endogenous opioid enkephalin, patches (or striosomes) are limbic-associate
234 protease cathepsin L for producing the (Met)enkephalin peptide neurotransmitter from proenkephalin (
241 ice, PDE10A content selectively increases in enkephalin-positive striatal neuronal bodies; moreover,
243 urons containing preprotachykinin and prepro-enkephalin (PPE) mRNAs were also activated, with the non
244 is entailed the solid-phase synthesis of two enkephalin precursor chains followed by a Cu(I)-catalyze
245 ne expression, leading to an upregulation of enkephalin precursor Penk mRNA and met-enkephalin protei
247 of the presynaptic delta-opioid receptor by enkephalin prevents the increase in neuronal Na(V)1.7 in
248 and related findings, we suggest endogenous enkephalins primarily set a background motivational tone
249 neutral antagonist 6beta-naltrexol; (2) pro-enkephalin, pro-opiomelanocortin, and pro-dynorphin KO m
250 or agonist [D-Ala(2), NMe-Phe(4), Gly-ol(5)]-enkephalin produces paradoxical behavioural responses: e
253 we used viral vectors utilizing dynorphin or enkephalin promoters to drive expression of 5-HT6 recept
255 In contrast, the levels of phospholipase A2, enkephalin, PSD-95, synaptophysin, or glutamate NMDA rec
256 method is illustrated by using a set of four enkephalin-related and acetylated peptides to generate 1
258 olesterol restored [D-Ala2,N-Me-Phe4,Gly5-ol]enkephalin responses back to control values, and were co
259 inhibition of neprilysin alone could enhance enkephalin responses to the same extent as inhibitors of
260 in highly increased cellular levels of (Met)enkephalin, resulting from the conversion of PE to enkep
263 /or efficacy of the orthosteric agonists leu-enkephalin, SNC80 and TAN67, as measured by receptor bin
264 er, desensitization of D-Ala(2)-Met(5)-Glyol-enkephalin-stimulated [(35)S]GTPgammaS binding following
265 emonstrated by reduced D-Ala(2)-Met(5)-Glyol-enkephalin-stimulated [(35)S]GTPgammaS binding to spinal
267 micro-domain within dorsal neostriatum where enkephalin surges are triggered by the opportunity to co
270 PENK is a stable surrogate analyte of labile enkephalins that is correlated inversely with renal func
271 GF) is an endogenous opioid peptide ([Met(5)]enkephalin) that interacts with the OGF receptor (OGFr)
272 roach, we have electroosmotically pulled Leu-enkephalin through OHSCs to identify ectopeptidase activ
273 lized with dynorphin, oxytocin, vasopressin, enkephalin, thyrothropin-releasing hormone, and corticot
274 mu-opioid agonist [D-Ala2,N-Me-Phe4,Gly5-ol]enkephalin to acutely inhibit adenylyl cyclase or to cau
275 lthough not affecting the ability of [Met](5)enkephalin to induce desensitization, acutely reversed t
276 is study clearly demonstrates the ability of enkephalins to disrupt insect sexual development and als
277 aine-trained mice, indicating that increased enkephalin tone on presynaptic mu opioid receptors was r
279 r prodrug - tyrosinyl(1)palmitate-leucine(5)-enkephalin (TPLENK) were coated with the polymer - N-pal
280 mportant GPCR peptides; namely, [Tyr(1)]-leu-enkephalin, [Tyr(4)]-neurotensin(8-13), and [Tyr(3)]-oct
281 nerve ligation is accompanied by D1R and met-enkephalin upregulation, acquired D1LR-mediated antinoci
282 ory cells that coexpress beta-endorphin, Met-enkephalin, uroguanylin, and Trpm5 exist in mouse duoden
284 ate release by a submaximal concentration of enkephalin was doubled by application of all three pepti
286 ally in close proximity to fibers containing enkephalin was noted in the NAmb of EA-treated cats (n=5
289 erivatization conditions for 1microM leucine-enkephalin were achieved when 10mM cysteine and 200U/ml
294 thalamic levels of the endogenous opioid Leu-enkephalin, which is derived from the KOR agonist precur
295 R signaling resulting from lowered levels of enkephalins, which is partly mediated through elevated e
296 n of the opioid growth factor (OGF) [Met(5)]-enkephalin with its receptor (OGFr) is a regulator of TC
297 se results indicate increased levels of (Met)enkephalin within secretory vesicles of the regulated se
299 morphine and DAMGO (D-Ala2-N-Me-Phe4-glycol5-enkephalin) without affecting agonist potency, the onset