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1 tussis toxin and by the kappa antagonist nor-binaltorphimine.
2 opioid peptide (KOP) receptor antagonist nor-binaltorphimine.
4 n-ThrNH2, 6.25 nmol) and kappa (Nor-BIN: nor-binaltorphimine, 10 nmol) opioid receptors were infused
7 ntagonism of kappa-opioid receptors with nor-binaltorphimine and by depletion of neurosecretory vesic
8 ective kappa opioid receptor antagonist, nor-binaltorphimine, blocks naloxone-evoked hyperalgesia in
9 P), delta (naltrinodole, NTI) and kappa (nor-binaltorphimine, BNI) opioid receptors were administered
10 oid receptor subtype antagonist nor-BNI (nor-Binaltorphimine), but not by the selective mu-opioid or
11 er, the kappa opioid receptor antagonist nor-Binaltorphimine decreased immobility in HSV-CREB- and HS
13 abolished by the kappa-opioid antagonist nor-Binaltorphimine dihydrochloride (nor-BNI; 100 nM), and b
14 inally, the kappa R-selective antagonist nor-binaltorphimine hydrochloride inhibits the binding of an
15 al injection of CTOP (micro antagonist), nor-Binaltorphimine (kappa antagonist), or saline, newborn (
16 depletes neurosecretory vesicles) and by nor-binaltorphimine (kappa-opioid receptor antagonist), but
17 tagonist, 2 micrograms/2 microliters) or nor-binaltorphimine (kappa-selective antagonist, 73.5 microg
18 atment with ultra-low-dose naltrexone or nor-binaltorphimine may selectively block signaling by endog
19 e reverse dialysis of the KOR antagonist nor-Binaltorphimine (nor-BNI) enhanced mPFC DA overflow.
21 and pretreatment with the KOR antagonist nor-binaltorphimine (nor-BNI) increased DA levels selectivel
22 r to Dyn A, the KOR-selective antagonist nor-binaltorphimine (nor-BNI) lacked specificity when used a
23 of the kappa-opioid receptor antagonist, nor-binaltorphimine (nor-BNI) or the mu-opioid receptor anta
24 lecule selective KOR antagonists such as nor-binaltorphimine (nor-BNI) that last weeks after a single
25 ntricular infusion of the KOR antagonist nor-binaltorphimine (nor-BNI) was assessed for the ability t
26 ceptor agonist (U-50,488) or antagonist (nor-binaltorphimine (NOR-BNI)) on D2 receptor-mediated activ
27 norphin(1-8) was reversed by 2 microM of nor-binaltorphimine (nor-BNI), a selective kappa opioid rece
28 rospinal fluid (aCSF) or aCSF containing nor-binaltorphimine (nor-BNI), a selective kappa-opioid rece
29 nt, push-pull perfusion of the MPOA with nor-binaltorphimine (nor-BNI), a specific kappa-opioid recep
30 n monkeys, the selective KOR antagonist, nor-binaltorphimine (nor-BNI), produces a long-lasting antag
31 rtate in the locus coeruleus (LC) during nor-binaltorphimine (nor-BNI)-precipitated withdrawal from b
33 -tetrahydroisoquinoline-3-carboxamide)], nor-binaltorphimine (nor-BNI); and (3R)-7-hydroxy-N-((1S)-1-
34 onists selective for either kappa- [e.g. nor-binaltorphimine (nor-BNI)] and mu- (e.g. beta-funaltrexa
36 ntra-CeA infusions of the KOR antagonist nor-binaltorphimine (nor-BNI; 0, 2, 4, or 6 mug) prior to op
37 ted by administering one of two doses of nor-binaltorphimine (nor-BNI; 1 and 5 mg/kg i.v.) before isc
38 ith the kappa opioid receptor antagonist nor-binaltorphimine (nor-BNI; 10 mg/kg, i.p.) blocked the st
39 periment 2, the kappa opioid antagonist, nor-binaltorphimine (Nor-BNI; 20.0 microg, i.c.v.) reproduce
40 A+/-the kappa-opioid receptor antagonist nor-binaltorphimine (NorBNI) under extinction conditions.
44 reincubation with the opioid antagonists nor-binaltorphimine or naltrexone, suggesting that these inh
46 ersely, injection of the KOR antagonist, nor-binaltorphimine, stimulated ethanol drinking in low-drin
47 spontaneously active neurones exposed to nor-binaltorphimine switched from phasic to continuous firin
48 ration of the long-acting KOR antagonist nor-binaltorphimine to wild-type mice increased DA dynamics.