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1 y inert drug-like and bioavailable compound (clozapine-N-oxide).
2  a concurrent gain in potency for the ligand clozapine N-oxide.
3 us administration of the inert DREADD ligand clozapine-N-oxide.
4 rent subsets using intravenous injections of clozapine-N-oxide.
5 Activation of the transfected Gi-DREADD with clozapine-N-oxide administered into the ventral pallidum
6 clozapine; a hM3Dq-miniG(q) complex bound to clozapine-N-oxide; and a hM3R-miniG(q) complex bound to
7  NAcC-projecting BLA neurons, treatment with clozapine N-oxide, but not vehicle, selectively prevente
8 ndicate that acute Gi-Dreadd activation with Clozapine-N-Oxide can reduce seizure severity.
9                                        While clozapine N-oxide (CNO) activation of interneurons suppr
10 g intracranial or systemic administration of clozapine N-oxide (CNO) and tested the ability of system
11 s approach, we encapsulate the designer drug clozapine N-oxide (CNO) into the optimal HOF nanocrystal
12              The prototypical DREADD agonist clozapine N-oxide (CNO) lacks brain entry and converts t
13                               Males received clozapine N-oxide (CNO) or vehicle injections before eac
14 mporally by the administration of the ligand clozapine N-oxide (CNO).
15 exclusively activated by the "designer drug" clozapine N-oxide (CNO).
16 ited SST-expressing neurons by administering Clozapine N-oxide (CNO).
17 hronically activated using the designer drug clozapine N-oxide (CNO).
18 nergic neurons, administration of the ligand clozapine-N-oxide (CNO) by systemic injection attenuated
19                                              Clozapine-N-oxide (CNO) did not affect conditioned freez
20                                Administering clozapine-N-oxide (CNO) enabled precise DREADD-dependent
21 coupled receptor with the synthetic compound clozapine-N-oxide (CNO) evoked a short and transient Ca(
22 combination of muscarinic-based DREADDs with clozapine-N-oxide (CNO) has been widely used, sluggish k
23 d and subsequently activated by their ligand Clozapine-N-oxide (CNO) in conjunction with fear extinct
24  adora2A-rM3Ds mouse, activation of rM3Ds by clozapine-N-oxide (CNO) induces DARPP-32 phosphorylation
25                            We confirmed that clozapine-N-oxide (CNO) itself did not alter the CD resp
26 ch, potential effects of the DREADD actuator clozapine-N-oxide (CNO) on sleep have never been systema
27 nd after administration of the DREADD ligand clozapine-N-oxide (CNO) or vehicle (saline).
28 und that activation of hM(4)D receptors with clozapine-N-oxide (CNO) potently reduced striatal neuron
29 ce expressing Gi-DREADD were normal, 1 mg/kg clozapine-N-oxide (CNO) produced a significant 3 h incre
30 CRF-neurons, we found that the DREADD ligand clozapine-N-oxide (CNO) produced an acute and robust act
31 er injection of saline or the hM3/hM4 ligand clozapine-N-oxide (CNO) under baseline conditions and un
32 livered after 4-weeks of alcohol intake, and clozapine-N-oxide (CNO) was administered to selectively
33  ligand, but can be efficiently activated by clozapine-N-oxide (CNO), an otherwise pharmacologically
34       However, several DREADD ligands, e.g., clozapine-N-oxide (CNO), have metabolic and off-target e
35 ctivation of hM4Di with the DREADD actuator, clozapine-n-oxide (CNO), would potentiate the discrimina
36                                Chemogenetic [clozapine-N-oxide (CNO)-hM4Di] perturbation of Tac1-Pet1
37 ated by an otherwise inert synthetic ligand, clozapine-N-oxide (CNO).
38 idal neurons and activated the receptor with clozapine-N-oxide (CNO).
39 tion to a bioinert drug-like small molecule, clozapine-N-oxide (CNO).
40 ons could be dose-dependently inactivated by clozapine-n-oxide (CNO).
41 lencer in the presence of its cognate ligand clozapine-N-oxide (CNO).
42 lly inactive and orally bioavailable agonist clozapine-N-oxide (CNO).
43 ated by an otherwise inert synthetic ligand, clozapine-N-oxide (CNO).
44 acologically inert, orally bioavailable drug clozapine-N-oxide (CNO).
45 NAc administration of the Gi-DREADD actuator clozapine-n-oxide (CNO).
46 d AAV-hSYN-eYFP vector that was treated with clozapine-N-oxide (CNO; 3 mg/kg, i.p.) before stage II s
47 cologically inert, but bioavailable, ligand (clozapine-N-oxide; CNO), while being non-responsive to e
48       Sustained activation of Gi-DREADD with clozapine-N-oxide delivered in drinking water over 4 day
49 the ventral hippocampal neurons and infusing clozapine N-oxide in the amygdala.
50 ted Cre/(td)Tomato(+) cells are activated by clozapine-n-oxide in vitro and in vivo, and that activat
51 ly shown that the prototypical DREADD ligand clozapine-N-oxide increased pharyngeal diameter in mice
52  nerve terminals by brainstem application of clozapine-N-oxide increased the firing rate of DMV neuro
53                                              Clozapine N-oxide-induced activation of Piezo2;hM3Dq-exp
54                                    Likewise, clozapine-N-oxide-induced inhibition of PV interneurons
55 tic activation of PVN(OT+) neurons following clozapine-N-oxide injection reduced binge-like alcohol d
56 tially before and for 1 hr after intravenous clozapine-N-oxide injection.
57  otherwise pharmacologically inert compound (clozapine-N-oxide), leading to the conditional activatio
58 was later activated by systemic injection of clozapine-N-oxide, neural activity in RSC was transientl
59     Chemogenetic activation (via intravenous clozapine-N-oxide) of nodose and jugular nociceptors evo
60 esigner drug (DREADD(Gi) ) by application of clozapine-N-oxide reduced the CO(2) response by ~20% and
61                 Chemogenetic activation with clozapine N-oxide resulted in delayed estrous cycles and
62 with intra-VTA microinfusions of the agonist clozapine-n-oxide to bidirectionally modulate dopamine n
63 ed for direct brainstem viral injections and clozapine-N-oxide toxicity diminished translational pote
64 , as it was reversible, and it was absent in clozapine N-oxide-treated rats expressing an empty contr
65 ly more potent than the parent drug, whereas clozapine N-oxide was essentially inactive.
66  M3D-arr using the otherwise inert compound, clozapine-N-oxide, we found that M3D-arr activation incr
67 o the P4-P6 peptide binding pockets, whereas clozapine N-oxide, which did not activate the TCC, bound