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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 g intracranial or systemic administration of clozapine N-oxide (CNO) and tested the ability of system
8 nergic neurons, administration of the ligand clozapine-N-oxide (CNO) by systemic injection attenuated
10 coupled receptor with the synthetic compound clozapine-N-oxide (CNO) evoked a short and transient Ca(
11 d and subsequently activated by their ligand Clozapine-N-oxide (CNO) in conjunction with fear extinct
12 adora2A-rM3Ds mouse, activation of rM3Ds by clozapine-N-oxide (CNO) induces DARPP-32 phosphorylation
14 und that activation of hM(4)D receptors with clozapine-N-oxide (CNO) potently reduced striatal neuron
15 ce expressing Gi-DREADD were normal, 1 mg/kg clozapine-N-oxide (CNO) produced a significant 3 h incre
16 er injection of saline or the hM3/hM4 ligand clozapine-N-oxide (CNO) under baseline conditions and un
17 ligand, but can be efficiently activated by clozapine-N-oxide (CNO), an otherwise pharmacologically
27 d AAV-hSYN-eYFP vector that was treated with clozapine-N-oxide (CNO; 3 mg/kg, i.p.) before stage II s
28 cologically inert, but bioavailable, ligand (clozapine-N-oxide; CNO), while being non-responsive to e
30 otherwise pharmacologically inert compound (clozapine-N-oxide), leading to the conditional activatio
31 was later activated by systemic injection of clozapine-N-oxide, neural activity in RSC was transientl
34 M3D-arr using the otherwise inert compound, clozapine-N-oxide, we found that M3D-arr activation incr
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