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1 influx was reduced by the GABA(B) antagonist saclofen.
2 lline, but not by the GABAB receptor blocker saclofen.
3 ptors with the selective GABA(B) antagonist, saclofen.
4 of bicuculline (0, 7.5, 75, 150, 300 ng) or saclofen (0, 0.5, 1.5, 3, 5 mug) into the other site wit
5 ABA(A) (bicuculline, 75-150 ng) and GABA(B) (saclofen, 1.5-3 microg) antagonists administered into th
6 , whereas GABAB receptor antagonists [10 mum saclofen; 10-50 mum CGP55845 (p-3-aminopropyl-p-diethoxy
7 a combination of picrotoxin (50 microM) and saclofen (100 microM), and thus appeared to be mediated
10 GABAB agonist baclofen decreased, while 2-OH-saclofen (a GABAB antagonist) increased DA release in th
11 induced feeding in that both bicuculline and saclofen administered into the nucleus accumbens shell,
12 aptoacetate-induced intake was eliminated by saclofen and significantly reduced by bicuculline in the
22 cted to the rostral lateral hypothalamus and saclofen (GABA-B receptor antagonist), biccuculine (GABA
27 treatment with either the GABA-B antagonist, saclofen, or the GABA-A antagonist, bicuculline, into th
28 duced by bicuculline and naltrexone, but not saclofen pretreatment, baclofen-induced feeding elicited
29 vated by microinjections of baclofen or 2-OH-saclofen, systemic injections of muscimol caused an inhi
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