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1 milar before and after the injections of the 5-HT(3) receptor agonists.
3 ione (DNQX) on the excitatory actions of the 5-HT3 receptor agonist 1-phenylbiguanide (PBG) were stud
4 This initial response was mimicked by the 5-HT3 receptor agonist, 2-methyl-5-HT, whereas 5-methoxy
6 data are consistent with the hypothesis that 5-HT3 receptor agonists activate DVMN neurones partly by
12 T(3B) with 5-HT(3A) modified the duration of 5-HT(3) receptor agonist-induced responses, linearized t
13 urrent by low concentrations of bath-applied 5-HT3 receptor agonists is compatible with the cyclic mo
14 Likewise, posterior IC administration of the 5-HT(3) receptor agonist m-chlorophenylbiguanide (mCPBG)
15 sed with the 5-HT1A receptor agonist and the 5-HT3 receptor agonist, m-chlorophenyl-biguanide (mCPBG;
17 These findings suggest that tachyphylaxis to 5-HT(3) receptor agonists may be due to the desensitizat
19 pressure and cardiac output elicited by the 5-HT(3)-receptor agonists, phenylbiguanide (100 microg/k
20 retic application of PBG, a highly selective 5-HT3 receptor agonist, significantly increased activity
22 ptor by intrathecal injection of a selective 5-HT(3) receptor agonist, SR57227, induced spinal glial
24 that phenyldiguanide (later recognized as a 5-HT3 receptor agonist) stimulated the firing of C-fibre
25 icrog kg(-1)) and PBG (100 microg kg(-1)), a 5-HT(3) receptor agonist, stimulated nine ischaemically
26 2-methylserotonin (100 microg kg-1, i.a.), a 5-HT3 receptor agonist, stimulated eleven of twelve affe
28 by white matter stimulation were reduced by 5-HT3 receptor agonists, whereas the frequency of sponta
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