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1 comitant decrease or increase in response to dopaminergic agonists.
2   The experiment examined the influence of a dopaminergic agonist (amphetamine) and an antagonist (ha
3 ce, which can be ameliorated by the indirect dopaminergic agonist, amphetamine, has been demonstrated
4 onjunction with pharmacological fMRI using a dopaminergic agonist and an antagonist.
5 nd this organization is influenced by both a dopaminergic agonist and an antagonist.
6 ivity whilst iontophoretically administering dopaminergic agonists and antagonists while rhesus macaq
7  psychiatric disorders commonly treated with dopaminergic agonists and antagonists.
8 tor activity in the presence or absence of a dopaminergic agonist (apomorphine) or an atypical antips
9 r phosphoinositide hydrolysis in response to dopaminergic agonist, apparently by coupling to a Gq-lik
10 controlled pharmacological fMRI study with a dopaminergic agonist (bromocriptine) and antagonist (sul
11 absent or blunted responses to stimulant and dopaminergic agonist drugs, in conjunction with near-com
12                                      Despite dopaminergic agonist efficacy in DoC patients equally po
13 rs contribute to the beneficial influence of dopaminergic agonists for the protection and restoration
14 etic pulses of glutamate, GABA, dopamine and dopaminergic agonists locally, onto layer 5 pyramidal ne
15                           Application of the dopaminergic agonist quinpirole to cotransfected cells i
16  present study challenge the prediction that dopaminergic agonists reduce STN activity predominantly
17            Treatment of GH4-121 cells with a dopaminergic agonist resulted in activation of PLD in bo
18 uence contributes to the effects of indirect dopaminergic agonists such as D-amphetamine on striatal
19             Three distinct classes of drugs: dopaminergic agonists (such as D-amphetamine), serotoner
20                                              Dopaminergic agonists, such as pramipexole, appear to ha
21                    The stimulation of PLD by dopaminergic agonists took place in the absence of any d
22 by measuring striatal c-Fos expression after dopaminergic agonist treatment at postnatal day 4 (P4) t
23 icantly lower in short photoperiod mice, and dopaminergic agonist treatment rescued the photopic ligh
24 TA-PCu/PCC connectivity can be affected by a dopaminergic agonist, we demonstrated in a separate set
25 utant mice were relieved using ropinirole, a dopaminergic agonist widely used for RLS treatment.