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1  given 20 min prior to the administration of harmaline).
2 in mice that were given the tremorgenic drug harmaline.
3 port was abolished in the presence of 0.2 mM harmaline.
4                                              Harmaline (10 mg/kg, s.c.) produced intense tremors and
5 mpletely blocked the tremorogenic effects of harmaline (10 mg/kg, s.c.).
6                                              Harmaline, a beta-carboline derivative thought to induce
7                                              Harmaline, a beta-carboline derivative, is known to prod
8                                              Harmaline, a closely related alkaloid that excites infer
9       However, the receptor(s) through which harmaline acts remains unknown.
10 group displayed slowing of lick rhythm after harmaline challenge.
11                                              Harmaline completely displaced saturable [3H]MK-801 bind
12 chrony was increased after administration of harmaline, consistent with an olivary origin.
13 ly reported that the tremorogenic actions of harmaline could be blocked by the noncompetitive NMDA ch
14         We have proposed that ibogaine, like harmaline, excites neurons in the inferior olive, leadin
15 s series exhibits potent in vivo activity in harmaline-induced cGMP formation in rat cerebellum, a fu
16 rsed the tremor phenotype in the traditional harmaline-induced essential tremor model.
17 ro evidence that the competitive blockade of harmaline-induced tremor by MK-801 occurs within the cal
18  olivo-cerebellar burst-firing occurs during harmaline-induced tremor.
19 n-mediated synchrony does not play a role in harmaline-induced tremor.
20                                              Harmaline-induced tremors were robust and indistinguisha
21                                              Harmaline is known to produce tremors and retard acquisi
22                       Our hypothesis is that harmaline produces tremor by acting as an inverse agonis
23 values are consistent with the high doses of harmaline required to produce tremor, e.g., 10-30 mg/kg.
24  site of action, these data demonstrate that harmaline's ability to activate the interior olivary nuc
25  This study examined whether the blockade of harmaline's action, in the rabbit, by MK-801 was due to
26        It was suggested that the blockade of harmaline's actions by dizocilpine may be occurring at N
27 er, the precise receptor systems involved in harmaline's actions remains unknown.
28 dy examined the role of the NMDA receptor in harmaline's actions.
29 t [3H]MK-801 bound to a single site and that harmaline's displacement of [3H]MK-801 binding to the NM
30 e report that harmine, tetrahydroharmine and harmaline, the three main alkaloids present in B. caapi,
31 een demonstrated to depend on the ability of harmaline to activate the inferior olive which gives ris
32 paired the coherence of muscle firing during harmaline tremor without affecting its rhythm.
33 vagus nerve stimulation (VNS) would suppress harmaline tremor, as measured with digitized motion powe
34 gnificantly different from 1 indicating that harmaline was producing a displacement of [3H]MK-801 fro
35                     Both of these effects of harmaline were significantly blocked by the prior admini