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1 given 20 min prior to the administration of harmaline).
2 port was abolished in the presence of 0.2 mM harmaline.
12 ly reported that the tremorogenic actions of harmaline could be blocked by the noncompetitive NMDA ch
14 s series exhibits potent in vivo activity in harmaline-induced cGMP formation in rat cerebellum, a fu
15 ro evidence that the competitive blockade of harmaline-induced tremor by MK-801 occurs within the cal
21 values are consistent with the high doses of harmaline required to produce tremor, e.g., 10-30 mg/kg.
22 site of action, these data demonstrate that harmaline's ability to activate the interior olivary nuc
23 This study examined whether the blockade of harmaline's action, in the rabbit, by MK-801 was due to
27 t [3H]MK-801 bound to a single site and that harmaline's displacement of [3H]MK-801 binding to the NM
28 e report that harmine, tetrahydroharmine and harmaline, the three main alkaloids present in B. caapi,
29 een demonstrated to depend on the ability of harmaline to activate the inferior olive which gives ris
31 vagus nerve stimulation (VNS) would suppress harmaline tremor, as measured with digitized motion powe
32 gnificantly different from 1 indicating that harmaline was producing a displacement of [3H]MK-801 fro
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