HA increases seizure threshold through an action on the brain H1 receptor, and high doses ofH1 antagonists have the opposite effect (Yokoyama etal. 1994,1996). H3 antagonists have an anticonvulsant effect, possibly due to the increased release of neuronal HA (Murakami et al. 1995; Kakinoki et al. 1998). Metoprine, the inhibitor of brain HA metabolism, has a similar effect (Kakinoki et al. 1998). High doses of H2 antagonists (which do not readily penetrate the brain) cause seizures, and some data suggest that the effects are due to H2 receptor actions (Shimokawa et al. 1996). This is not likely to be the case, however, since large doses of the brain-penetrating H2 antagonist zolantidine do not induce seizures (Hough unpublished).
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