Electrophysiological experiments were carried out to evaluate the mechanism of the central depressive effect of magnolol and honokiol. Magnolol (30 mg/kg) caused a decrease in spontaneous arousal pattern in the hippocampus and induced periodic spindle bursts in the sensory and motor cortices (Watanabe et al., 1983a). Comparatively higher concentrations of magnolol (10-5 and 10-4 M) selectively inhibited the size of spontaneous ventral root potential without eliciting a marked change in the dorsal root potential, and also inhibited the ventral root potential induced by glutamate and aspartate (Kudo and Watanabe, 1984). However, the GABA-induced potential could not be inhibited by magnolol. These findings indicate that the muscle relaxing effect of high doses of magnolol is produced via inhibition of the stimulatory neurotransmission and increase in the threshold of firing of motor neurons.
Neurochemical evaluation revealed that honokiol (1-10 |iM), but not magnolol (1-10 |iM), elicited a concentration-dependent enhancement of 25 mM K+-evoked acetylcholine (ACh) release from rat hippocampus slices (Tsai et al., 1995b). Addition of tetrodotoxin (1 |iM), pilocarpine (1 |iM) or methoctamine (1 |iM) had no effect on the enhanced ACh release by honokiol. These results indicate that part of the central depressive effect of honokiol is produced through an enhancement of K+-evoked ACh release directly on hippocampal cholinergic terminals via receptors other than M2 cholinergic subtypes. Taken together, the results from the behavioral, electrophysiological and neurochemical evaluations strongly suggest that magnolol and honokiol show an inhibitory effect on several areas of the brain such as the hypothalamic and reticular formation ascending activating systems as well as the spinal cord.
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