Author(s): Onodera K
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Abstract Male Wistar rats maintained on a thiamine deficient diet showed mouse-killing behavior (muricide). On the 30th day of experimental feeding, the incidence of the muricide was 70\%. Intraperitoneal (i.p.) injection of 3-(3,4-dihydroxyphenyl)-l-alanine (l-dopa) suppressed the muricide in a dose-dependent manner. This suppressive effect was potentiated with carbidopa, but was quite reduced by pretreatment with alpha-monofluoromethyldopa or FLA-63. These results indicated that the effect of l-dopa was dependent on its decarboxylation, and its conversion to noradrenaline (NA) essential for muricidal suppression in the brain. The NA precursors, l-dopa, l-threo-dops or maprotiline and Y-8894, which can increase the availability of synaptic catecholamines (CA), also showed muricidal suppression. CA depletors (alpha-methyl-p-tyrosine, FLA-63 and alpha-monofluoromethyl-p-tyrosine) did not significantly increase the incidence of muricide induced by thiamine deficiency nor decrease the number of killer-rats. These findings suggest that brain CA may not participate in the mediation of muricide induced by thiamine deficiency in this experiment, but such muricide can be pharmacologically characterized by the effects which are brought about by catecholaminergic agents.
This article was published in Arch Int Pharmacodyn Ther
and referenced in Journal of Alzheimers Disease & Parkinsonism