Subsequent tests revealed that amygdala-lesioned animals only expressed juice preferences if they differed in ‘sweetness’. Unlike controls, orbitofrontal cortex-lesioned and medial prefrontal cortex-lesioned animals, they were unable to display preferences between juices matched for ‘sweetness’ i.e. 5% sucrose solutions BYL719 aromatised with different essential oils. The most parsimonious explanation is that
the amygdala contributes to the expression of food preferences based on learnt cues but not those based on an innate preference for sweetness. “
“Brain histamine is involved in the regulation of the sleep–wake cycle and alertness. Despite the widespread use of the mouse as an experimental model, the periodic properties of major markers of the mouse histaminergic system have not been comprehensively characterized. We analysed the daily levels of histamine and its first metabolite, 1-methylhistamine, in different brain structures of C57BL/6J and CBA/J mouse strains, and the mRNA level and activity of histidine decarboxylase and histamine-N-methyltransferase PD0325901 molecular weight in C57BL/6J mice. In the C57BL/6J strain, histamine
release, assessed by in vivo microdialysis, underwent prominent periodic changes. The main period was 24 h peaking during the activity period. Additional 8 h periods were also observed. The release was highly positively
correlated with active wakefulness, as shown by electroencephalography. In both mouse strains, tissue histamine levels remained steady for 24 h in all structures except for the hypothalamus of CBA/J mice, where 24-h periodicity was observed. Brain tissue 1-methylhistamine levels in both strains reached their maxima in the periods of activity. The mRNA level of histidine decarboxylase in the tuberomamillary nucleus and the activities of histidine decarboxylase and histamine-N-methyltransferase in the striatum SSR128129E and cortex did not show a 24-h rhythm, whereas in the hypothalamus the activities of both enzymes had a 12-h periodicity. These results show that the activities of histamine-metabolizing enzymes are not under simple direct circadian regulation. The complex and non-uniform temporal patterns of the histaminergic system of the mouse brain suggest that histamine is strongly involved in the maintenance of active wakefulness. The histaminergic system is involved in the regulation of sleep, feeding behaviour, and hibernation (Haas & Panula, 2003). Gene knockout of the key histamine-synthesizing enzyme, histidine decarboxylase (HDC), leads to alterations in the circadian rhythm of motor activity and the expression of key genes involved in the mechanism of the biological clock, i.e. Period1 and Period2, in several brain areas in mice (Abe et al., 2004).