“…Further, administration of histamine or drugs which enhance histaminergic transmission leads to desynchronization of the EEG and wakefulness (Wolf & Monnier, 1973;Monti et al, 1986;Lin et al, 1988), and histamine may also modulate the activity of medullary neurones (Jones et al, 1983;Bradley et al, 1984). Circadian rhythms in the level of histamine have been found in various regions of the brain (Friedman & Walker, 1968;Orr & Quay, 1975), and the rate of formation of histamine is elevated in rodents during the period of darkness when spontaneous activity is maximal (Schwartz et al, 1976). Nevertheless, it is possible that pharmacological activity other than H1 antagonism may give rise to sedation with antihistamines, and the drugs used in the present study, in particular chlorpheniramine, are not specific H1-receptor antagonists.…”