Histamine stimulates brain phospholipid turnover through a direct, H-1 receptor-mediated mechanism

Intracisternal administration of histamine produced a dose-dependent increase of incorporation of 33Pi into brain phospholipids. The effect could not be mimicked by administration of compound 48/80, indicating lack of involvement of non-neuronal histamine. The stimulation was not attenuated by prior depletion of catecholamines with reserpine, indicating that the effect of histamine on phospholipid turnover was mediated by direct histaminergic mechanisms. An H-1 receptor appeared to be involved, as demonstrated by studies with specific histaminergic agonists and antagonists. Incorporation of 33Pi into phospholipids may be a valuable tool in evaluating cellular effects mediated through H-1 receptors.