Phospholipids and Membrane Phenomena Involved in the Release of Mediators of Anaphylaxis

Abstract

The anaphylactic model is of particular interest in the study of inflammatory processes, but it can also inform us of some biological mechanisms in the central or peripheral nervous system. Histamine is now considered as a neuromediator (Schwartz et al., 1979a): histaminergic pathways have been studied in rat brain (Garbarg et al., 1980) and histamine H₁ and H₂ receptors have been described in the brain (Schwartz et al., 1979b). Non neuronal histamine-storing cells having properties strongly resembling those of typical mast cells have also been identified by biochemical and pharmacological approaches (Kruger, 1974). The functional role of mast cells in the central nervous system as in peripheral tissues is far from clear. In peripheral tissues it is generally assumed that they are involved in vascular control under particular pathophysiological conditions, i. e. during immune and inflammatory processes. It can be hypothezised that cerebral mast cells are involved in similar processes. Anaphylactic phenomena involved in tissues are closely interwoven with peripheral nervous system endings disturbances (Boushey et al., 1980). Interactions between inflammatory mediators and neuromediators have already been described (Besedovski et al., 1983). The immune system is now thought to be a sensory organ (Blalock, 1984). It seems probable that the sensory function of the immune system may mimic the neuroendocrine system in terms of a given stimulus eliciting a particular set of hormones and thus a physiological response. Molecular targets of neuromediators have been particularly studied in brain tissue; but these studies benefited from other studies on immune cells or adrenal medulla for example.