Noradrenalin is an endogenous local immune-suppressive mediator in the central nervous system of mammals (Feinstein et al., NeurochemInt 2002). b-adrenergic receptor stimulation inhibits expression of pro-inflammatory factors in cultured astrocytes and microglia, immune-competent cells in the nervous system. The noradrenergic ascending projections originate from neurons in the locus coeruleus. These neurons not only synthesize noradrenalin but also express the bioactive peptide, galanin. Accordingly, projections from locus coeruleus neurons in cortex and hippocampus show a co-localization of noradrenalin and galanin (Hökfelt et al., Ann NY AcadSci 1998). Recently, we found that b-adrenergic stimulation with isoproterenol suppresses phagocytosis via a cAMP - Epac-dependent pathway in murine microglial cells (Steininger et al., Brain Res 2011). However, microglial cells express not only a- and b-adrenergic receptors, but also galanin receptors (Ifuku et al.,J Neurochem.2011). In the present study, we were interested in the interaction of noradrenalin and galanin on phagocytosis. Particle uptake was studied using polystyrene microsphere and scanning electron microscopy.

Exposure of microglial cells to noradrenalin suppressed uptake of polystyrene microspheres. The most effective concentration was 1 pM. Galanin enhanced engulfment of microspheres in a biphasic mode. Maximum effect was detected at 1 nM. Galanin concentrations above or below 1 nM were less effective. Simultaneous exposure of cells to noradrenalin (1 pM) as well as galanin (1 nM) revealed a suppression of particle uptake.