Inhibition of surface capping of macromolecules by local anaesthetics and tranquillisers

Abstract

IMMUNOGLOBULIN (Ig) molecules on the surface of B lymphocytes aggregate into a ‘cap’¹ when the cell is treated with anti-Ig^1–3. A similar process occurs with concanavalin A (con A) on neutrophil polymorphonuclear leukocytes (PMN)⁴. Capping occurs in two stages in both of these cell types^4,5: first, the ligand-receptor complexes aggregate into multiple clusters of variable size, leaving intervening bare membrane; and second, the clusters are swept into a single mass. Both stages are temperature-dependent (that is, they do not occur in the cold), but only the latter is energy-dependent (that is, clustering occurs but capping is inhibited on cells treated with metabolic inhibitors)^4–6. The formation of clusters can be attributed to the ability of the ligand to cross-link receptors⁵; some form of membrane activity then sweeps the clusters into the cap. Capping can occur in the absence of cell locomotion^4,7, but if locomotion does occur the cap is found at the trailing end of the cell⁴. These aspects of capping have recently been analysed in detail^4,7.