ABSTRACT
This chapter focuses on aging-dependent changes in transmembrane signaling mechanisms and functional aspects around the metabotropic and the ionotropic types in cellular signal transduction. Changes in membrane properties during aging may occur in many physiological and pharmacological situations. In general, changes in membrane composition with aging cause membranes to become more rigid in rat cortex and bladders. Aging has been shown to increase functional neuronal cytoplasmic calcium levels, increase membrane-lipid peroxidation, and reduce brain membrane fluidity — each of which conceivably could alter the coupling between calcium uptake and transmitter release. Critical issues for studies of brain aging concern questions of how and what cellular changes may lead to desensitization of calcium homeostasis within the cytosol and/or disruption of calcium-mediated signal transduction processes. The "Ca2+ hypothesis of aging" proposed that cellular mechanisms which regulate the homeostasis of cytosolic free Ca2+ ion play a critical role in aging.
