Drugs or toxins that alter the transport properties of these communication channels can profoundly alter cell function. The key property of membrane receptor function, irrespective of which signaling mechanism is used, lies in the ability of the ligand to act as an allosteric regulator of the receptor's activity. In other words, the ligand, the molecule that binds to the receptor in the membrane surface, changes the configuration of that receptor and initiates the transmembrane signaling. A wide variety of ligands bind to membrane receptors that are coupled to intracellular effector enzymes by guanosine- triphosphate proteins. The guanosine-triphosphate proteins are in turn important participants in polypeptide protein synthesis in the interior of the cell.
Some membrane receptors are ligand-gated ion channels.
Since the workings of ion channels are the key processes in the behavior of electrical behavior of nerve cells and muscle cells, particularly cardiac muscle cells, these membrane receptors are of great physiological and clinical importance. Other membrane receptors are membrane associated allosteric enzymes, membrane-bound catalysts for specific biochemical reactions which in turn are important elements in cascades of biochemical events. Given the crucial importance of the cell membrane in mediating not only intrinsic cell processes, but also the interactions of biological cells with pathogens and pharmacological agents, one can understand the fervor with which biochemists and biologists and medical scientists currently strive to understand the details of the operation of the cell membrane. With transmembrane signaling, the biological cell membrane is now recognized as a full participant in all important cellular processes, a structure not only mediating, but in many cases controlling the interaction of the cell with its environment. We are a long way from the primitive permeability experiments of the turn of the century, and the simple physico- chemical investigations of the 1930s and 1940s.