Neuronal and Glial Signaling

The major function of the nervous system is to rapidly transfer and integrate information with a view to organizing the diverse functions of multicellular organisms. Our present understanding as to how nerve cells communicate originates with studies in the nineteenth century on the anatomy of the nervous system. Work conducted by Camillo Golgi and Santiago Ramon y Cajal defined the fine structure of neurons for the first time. Golgi favored the idea that all the nerves in the nervous system existed as a sort of reticular net, rather than as separate entities. Cajal, in contrast, concluded that neurons were independent entities and that a minute gap existed between the ends of nerve fibers and other nerve cells or the muscles that they innervate. This gap was ultimately named a “synapse” by the great neurologist Sir Charles Sherrington in 1897, from the Greek meaning “to clasp”. Cajal also argued that neurotransmission was basically a unidirectional process, information being received by dendrites and being transmitted unidirectionally along axons. The actual existence of the synapse as a structure was not confirmed until the development of the electron microscope in the 1950s. Around this time a fierce debate took place between two opposing sets of scientists (Valenstein, 2005). One set, primarily electrophysiologists, held the view that information was transmitted between nerves and between nerves and muscles by purely electrical processes. The other group, primarily pharmacologists, suggested that chemical messenger molecules were released by the presynaptic nerve and carried the information across the synapse. The nature of the chemicals that constitute neurotransmitters was gradually revealed by the work of several important investigators who characterized the effects of different substances that mimicked or blocked the actions of neurotransmitters on fast skeletal muscles and in the autonomic nervous system. This finally culminated in the demonstration by Otto Loewi in 1921 that the vagus nerve secreted a chemical (“Vagusstoff”) that mediated the slowing effect of vagal stimulation on the heart. This substance turned out to be acetylcholine.