ELEVATION OF INTRACELLULAR CALCIUM LEVELS IN NEURONS BY NICOTINIC ACETYLCHOLINE-RECEPTORS

The recognition that intracellular free calcium serves as a ubiquitous intracellular signal has motivated efforts to elucidate mechanisms by which cells regulate calcium influx. One route of entry that may offe r both spatial and temporal fine resolution for altering calcium level s is that provided by cation-permeable, ligand-gated ion channels. Bio physical measurements as well as calcium imaging techniques demonstrat e that neuronal nicotinic acetylcholine receptors as a class have a hi gh relative permeability to calcium; some subtypes equal or exceed all other known receptors in this respect. Activation of nicotinic recept ors on neurons can produce substantial increases in intracellular calc ium levels by direct passage of calcium through the receptor channel. When multiple classes of nicotinic receptors are expressed by the same neuron, each appears capable of increasing calcium in the cell but ma y differ with respect to location, temporal response, agonist sensitiv ity, or regulation in achieving it. As a result, nicotinic receptors m ust be considered strong candidates for signaling molecules through wh ich neurons regulate a diverse array of cellular events.