Regulation of Voltage-Sensitive Calcium Channels in Brain by Micromolar Affinity Benzodiazepine Receptors

Abstract

Ca²⁺ is an important mediator of molecular events in the functioning nerve terminal (1, 2). An increase in cytoplasmic Ca²⁺ has been shown to regulate a variety of neuronal cell functions, including neurotransmitter release, stimulation of protein phosphorylation, and synaptic morphological changes (3). It is well-established that these events are directly dependent on the entry of extracellular Ca²⁺ into the presynaptic nerve terminal through specific voltage-gated Ca²⁺ channels (4,6). The central role of Ca²⁺ channels in stimulus-secretion coupling mechanisms has led to the extensive investigation of Ca²⁺ channel function in a wide variety of intact and broken cell preparations (7). Despite extensive electrophysiological characterization of Ca²⁺ channels in brain, the molecular nature and pharmacological characteristics of this major neuronal Ca²⁺ channel remain largely unclear.