Calcium entry blocker (CEB) use has been proposed in a variety of neurological dysfunctions. Some of the new clinical applications suggest a direct non-vascular action on neuronal activity. This view is supported by the observation that in brain CEBs bind preferentially to neuronal terminals and not to vascular elements. The data reported indicate that CEBs modify both in vitro and in vivo neurotransmitter release using brain slices and that their binding sites display some degree of plasticity in various experimental conditions altering neuronal transmission.
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