Channels involved in the influx and intracellular mobilization of calc
ium have been implicated as targets of diverse genetic and immune-medi
ated neurological diseases. These include the L-type voltage-gated cal
cium channel of skeletal muscle (hypokalemic periodic paralysis), the
neuronal P/Q-type voltage-gated calcium channel (familial hemiplegic m
igraine, episodic ataxia type 2, spinocerebellar ataxia 6, and Lambert
-Eaton myasthenic syndrome), and the skeletal muscle ryanodine recepto
r (malignant hyperthermia and central core disease). The discovery of
these and other calcium channelopathies should help to clarify how dif
ferent mutations affect channel function and how altered channel funct
ion produces disease, and may lead to new treatments for these conditi
ons.