Voltage-dependent Ca( 2+ ) channels not only mediate the entry of Ca( 2+ ) ions into excitable cells but are also involved in a variety of Ca( 2+ )-dependent processes, including muscle contraction, hormone or neurotransmitter release, and gene expression. The alpha-1A isoform is abundantly expressed in neuronal tissue and corresponds to the P/Q Ca( 2+ ) channel type. The P/Q Ca( 2+ ) channel is responsible for presynaptic neurotransmitter release. Abnormalities in this channel could lead to abnormal neurotransmitter release. The affected CACNA1A gene encodes the pore-forming α 1A subunit of the P/Q-type channel (Ca V 2.1), a predominant mediator of voltage-gated Ca 2+ entry and transmitter release at many synapses in the central nervous system. Alterations in synaptic signaling are of likely importance for cross-talk between an ascending pain transmission pathway and inhibition by a powerful descending modulatory system, interactions that ultimately govern the generation of headache pain.Migraine, Childhood Syndromes