Is catecholaminergic polymorphic ventricular tachycardia caused by mutation-linked defective conformational regulation of the ryanodine receptor?
A single point mutation within the RyR2 sensitizes the channel to agonists and reduces the threshold of luminal [Ca(2+)] for activation, primarily mediated by defective interdomain interaction within the RyR2.
These results provide further evidence of a role for serotonergic transmission in the modulation of cortical excitability. Differential effects on the measures under study suggest a pattern of prioritization in bioamine regulation of cortical inhibition.