Efficient neuronal communication is key in several mental processes like motor performance, computation, learning and memory. To keep neurons in communication, connection requires the fusion of small vesicles which contains the neurotransmitter signal. This simple process is extremely fast and complex in nature. At release sites, a series of proteins re-arrangement progressively brings the synaptic vesicles to terminal plasma membrane and keeps they ready for an imminent fusion. Hence, when the electrical impulse arrives to the nerve-endings, its induces a concerted Ca2+ influx in the communicating nerve-terminals, triggering along the connections a synchronized vesicle fusion. After decades searching the neuronal Ca2+sensor, which drives the concerted vesicle fusion along neurons, a family of Ca2+ sensors called Synaptotagmin were identified. Recently, faculty and ex-faculty of the Neuroscience Department from UCC in collaboration with investigators from Texas Tech University and MIT as the leading group, have identified several mutations which alter the normal functioning of the faster neuronal Ca2+-sensor, Synaptotagmin-1. Since, several Synaptotagmin dysfunctions have been observed in inherited neuronal conditions like myasthenia and epilepsy, this research will help in understanding neuronal communication and the synaptic pathophysiology observed in patients.