Seminar

Calmodulin, epilepsy and mental retardation

Alvaro villarroel, PhD

Neuronal excitability is the landmark for the functioning of the brain. Under normal circumstances, neuronal activity is orchestrated and the flow of information is adequate for proper function. However, sometimes some areas of the brain lose control, and may lead to pathological situations such as epilepsy, or even derive in more severe situations as ischemia. There are many mechanisms to prevent pathological overexcitability. Among them, Kv7 channels, the product of KCNQ genes, play a critical role. Mutations in these genes lead to epileptogenic encephalopathyes, whereas increasing the activity of these channels prevents epilepsy. A key component in regulation of Kv7 activity is the ubiquitous calcium binding protein. I will describe the mechanisms by which this protein affect the density of Kv7 channels in the membrane, and how increasing the density of these channels can protect the brain from irreversible damage in animal models of overexcitability.