Fever, molecular excitability and epilepsy.

The transmission of the electrical impulse across neuronal membranes relies on innumerable excitable molecules that visit an array of conformations. It is not surprising, then, that the best recognized manifestation of cerebral hyperexcitability, a seizure, should exhibit some temperature dependence. From an enzyme catalysis perspective, a brief temperature i e w i b e l r N a c o 7 e b p r c g i h e t d s a protagonism of non-ion channel – and even of extraneuronal – molecules in genetic epilepsy. In both old and new epileptic phenotypes, inexcitable-protein genes such as the G-proteincoupled receptor fragment VLGR1 gene MASS1 [6], the soluble protein gene LGI1 [1], and, now, the casein kinase 2 gene CSNK1G2 [3], are receiving close attention, while three