Thiamine deficiency in the body occurs primarily by hepatic degradation and the central and peripheral nervous system. For this effect to a large extent corresponds to the universal metabolic function of thiamine pyrophosphate, a cofactor of the enzymes involved in the metabolism of carbohydrates and energy metabolism of cells. Data collected in the last years, numerous observations suggest however additional, non cofactor role of thiamine derivatives, thiamine triphosphate particularly selective for the nervous system. Reported three hypotheses that attempt to explain the neurochemical role of thiamine triphosphate at the molecular level. The first two of its postulated effect on ion channels: ligand-gated sodium and voltage-gated chloride. Last hypothesis postulates thiamine triphosphate operation of the mechanism of neurotransmission, as a specific phosphate group donor in the process of the phosphorylation of certain regulatory proteins.