The aim of the presented paper is the description of disturbances in the central nervous system (OUN) functions of fa/fa Zucker rats, in which the development of morbid obesity is observed as a result of a defect in leptin functioning. Zucker fa/fa rats possess a defect in a gene, which codes leptin receptor. A single exchange of adenine to cytosine in the 806th position of extracellular domain of the receptor results in coding proline instead of glutamine (Gln269Pro).