This chapter focuses on the central function of carnosine and its homologs on behavior in young chicks as a model for humans. In this regard, the organization of the human genome is closer to that of the chicken than it is to that of the mouse. The function of brain carnosine and its homologs was investigated, using young chicks. Both carnosine and anserine were found to inhibit food intake in a dose-dependent fashion when injected intracerebroventricularly. The constituents of carnosine - β-alanine (β-Ala) and l-histidine (l-His) - were also found to inhibit food intake, but their effects were weaker than that of carnosine itself. Coadministration with β-Ala and l-His inhibited food intake in a similar way to carnosine, but also altered other behaviors. Hyperactivity was induced by the injection of carnosine, also leading to an increased plasma corticosterone level, which may be regulated by the generation of nitric oxide via the constitutive nitric oxide synthase. Replacing the carboxyl terminus of l-histidine with branched chain amino acids induced hyperactive behavior similar to that observed with carnosine. On the contrary, however, replacing the amino terminus β-alanine with l-serine or l-isoleucine induced hypoactivity. When the positions of β-alanine and l-histidine of carnosine were reversed, the central function was also reversed to one of hypoactivity. Mental motivation in humans may be modified by carnosine and its homologs.