L-DOPA (DOPA) is generally believed to be an inert amino acid, and to relieve the symptoms of Parkinson's disease by converting to dopamine. However, we propose that DOPA is a neurotransmitter. Recently, the gene product of ocular albinism 1 (OA1) was reported to possess the binding activity against DOPA. By knockdown of OA1 using shRNA, we demonstrated that OA1 mediates depressor and bradycardiac response to DOPA in the nucleus tractus solitarii (NTS) of anesthetized rats. However, the roles of DOPA-OA1 signaling in the central nervous system remain to be elucidated. Here, we investigated the expression profile of OA1 by immunohistochemical examination with specific anti-OA1 antibody in the rat brain. We found that OA1 was expressed in the olfactory bulb, cortex, striatum, hippocampus, hypothalamus, Nigra and NTS. All the OA1 immunoreactive signals were inhibited by synthetic OA1 peptide immunogen against the OA1 antibody. We also generated oa1-deficient mice. We confirmed that the OA1 immunoreactive signals in the same regions as those in the rat brain were abolished in oa1-deficient mice. Furthermore, we found DOPA-induced depressor and bradycardiac response in the NTS of wild-type mice were not seen in oa1-deficient mice. These findings demonstrated an unique distribution pattern of OA1 expression, and suggested that DOPA-OA1 signaling may have some functions in the central nervous systems.