Abstract
The classical biomedical research approach begins with modeling the etiology of a disease, such as a genomic mutation, in an animal model to elucidate the pathology, develop new diagnostic methods, and explore new therapeutic strategies. However, genomic studies of psychiatric disorders such as schizophrenia have revealed that they cannot be explained by a few genomic mutations, making it difficult to take this approach. Although clinical studies have identified a variety of environmental factors, the translation of those environmental factors into animal models is not straightforward. On the other hand, monoamines are targets of drug therapy and their importance and involvement in psychiatric disorders are clear. Yet, how the various monoamines act on the various receptors to regulate brain function are not well understood. In order to advance animal model research under these circumstances, I suggest an approach for psychiatric disorders in animal models by clarifying the monoaminergic functions on neural circuits and molecular synaptic cellular mechanisms, modeling symptoms of psychiatric disorders based on monoamine functions, and mapping such neural bases to etiological candidates.
