Conclusions

It is clear that transgenic mice modeling different aspects of 5-HT2CR function have provided important and otherwise unobtainable knowledge of how serotonergic neurotransmission affects cellular function and whole organism behavior. In fact, there is still much future work to be accomplished. For example, the generation of currently unavailable mouse models with tailored 5-HT2CR function (e.g., overexpression, lesions, or specific edited receptor isoforms) restricted to important CNS regions, including but not limited to the striatum, nucleus accumbens, bed nucleus of stria terminalis, and amygdala, will further clarify how 5-HT2CRs regulate the behavioral response to environmental stressors and appetitive/aversive stimuli. Temporal control of 5-HT2CR function would similarly allow investigators to determine if later-life loss of 5-HT2CR function is ameliorated in the presence of intact function in neonate and young mice, and conversely, if reestablishment of 5-HT2CR function in later adulthood can avert the development of middle-aged obesity and type II diabetes in animals born with genetic lesions of 5-HT2CR expression. It is also intriguing to note that many of the therapeutic agents currently used to treat highly morbid psychiatric diseases (including schizophrenia, bipolar disorder, major depression, anxiety disorders, and substance abuse disorders) in part function through their actions on 5-HT2CRs. Thus, further elucidation of how 5-HT2CRs specifically affect the function of individual neuronal ensembles, and how these effects change the overall regulation of organism behavior, may provide important therapeutic insights to treat these major psychiatric illnesses.

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