Oxtr expressed in GABA neurons at the MeA are suspected to control social memory

Shinji Miyazaki,Yuuichi Hiraoka,Shizu Hidema & Katsuhiko Nishimori

Lab. of Mol. Biol., Grad. Sch. of Agric. Sci., Tohoku Univ., Japan

OXT/OXTR system is well known as one of the regulating mechanism for social behavior, and thus OXTR deficient mice are considered as a useful model to study the neural mechanisms which govern social memory. We used this model to reveal regions and neuronal subtypes which control the social memories. In this study, we found that OXTR positive GABAergic neurons in Medial Amygdaloid nuclei (MeA) play an important role for constructing social memories. First, we found social stimulation induced neural activation in MeA. This finding implies that MeA contributes important role in constructing social memory. We next analyzed histologically to clarify neuronal subtypes of OXTR positive neurons in MeA. Interestingly, in situ hybridization analysis reveals that 30% of GABAergic neurons in MeA were expressing OXTR. It was acceptable because previous studies suggest that loss of GABAergic neurons causes dysfunction of social memory as same as OXTR deficient mice. Then we hypothesize these OXTR positive GABAergic neurons are necessary for social memory function. To test this hypothesis, we generated GABAergic neuron specific OXTR deficient mice by crossing loxP flanked OXTR mice and vesicular GABA transporter locus cre recombinase knocked in mice. This conditional knockout mouse showed social memory abnormality in our behavioral analysis. Taken together, these findings propose that OXTR positive GABAergic neurons in MeA play an important role in social memory, and it might be potential mechanism of pathology of mental disorder such as autism.