EXPRESSION OF FOXP2 IN OTP AND NON-OTP NEURONS OF THE MEDIAL EXTENDED AMYGDALA

The medial extended amygdala (EAme) contains multiple neuron subtypes involved in either promotion or inhibition of social behaviors. In particular, glutamatergic neurons of the posterior medial amygdala inhibit social behavior and promote anxiety, resembling autism. These look like those expressing the transcription factor Otp, which originate near the telencephalon-hypothalamic frontier. We hypothesized that these neurons might express risk genes of autism and/or other social communication deficits during critical moments of their development. One of such genes is FoxP2, which encodes a transcription factor critical in language or vocalization learning and in social interactions. However, its expression in EAme is poorly understood. A previous study in songbirds suggested that FOXP2 is expressed in subsets of GABAergic and glutamatergic neurons of EAme with different embryonic origins. However, in the mouse medial amygdala, FOXP2 was found in a subset of GABAergic neurons, distinct from the Otp glutamatergic neurons. Since this study only analyzed the posterior medial amygdala, we aimed to analyze FOXP2 expression in Otp neurons of all EAme subdivisions. We processed brain sections from Otp-eGFP mice for double immunofluorescence for GFP and FOXP2. We found that nearly all Otp neurons of the anterior medial amygdala expressed FOXP2, but those in the posterior part did not. We also observed FOXP2 expression in a subset of Otp neurons of the medial bed nucleus of the stria terminalis. These results open the venue to investigate the contribution of these Otp and non-Otp neurons to the social impairments observed following FoxP2 disruption.
Funding: AEI/MICIU PID2023-151927OB-I00, PREP2023-002019