Steroidal/neuropeptide interactions in hypothalamus and amygdala related to social anxiety.

Oestrogens (E) influence the activity of oxytocin (OT) producing neurons and heighten the rate of transcription of the oxytocin receptor (OTR) gene. Working through synergistic activities of two different oestrogen receptors (ERs), likely gene duplication products, in the hypothalamus and amygdala, E supports social recognition by mice. As part of social recognition and approach, it is important for mice to assess the risks of social interactions, thus to reduce the social anxiety. Here we argue that hyperactivity in ascending central nervous system arousal systems would work in the opposite direction: increasing social anxiety by potentiating fear-related mechanisms in the amygdala. In humans, such increased social anxiety might account for some features of autism.