1. ¹Department of Psychiatry, Columbia University, New York, NY, USA
2. ²Department of Neuroscience, Columbia University, New York, NY, USA
3. ³Division of Integrative Neuroscience, The New York State Psychiatric Institute, New York, NY, USA

Correspondence: Dr R Hen, Department of Psychiatry and Neuroscience, Columbia University, The New York State Psychiatric Institute, 1051 Riverside Drive, Unit 87, New York, NY, USA. Tel: +1 212 543 5328; Fax: +1 212 543 5410; E-mail: rh95@columbia.edu

Received 27 June 2007; Revised 9 August 2007; Accepted 13 August 2007; Published online 12 September 2007.

Abstract

There is increasing recognition that many psychiatric disorders including anxiety disorders are neurodevelopmental in their origins. Here, we review and integrate data from human studies and from animal models that point to a critical period during which neural circuits that mediate anxiety develop. We then postulate that this highly plastic critical period is a time of heightened responsiveness that is particularly susceptible to adverse events. We discuss these concepts in the context the current heightened interest in gene by environment interactions in psychiatric illness emphasizing the importance of the temporal relationship between gene action and environmental milieu.