1. ¹Department of Psychiatry, University of Pittsburgh, Pittsburgh, PA, USA
2. ²Department of Psychology, University of Pittsburgh, Pittsburgh, PA, USA
3. ³Department of Human Genetics, University of Pittsburgh, Pittsburgh, PA, USA

Correspondence: Dr AR Hariri, PhD, Department of Psychiatry, University of Pittsburgh School of Medicine, Pittsburgh, PA 15213, USA. E-mail: haririar@upmc.edu

Received 24 February 2005; Revised 5 May 2005; Accepted 13 June 2005; Published online 26 July 2005.

Abstract

Recent studies have indicated that a newly identified second isoform of the tryptophan hydroxylase gene (TPH2) is preferentially involved in the rate-limiting synthesis of neuronal serotonin. Genetic variation in the human TPH2 gene (hTPH2) has been associated with altered in vitro enzyme activity as well as increased risk for mood disorders. Here, we provide the first in vivo evidence that a relatively frequent regulatory variant (G(-844)T) of hTPH2 biases the reactivity of the amygdala, a neural structure critical in the generation and regulation of emotional behaviors.