1. ¹Department of Psychiatry, Yale University School of Medicine and Connecticut Mental Health Center, New Haven, CT, USA
2. ²Department of Psychology, University of Vermont, John Dewey Hall, Burlington, VT, USA
3. ³Department of Psychology, Northern Illinois University, DeKalb, IL, USA

Correspondence: Dr SA Josselyn, Current address: Integrative Biology and Brain and Behaviour Program, Hospital for Sick Children, 555 University Ave, Department of Physiology, University of Toronto, Toronto, ON, M5G 1X8, Canada. Tel: +416 813 7664 ext 1824; Fax: +416 813 6846; E-mail: sheena.josselyn@sickkids.ca

⁴Current address: Department of Psychology, University of Minnesota, Elliott Hall, 75 East River Rd, Minneapolis, MN 55455, USA.

⁵Current address: Department of Psychiatry, Emory University School of Medicine, 1639 Pierce Dr., Suite 4311, Atlanta, GA 30322, USA.

Received 3 May 2004; Revised 14 June 2004; Accepted 17 June 2004; Published online 14 July 2004.

Abstract

Although considerable progress has been made towards understanding the neural systems mediating conditioned fear, little is known about the neural mechanisms underlying conditioned inhibitors of fear (or safety signals). The present series of experiments examined the involvement of the nucleus accumbens (NAC) in mediating the effects of safety signals on behavior using a conditioned inhibition of fear-potentiated startle paradigm. Neither increasing dopaminergic nor decreasing glutamatergic function in the NAC altered the magnitude of conditioned fear or conditioned inhibition of fear in rats. Furthermore, large pre- or post-training electrolytic lesions of the NAC did not affect acquisition or expression of fear-potentiated startle or conditioned inhibition of fear-potentiated startle. Taken together, these data suggest that the NAC is not critically involved in the acquisition or expression of fear-potentiated startle or conditioned inhibition of fear-potentiated startle. Previous research has implicated the NAC in 'reward-attenuated startle' in which presentation of a stimulus paired with food decreased startle responding. The present results, therefore, indicate important neural dissociations between the processing of appetitive and safety signals, even though behavioral studies and learning theories have suggested that these two forms of learning share some commonalities.