Psychosocial stress has been shown to contribute to depressive and anxious symptoms in patients with affective illness (Caspi et al, 2003; Hammen, 2005; Hammen et al, 2004; Melchior et al, 2007). Environmental and psychological stressors can recapitulate biochemical, structural, and behavioral aspects of depressive illness in laboratory animals (see Pittenger and Duman, 2008 for review). Recent studies have pointed to the endocannabinoid (eCB) system as an important modulator of stress responses and emotional regulation (Hill and Gorzalka, 2005; Moreira and Lutz, 2008; Patel and Hillard, 2008; Viveros et al, 2005). In addition, the type-1 cannabinoid receptor (CB1) gene variants modulate the vulnerability to develop depressive symptoms following stressful life events (Juhasz et al, 2009). Taken together, these data suggest an interaction between stress, eCB signaling, and mental illness. Understanding the neuroadaptations that occur in the eCB system in response to chronic stress could shed light on the neural mechanisms subserving stress-induced exacerbation of affective disorders in humans.
