Stable (i.e., trait-like) negative cognitive biases increase vulnerability for affective psychopathology (Alloy et al., 2006
). In addition, stress triggers psychopathological symptomatology in some but not all individuals (Monroe and Harkness, 2005
). However, the mechanisms responsible for inter-individual differences in vulnerability to stressors are not completely understood. One aspect of vulnerability to stress may involve inter-individual differences in the effects of stress on neurocognitive processes (e.g., emotional memory biases in depression; over-consolidation of threat-related material in Posttraumatic Stress Disorder; PTSD).
Elevation in the stress hormone cortisol is a primary mechanism through which stress alters neurocognitive processes (de Kloet et al., 1999
). The direction of effects of glucocorticoids (GCs; i.e., cortisol in primates and corticosterone in rodents) on learning vary depending on the magnitude of GC elevation -- mild-to-moderate elevations in GCs enhance many neurobiological processes associated with memory formation, but extremely elevated cortisol levels often dampen memory formation (Lupien and McEwen, 1997
; Pittenger and Duman, 2008
). In addition, the facilitatory effects of GCs on memory formation depend on emotional arousal at the time of GC elevation (Okuda et al., 2004
; Abercrombie et al., 2006
). Arousal-related noradrenergic activation in the basolateral amygdala is required in order for GCs to affect memory (Roozendaal et al., 2006b
). In summary, extensive work has examined how factors at the time of GC elevations (e.g., current neural milieu and emotional state) moderate GC’s effects on memory. However, it is not known how long-lasting inter-individual differences (or “traits”) moderate effects of stress hormones on emotional memory.
Dispositional “affective style” refers to consistent inter-individual differences in mood, emotional reactivity, and emotion regulation (Davidson, 2000
). Studies examining a constellation of behavioral and physiological measures (Davidson, 2000
) show that affective style can be indexed by biological measures as well as measures of self-reported trait affect. In the current project, we use the Positive Affect and Negative Affect Schedule (PANAS) – Trait Version (Watson et al., 1988
) as an index of inter-individual differences in trait affective arousal.
We used two different paradigms to examine in healthy individuals how trait affective arousal moderates the relation between acute cortisol elevations and memory formation. In Study 1 we included only males, and manipulated endogenous
cortisol levels using a laboratory-based stressor immediately after encoding emotional and neutral stimuli. Data from Study 1 examining the moderating effects of acute increases in negative affect (i.e., “State NA”) on cortisol’s relation with memory facilitation have been previously published (Abercrombie et al., 2006
). Study 2 included males and females, and we manipulated cortisol levels exogenously
using hydrocortisone or placebo administration during memory encoding.
Because research shows that cortisol facilitates memory formation preferentially in individuals in an emotionally aroused state
(mentioned above), we hypothesized that these findings would extend to trait
measures of emotional arousal. In other words, we hypothesized that cortisol would facilitate emotional memory formation preferentially in individuals reporting higher levels of trait emotional arousal (in particular, negative emotional arousal). Furthermore, a rapidly growing literature has established sex differences in the relation between memory and stress (Shors, 2006
; Andreano and Cahill, 2009
; Wolf, 2009
). We therefore hypothesized that the role of trait emotional arousal as a moderator may vary by sex.
In order to make firm inferences about the role of cortisol in cognition, it is essential to jointly examine studies that pharmacolocially manipulate cortisol and studies that manipulate cortisol levels naturalistically (e.g., with a stressor). Studies that manipulate cortisol levels using a lab-based stressor limit inferences about the role of cortisol per se because other elements of a stress response (e.g., autonomic response; activation of neural circuitry) could be responsible for observed effects (which may simply co-vary with cortisol elevations). Studies that pharmacologically manipulate cortisol (vs. placebo) permit firm conclusions regarding the causal role of cortisol elevation, but do not readily allow for generalization of conclusions because of the artificial drug-induced physiological state (i.e., a cortisol elevation absent of other aspects of a stress response). Thus, we used two different studies (one with manipulation of endogenous cortisol, and the other manipulating cortisol exogenously) to examine whether findings replicate across both types of studies.