Another explanation for numbing symptoms—and corresponding forgetting or dissociation from traumatic memory—may be related to the action of the dopaminergic (opiate) modulatory system as well as the noradrenergic (NE) modulatory system during memory encoding orchestrated by the amygdala and hippocampus (Abel et al., 1995; Petty, Kramer, Wu, & Davis, 1997). Petty et al. suggest that initial dopamine release at the traumatic event can lead to increased serotonin uptake and depletion. In animal studies, learned helplessness as a result of inescapable stress is correlated with serotonin depletion and alleviated by adequate amounts of norepinephrine in the hippocampus. The human correlate to learned helplessness articulated from the results of animal
studies (Peterson, Maier, & Seligman, 1993) may be numbing, an avoidance symptom, that tends to alternate with arousal symptoms and is correlated with alexithymia (see point 4) (Badura, 2003). Research findings by McGaugh et al. (1989) and Gallagher et al. (1985) (as cited in Abel et al.) suggest repression [dissociation (Tryon, 1993b)] might occur when naturally produced “opiates are released in response to the [traumatic] experience”
Endnote 18 and in turn “interfere with the memory storage process”
(p. 318). Abel et al. suggest that perhaps flashbacks represent repressed (dissociated) memories “retrieved when their noradrenaline [NE] system is activated”
(p. 319). Thus, forgetting and remembering (or re-experiencing) may be related to oscillating activations of the PNS and SNS dependent upon the presence of reminders of the traumatic eventEndnote 19.