It has been known since 1967 that exposure to stressors over which the organism has no behavioral control produce a constellation of behavioral and neurochemical sequelae that do not occur if an element of behavioral control over the stressor is possible. “Learned Helplessness” points of view developed by me and Seligman explained this difference by arguing that when confronted with an uncontrollable stressor the organism learns that it is uncontrollable, and that this learning sets off a cascade of events that produce the behavioral and neurochemical outcomes. Here, controllable aversive events fail to produce the outcomes because they lack the critical element of uncontrollability, not because they lead to an active process.
Recent neurocircuitry work will be described which indicates that this original view had it exactly backwards. Instead, a) specific circuits (prelimbic cortex to dorsomedial striatum and mediodorsal thalamus to prelimbic cortex) detect/process the presence of control, and b) when control is detected separate projections from the prelimbic cortex actively inhibit stress-responsive limbic and brainstem structures that are activated by both uncontrollable and controllable aversive events and that are the proximate mediators of the behavioral changes. In addition, there are strong sex differences in these processes which will be described. Finally, implications of this neurocircuitry work, especially for controllable stressor-induced changes in behavior outside the realm of aversively motivated behavior, such as generalized persistence/perseverance, will be discussed.
