Effects of Acute Exposure to Stressors on Subsequent Avoidance-Escape Behavior*

Abstract

This paper attempts to show that severely stressful conditions can lead to a deficit in avoidance-escape responding by reducing noradrenergic activity in the brain. It is argued that this stress-induced neurochemical change explains more adequately an avoidance-excape deficit seen previously in dogs after severe inescapable shock than does the "learned helplessness" explanation originally offered for this effect. A series of six experiments are described that test the stress-neurochemical change explanation, which is called the "motor activation deficit" hypothesis. The first experiment showed that a brief exposure to cold swim, which reduced central noradrenergic activity but did not induce "learned helplessness," produced an avoidance-escape deficit similar to that observed after inescapable shock in the original "learned helplessness" studies. Subsequent experiments demonstrated that the deficit induced by cold swim was also similar to the original deficit in that it too dissipated with the passage of time and was reduced by pretraining animals in the correct response. Further experiments then showed that the deficit induced by cold swim was (a) aggravated by raising the height of the barrier between compartments in the shuttle box, and (b) did not occur if the avoidance-escape task used required little motor activity, both of the findings being predicted by the "motor activation deficit" hypothesis. Finally, an avoidance-escape deficit was produced by inescapable shock, and it was found that this stressor likewise did not impair avoidance-escape responding if the task required little skeletal activity, a result not predicted by the "learned helplessness" hypothesis. The paper concludes by discussing how the results presented in this paper, as well as in succeeding papers, support the "motor activation deficit" explanation for certain avoidance-escape deficits, defining the cases to which the explanation applies and discussing the neurotransmitters involved.

Estrogen-mediated effects on depression and memory formation in females

“…Adding to its usefulness as an animal model of depression, treatment with standard antidepressants such as the SSRIs and lesions to the serotonergic system ameliorated some if not all of the performance deficits (Maier et al, 1993). Although compelling, there is concern that some of these effects of stress on learning are attributable to nonspecific effects on performance (Maier and Jackson, 1979;Weiss and Glazer, 1975). For example, exposure to stressful events as used in these studies can induce neophobia and a decrease in activity, both of which can impair learning when activity is necessary.…”

The role of prior stressor controllability and the dorsal raphé nucleus in sucrose preference and social exploration

“…These outcomes reflect the stress history of the subject and have been argued to correlate with anxious [27] or depressed states [51]; for this reason variations of these procedures are commonly used as preclinical screens for novel anxiolytic or antidepressant compounds. Poor performance in the shuttlebox has been argued to reflect associative deficits [25], motor impairment [50], fatigue [30] and reduced pain sensitivity [18], as well as anxiety [27]. Thus, the meaning of poor shuttlebox escape is unclear.…”

Freewheel Running Prevents Learned Helplessness/Behavioral Depression: Role of Dorsal Raphe Serotonergic Neurons

“…For example, sedentary rats exposed to uncontrollable shocks, relative to controllable shocks, later exhibit a deficit in learning to escape from escapable stress (Seligman and Beagley, 1975;Weiss and Glazer, 1975) and exaggerated fear responding (Maier, 1990). LH behaviors expressed in laboratory animals resemble those of human depression and anxiety (Anisman and Zacharko, 1992;Yehuda and Antelman, 1993;Maier and Watkins, 1998) and are sensitive to antidepressant and anxiolytic drugs (Maier et al, , 1994Martin and Puech, 1996;Maudhuit et al, 1997).…”