Effects of Chronic Exposure to Stressors on Avoidance‐Escape Behavior and on Brain Norepinephrine*

@article{Weiss1975EffectsOC,
  title={Effects of Chronic Exposure to Stressors on Avoidance‐Escape Behavior and on Brain Norepinephrine*},
  author={JAY M. Weiss and Howard I. Glazer and Larissa A. Pohorecky and John Brick and Neal E. Miller},
  journal={Psychosomatic Medicine},
  year={1975},
  volume={37},
  pages={522–534}
}
&NA; A single exposure to a severe stressor (either cold swim or inescapable shock) impairs subsequent performance in a shuttle avoidance‐escape task (1), a deficit attributed to reduction in brain noradrenergic activity produced by these stressors. In the present paper, two experiments are described which examine how repeated exposure to such stressors affects (a) shuttle avoidance‐escape performance (Experiment 1), and (b) aspects of brain norepinephrine metabolism (Experiment 2). Experiment… 
Effects of Acute Exposure to Stressors on Subsequent Avoidance‐Escape Behavior*
TLDR
How the results presented in this paper, as well as in succeeding papers, support the “motor activation deficit” explanation for certain avoidance‐escape deficits are discussed, defining the cases to which the explanation applies and discussing the neurotransmitters involved.
Monamines as Mediators of Avoidance‐Escape Behavior*
TLDR
Three experiments test the hypothesis that the avoidance‐escape deficits observed following certain highly stressful conditions result from changes in activity of noradrenergic (or other monominergic) neural systems and indicate that depletion of monamines by a single injection of tetrabenazine produces an active avoidance‐ Escape deficit.
Catecholamine depletion in mice upon reexposure to stress: mediation of the escape deficits produced by inescapable shock.
  • H. Anisman, L. Sklar
  • Biology, Psychology
    Journal of comparative and physiological psychology
  • 1979
TLDR
It is suggested that the long-term effects of inescapable shock may be due to sensitization effects or conditioned amine depletion, and catecholamine mediation of escape performance through variations in response maintenance abilities is suggested.
Behavioral analysis of stress controllability effects in a new swim stress paradigm
Effect of stressor intensity on habituation and sensitization of glucocorticoid responses in rats.
TLDR
The data extend the dual process theory of Groves and Thompson (1970) to an endocrine respondent and suggest that an explanation as to discrepancies in the literature concerning adrenocortical response to repeated presentation of stressors may relate to differences in the stressor parameters used.
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References

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Effects of Acute Exposure to Stressors on Subsequent Avoidance‐Escape Behavior*
TLDR
How the results presented in this paper, as well as in succeeding papers, support the “motor activation deficit” explanation for certain avoidance‐escape deficits are discussed, defining the cases to which the explanation applies and discussing the neurotransmitters involved.
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TLDR
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TLDR
The shock-induced decrease in norepinephrine failed to occur in animals treated with a monoamine oxidase inhibitor (Catron, tranylcypromine or harmaline), and a catechol O-methyl transferase inhibitors (pyrogallol) did not affect the stress-induced disappearance of the amine.
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Rats received electric shock that was preceded by either a warning signal, a series of signals forming an "external clock," or no signal at all. In all conditions, subjects which could avoid and/or
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TLDR
Exposure of dogs to inescapable shocks under a variety of conditions reliably interfered with subsequent instrumental escape-avoidance responding in a new situation, indicating that interference is not due to acquisition, during the period of exposure to in unavoidable shocks, of inappropriate, competing instrumental responses.
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TLDR
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TLDR
Changes in NE turnover regulation induced by electric foot shocks were studied in various conditions and there was an enhanced turnover of NE in the brainstem-mesencephalon when higher intensities of stimulation were used; this was associated with an increased accumulation of H 3 -normetanephrine.
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TLDR
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