Preshock-produced intensification of passive avoidance responding and of elevation in corticosteroid level

doi:10.1016/0031-9384(71)90141-7

Physiology & Behavior

Volume 7, Issue 5, November 1971, Pages 733-736

https://doi.org/10.1016/0031-9384(71)90141-7 Get rights and content

Abstract

The adrenocortical steroid response and passive avoidance behavior were studied in rats that had been exposed to inescapable intense shock (preshock). Previously preshocked animals exhibited a greater adrenocortical steroid response to mild shock than nonpreshocked controls; in addition, passive avoidance behavior was facilitated in the preshocked animals.

References (12)

D.C. Anderson et al.
Variations in unsignaled inescapable preshock as determinants of responses to punishment
J. comp. physiol. Psychol. Monogr. Suppl.
(1968)
D.C. Anderson et al.
Intensification of passive-avoidance learning as a function of preshock and a 39 KHz tone
D.C. Anderson et al.
Adrenocorticotrophic hormone and acquisition of a passive avoidance response: A replication and extension
J. comp. physiol. Psychol.
(1968)
D.C. Anderson et al.
Number and duration of inescapable preshocks and variation in time of testing as determinants of escape-avoidance learning in the rat
K.H. Brookshire et al.
Residual of shock-trauma in the white rat: a three-factor theory
Psychol. Monogr.
(1961)
B.A. Campbell et al.
Electrical and behavioral effects of different types of shock stimuli on the rat
J. comp. physiol. Psychol.
(1958)

There are more references available in the full text version of this article.

Cited by (16)

PTSD and stress sensitisation: A tale of brain and body Part 2: Animal models
2007, Neuroscience and Biobehavioral Reviews
Citation Excerpt :
One week after pre-shocks, the plasma corticosterone response to a novel cage is increased compared to non-shocked controls (Weinberg et al., 1980). Two weeks after pre-shocks, the corticosterone response to a reminder footshock (Madden et al., 1971), but also to a novel open field (Levine and Madden, 1973), to a startle apparatus (Chalmers et al., 1974) and to heat-induced pain (Caggiula et al., 1989), the ACTH response to noise in a novel cage (van Dijken et al., 1993) and the ACTH and corticosterone response to a novel, electrified prod in the home cage (Bruijnzeel et al., 2001a) are all greater than in non-shocked controls. Even though peak corticosterone levels in the noise test are not greater in previously shocked rats, the temporal dynamics seem to point to a faster negative feedback (van Dijken et al., 1993).
Animal models that are characterised by long-lasting conditioned fear responses as well as generalised behavioural sensitisation to novel stimuli following short-lasting but intense stress have a phenomenology that resembles that of PTSD in humans. These models include brief sessions of shocks, social confrontations, and a short sequence of different stressors. Subgroups of animals with different behavioural traits or coping styles during stress exposure show a different degree or pattern of long-term sensitisation. Weeks to months after the trauma, treated animals on average also show a sensitisation to novel stressful stimuli of neuroendocrine, cardiovascular and gastrointestinal motility responses as well as altered pain sensitivity and immune function. Functional neuroanatomical and pharmacological studies in these animal models have provided evidence for involvement of amygdala and medial prefrontal cortex, and of brain stem areas regulating neuroendocrine and autonomic function and pain processing. They have also generated a number of neurotransmitter and neuropeptide targets that could provide novel avenues for treatment in PTSD.
Exposure to repeated low-level formaldehyde in rats increases basal corticosterone levels and enhances the corticosterone response to subsequent formaldehyde
2001, Brain Research
Citation Excerpt :
Previous work examining the effect of repeated stress has demonstrated a variety of outcomes regarding CORT responses. Some studies have demonstrated no changes in CORT levels after repeated presentations of stress [23,36], while others have demonstrated a sensitization of basal and/or stress-induced CORT responses after repeated stress [17,23,26,27,34], and even a single pre-exposure to a stressor is sufficient to sensitize the CORT response [7]. However, the literature also supports an habituation response of CORT to repeated stressor presentation ( [21,22,25,51]; also, see [12] and references therein).
Low-level exposure to volatile organic compounds may produce symptoms in humans reporting multiple chemical sensitivity (MCS) through altered hypothalamic–pituitary–adrenal (HPA) axis functioning. We determined whether repeated formaldehyde (Form) exposure would alter corticosterone (CORT) levels in a rat model of MCS. Male Sprague–Dawley rats were given acute chamber exposures to Air or Form (0.7 or 2.4 ppm), and trunk blood was collected 20 or 60 min later. All groups showed increased CORT levels above naı̈ve basal levels at 20 min and a return to baseline by 60 min, with no differences between treatment groups. The second experiment examined the effect of repeated Form exposure (1 h/day×5 days/week×2 or 4 weeks) on basal CORT levels and after a final challenge. Basal CORT was increased above naı̈ve values after 2 week exposure to Air or 0.7 ppm Form. By 4 week, CORT levels in the Air group returned to naı̈ve values, but remained elevated in the 0.7 ppm Form group. There were no differences in basal CORT levels among either 2.4 ppm exposed groups. After a final Air or Form challenge, the 2 and 4 week Air and 0.7 ppm Form groups had elevated CORT levels similar to their acute response, while the 2 and 4 week 2.4 ppm Form groups had elevated CORT levels compared to their acute response, indicating enhanced reactivity of the HPA axis to subsequent Form. These findings suggest that altered HPA axis functioning occurs after repeated low-level Form exposure, and may have implications for mechanisms mediating MCS in humans.
Sensitization of amphetamine-stereotypy reduces plasma corticosterone: Implications for stereotypy as a coping response
1991, Behavioral and Neural Biology
The potential coping functions of amphetamine-induced stereotypy were investigated using a physiological index of stress or arousal, plasma corticosterone level. A series of five injections of d-amphetamine was used to enhance stereotyped behavior in control animals as well as in rats with bilateral dopamine-depleting lesions of the caudate-putamen. This regimen of amphetamine injections significantly increased stereotyped behavior and also reduced the normal elevation in corticosterone produced by treatment with d-amphetamine. This effect was apparent in both control and lesioned animals. These results support the hypothesis that amphetamine-induced stereotyped behavior functions to reduce stress or arousal and additionally suggest that this effect is largely independent of underlying dopaminergic mechanisms.
Serial stressors: Prior exposure to a stressor modulates its later effectiveness on gastric ulceration and corticosterone release
1986, Behavioral and Neural Biology
Several studies have focused on the proactive effects of prior exposure to a stressor on ulcerogenic and endocrine responses to exposure to a similar final stressor. In the present study, we explored the effects of prior exposure of Møll—Wistar rats to water-restraint stress on gastric ulceration and corticosterone responses to a final stressor. The number of prior exposures to water-restraint challenge was varied from one to four, and the durations of the prior exposures varied from 30 min to 2 h. The duration of the final stress challenge was 75 min. The two indices of the stress response to the final stressor challenge yielded different results. For neither index was the duration of prior exposures a significant factor in modulating the response to the final challenge. For gastric ulceration, those animals receiving one prior exposure, but not four, exhibited less gastric ulceration than animals receiving no prior exposure. These animals also developed less ulceration than those receiving four prior exposures. For corticosterone, those animls receiving four prior exposures exhibited a lower adrenocortical response to the final stressor than did animals receiving no prior exposure, or only one prior exposure. The results indicate the complexity of proactive effects of earlier stress experience on responses to a final stressor challenge.
Adjunctive drinking and the pituitary-adrenal response: Effects of prior aversive stimulation (preshock)
1982, Physiology and Behavior
Shock-induced fighting attenuates the effects of prior shock experience in rats
1980, Physiology and Behavior
We compared the responses of animals exposed singly to inescapable shock with those of animals exposed to the same shock in pairs and thus able to fight in response to shock. During the shock sessions animals shocked in pairs showed a reduced ACTH response when compared with animals shocked individually, and the reduction in ACTH was not dependent on the amount of fighting which occurred. In addition, if animals had previous opportunities to fight, the response to shock was still attenuated even when the partner was no longer present. When subsequently tested in a novel task it was observed that fighters, like controls, showed a reduced pituitary-adrenal response to novelty when a consummatory response was available. Singly shocked animals, however, exhibited elevated levels of plasma corticosterone whether or not they could drink in the novel chamber. We hypothesized that fighting is a consummatory response, and that the reinforcement provided by performance of this consummatory response reduced the ACTH response to shock and permanently altered subsequent responsiveness.

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^☆: This research was supported in part by NIMH grant MH 14436-02 and 03 to D. Chris Anderson, NGL 05-020-326 (NASA) and ONR Contract N00014-67-A-0112-0009 (Navy) to Seymour Levine. The valuable assistance of Saku Mantena is gratefully acknowledged.

²: Now at the Department of Psychology, University of Pennsylvania.

³: Supported by USPHS Research Scientist Award 1-K05-MH-19936 from the National Institute of Mental Health.

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Preshock-produced intensification of passive avoidance responding and of elevation in corticosteroid level☆

Abstract

Variations in unsignaled inescapable preshock as determinants of responses to punishment

J. comp. physiol. Psychol. Monogr. Suppl.

Intensification of passive-avoidance learning as a function of preshock and a 39 KHz tone

Adrenocorticotrophic hormone and acquisition of a passive avoidance response: A replication and extension

J. comp. physiol. Psychol.

Number and duration of inescapable preshocks and variation in time of testing as determinants of escape-avoidance learning in the rat

Residual of shock-trauma in the white rat: a three-factor theory

Psychol. Monogr.

Electrical and behavioral effects of different types of shock stimuli on the rat

J. comp. physiol. Psychol.