Adrenocortical and behavioral responses to repeated stressors: toward an animal model of chronic stress and stress-related mental illness

Ottenweller, John E.; Natelson, Benjamin H.; Pitman, David; Drastal, Susan

doi:10.1016/0006-3223(89)90123-6

Cited by 144 publications

(80 citation statements)

References 20 publications

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“…This result might seem contrary to those from studies using other stressors in which the THPVP appears to be play a role in the habituation of the ACTH response to repeated experience of the homotypic stressor (Bhatnagar et al, 2000(Bhatnagar et al, , 2002Jaferi et al, 2003;Jaferi and Bhatnagar, 2006;Ottenweller et al, 1989). However, we do not observe consistent habituation of the HPA response in our recurrent hypoglycemia model, with only modest decrements of ACTH and CORT.…”

Section: Discussioncontrasting

confidence: 99%

“…Activity of the THPVP has been implicated in the altered neuroendocrine response to the repeated experience of other stressors, including the phenomenon of stress habituation (decreased HPA activation): the THPVP contributes to feedback inhibition by glucocorticoids on the HPA axis, in chronically but not acutely stressed rats (Jaferi et al, 2003). Bhatnagar and others have demonstrated that permanent inactivation of the THPVP, via electrolytic lesion, prevents the blunted ACTH response that occurs with multiple experience of restraint stress, whereas the HPA response to a novel, heterotypic, stressor is not altered by THPVP lesion (Bhatnagar et al, 2000(Bhatnagar et al, , 2002Jaferi et al, 2003;Jaferi and Bhatnagar, 2006;Ottenweller et al, 1989). These data suggest that the THPVP is linked to the CNS 'memory' of a stressor experience.…”

Section: Introductionmentioning

confidence: 99%

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Acute THPVP inactivation decreases the glucagon and sympathoadrenal responses to recurrent hypoglycemia

et al. 2008

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The posterior paraventricular nucleus of the thalamus (THPVP) has been identified as a forebrain region that modulates the central nervous system (CNS) response to recurrent experiences of stressors. The THPVP is activated in response to a single (SH) or recurrent (RH) experience of the metabolic stress of hypoglycemia. In this study, we evaluated whether temporary experimental inactivation of the THPVP would modify the neuroendocrine response to SH or RH. Infusion of lidocaine (LIDO) or vehicle had no effect on the neuroendocrine response to SH, comparable to findings with other stressors. THPVP vehicle infusion concomitant with RH resulted in a prevention of the expected impairment of neuroendocrine responses, relative to SH. LIDO infusion with RH resulted in significantly decreased glucagon and sympathoadrenal responses, relative to SH. These results suggest that the THPVP may contribute to the sympathoadrenal stimulation induced by hypoglycemia; and emphasizes that the THPVP is a forebrain region that may contribute to the coordinated CNS response to metabolic stressors.

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Section: Discussioncontrasting

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Acute THPVP inactivation decreases the glucagon and sympathoadrenal responses to recurrent hypoglycemia

et al. 2008

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“…The current study tested whether repeated restraint caused similar effects on BLA neuronal physiology in resilient and vulnerable populations. Resilience and vulnerability were defined based on a well-established biological index of stress, adrenal gland weight (Selye, 1936;Bassett and Cairncross, 1975;Dallman, 1984;Ottenweller et al, 1989;Marquez et al, 2004), and cross checked by EPM and body weight. EPM and body weight are both validated measures of effects of repeated stress in vulnerable rats (Willner et al, 1996;Stone and Quartermain, 1997;Caldji et al, 2000;Maslova et al, 2002;Vyas et al, 2002;Marquez et al, 2004;Weiss et al, 2004;McLaughlin et al, 2007;Pohl et al, 2007;Zhang and Rosenkranz, 2012), further validating the subdivision of populations.…”

Section: Discussionmentioning

confidence: 99%

Distinct Effects of Repeated Restraint Stress on Basolateral Amygdala Neuronal Membrane Properties in Resilient Adolescent and Adult Rats

Hetzel

Rosenkranz

2014

Neuropsychopharmacol

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Severe and repeated stress has damaging effects on health, including initiation of depression and anxiety. Stress that occurs during development has long-lasting and particularly damaging effects on emotion. The basolateral amygdala (BLA) plays a key role in many affective behaviors, and repeated stress causes different forms of BLA hyperactivity in adolescent and adult rats. However, the mechanism is not known. Furthermore, not every individual is susceptible to the negative consequences of stress. Differences in the effects of stress on the BLA might contribute to determine whether an individual will be vulnerable or resilient to the effects of stress on emotion. The purpose of this study is to test the cellular underpinnings for age dependency of BLA hyperactivity after stress, and whether protective changes occur in resilient individuals. To test this, the effects of repeated stress on membrane excitability and other membrane properties of BLA principal neurons were compared between adult and adolescent rats, and between vulnerable and resilient rats, using in vitro whole-cell recordings. Vulnerability was defined by adrenal gland weight, and verified by body weight gain after repeated restraint stress, and fecal pellet production during repeated restraint sessions. We found that repeated stress increased the excitability of BLA neurons, but in a manner that depended on age and BLA subnucleus. Furthermore, stress resilience was associated with an opposite pattern of change, with increased slow afterhyperpolarization (AHP) potential, whereas vulnerability was associated with decreased medium AHP. The opposite outcomes in these two populations were further distinguished by differences of anxiety-like behavior in the elevated plus maze that were correlated with BLA neuronal excitability and AHP. These results demonstrate a substrate for BLA hyperactivity after repeated stress, with distinct membrane properties to target, as well as age-dependent factors that contribute to resilience to the effects of stress.

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“…Hence, the normal activity of the HPA axis, characterized by wide circadian variations with morning zeniths and evening nadirs, becomes altered during chronic stress (Halbreich, Asnis, Schindledecker, Zumoff, & Nathan, 1985). This results in a sustained increase of cortisol levels (Ottenweller, Natelson, Pitman, & Drastal, 1989), with a blunted circadian curve due to increased levels in the evening and discrete decline in the morning (Chrousos & Gold, 1998). This hyperactivation, with the resulting hypercortisolism, has long been associated with different clinical conditions, such as depression and anxiety disorders (Gold, Goodwin, & Chrousos, 1988a, 1988b.…”

mentioning

confidence: 99%

Regulation of hypothalamic-pituitary-adrenal activity in response to cognitive therapy in patients with generalized anxiety disorder

Tafet

Feder

Abulafia

et al. 2005

Cognitive, Affective, & Behavioral Neuroscience

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Adrenocortical and behavioral responses to repeated stressors: toward an animal model of chronic stress and stress-related mental illness

Cited by 144 publications

References 20 publications

Acute THPVP inactivation decreases the glucagon and sympathoadrenal responses to recurrent hypoglycemia

Acute THPVP inactivation decreases the glucagon and sympathoadrenal responses to recurrent hypoglycemia

Distinct Effects of Repeated Restraint Stress on Basolateral Amygdala Neuronal Membrane Properties in Resilient Adolescent and Adult Rats

Regulation of hypothalamic-pituitary-adrenal activity in response to cognitive therapy in patients with generalized anxiety disorder

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