Habituation to repeated restraint stress is associated with lack of stress-induced c-fos expression in primary sensory processing areas of the rat brain

Girotti, Milena; Pace, Thaddeus W.W.; Gaylord, Reginald I.; Rubin, B. A.; Herman, James P.; Spencer, Robert L.

doi:10.1016/j.neuroscience.2005.12.002

Cited by 210 publications

(172 citation statements)

References 68 publications

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“…In these rats, sensitivity to pain was linked to estrous cycle stage, indicating that variability in nociceptor responsiveness within a female population is determined principally by the hormonal profile that characterizes the particular stage of the estrous cycle rather than trait differences between individuals. Moreover, habituation to the testing paradigm on a second exposure, as has been reported for male rats after repeated exposure to a mild anxiogenic stressor (Weinberg et al, 2009;Girotti et al, 2006), did not seem to be present in females.…”

Section: Effect Of Estrous Cycle On Vibration Stress-evoked Changes Imentioning

confidence: 58%

“…AJ Devall and TA Lovick da Costa Gomez and Behbehani, 1995;Figueiredo et al, 2002;Girotti et al, 2006;Salchner and Singewald, 2002;Gerrits et al, 2003;Rizvi et al, 1991;Rocher et al, 2004;Brown et al, 2005;Floyd et al, 2000;Keay and Bandler, 2001). In particular, activation of the orbitofrontal cortex has been shown to induce biphasic changes in nociceptive threshold: hypoalgesia followed by a delayed hyperalgesia, and both effects could be blocked by inhibiting transmission through the ventrolateral PAG (Zhang et al, 1997).…”

Section: Stress-induced Hyperalgesia In Female Ratsmentioning

confidence: 99%

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Differential Activation of the Periaqueductal Gray by Mild Anxiogenic Stress at Different Stages of the Estrous Cycle in Female Rats

Devall¹,

Lovick²

2010

Neuropsychopharmacol

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The effect of acute exposure to mild anxiogenic stress on cutaneous nociceptive threshold was investigated in female Wistar rats at different stages of the estrous cycle. Baseline tail flick latencies did not change significantly during the cycle. However after brief exposure to vibration stress (4 Hz for 5 min), rats in late diestrus, but not at other cycle stages, developed a hyperalgesia (decrease in tail flick latency). Animals in late diestrus revealed a more than fivefold increase in the density of Fos-like immunoreactive nuclei in the dorsolateral, lateral, and ventrolateral columns in the caudal half of the periaqueductal gray matter (PAG). There was no change in the density of Fos-like immunoreactive nuclei in the PAG in rats in estrus and early diestrus, although rats in proestrus showed a smaller (50%) but significant increase. Rats undergoing withdrawal from a progesterone dosing regimen (5 mg/kg i.p. twice daily for 6 days) designed to mimic the fall in progesterone that occurs naturally during late diestrus, exhibited a stress-induced hyperalgesia that was similar to animals in late diestrus and a significant increase in Fos-positive cells in the PAG. We suggest that falling levels of progesterone during late diestrus may be a predisposing factor for the development of stress-induced hyperalgesia, which is linked to differential activation of descending pain control circuits in the PAG. Similar changes in women, when progesterone levels fall during the late luteal phase of the menstrual cycle, may contribute to the development of premenstrual symptoms that include increased anxiety and hyperalgesia.

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Section: Effect Of Estrous Cycle On Vibration Stress-evoked Changes Imentioning

confidence: 58%

Section: Stress-induced Hyperalgesia In Female Ratsmentioning

confidence: 99%

Differential Activation of the Periaqueductal Gray by Mild Anxiogenic Stress at Different Stages of the Estrous Cycle in Female Rats

Devall¹,

Lovick²

2010

Neuropsychopharmacol

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“…The most likely reason is that we only collected one blood sample at 30 minute and it is possible that corticosterone habituates at a time following termination of restraint. The possibility remains that changes in adrenal responsivity or intra-adrenal mechanisms prevent habituation at the adrenal level though many studies have observed habituation of both ACTH and corticosterone [4,10,11,16]. In animals exposed to restraint after repeated swim in Experiment 2, ACTH and corticosterone levels are similar to those of acutely restrained rats.…”

Section: Discussionmentioning

confidence: 94%

“…Repeated restraint exposure leads to decreases in hypothalamic-pituitary-adrenal (HPA) activation and fos mRNA expression in stressresponsive brain areas to the familiar restraint, a phenomenon known as habituation [4,10,11,16]. In contrast, in animals with a history of repeated experience with a different stressor, acute restraint can lead to facilitation, in which HPA and sympathetic activity meets or exceed the responses induced by naive exposure to acute restraint [3,5,6].…”

Section: Introductionmentioning

confidence: 99%

Struggling behavior during restraint is regulated by stress experience

Grissom

Kerr

Bhatnagar

2008

Behavioural Brain Research

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Restraint elicits a number of physiological stress responses that can be increased or decreased in magnitude based on prior stress history. For instance, repeated exposure to restraint leads to habituation of hypothalamic-pituitary-adrenal (HPA) activation to restraint. In contrast, acute restraint after a different repeated stressor leads to facilitation of HPA activity to the novel stress. Acute restraint also elicits a variety of behaviors including struggling, but the effect of prior stress in regulating behavioral responses to restraint is not clear. The goal of the present studies was to assess struggling during restraint with or without a prior history of repeated stress. Using automated behavioral analysis software (EthoVision), we quantified struggling during restraint. We found that acutely restrained rats exhibit vigorous struggling behavior that declines during a single restraint period. Repeated restraint lead to habituated struggling behavior, whereas acute restraint after repeated swim elicited facilitated struggling behavior. These effects on struggling were found alongside expected differences in HPA activity. Removing stress-induced increases in corticosterone via adrenalectomy did not significantly affect struggling responses to restraint. Overall, restraintinduced struggling appears to be regulated in a manner similar to HPA responses to restraint, but is not dictated by adrenal hormones.

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“…Comparison of the responses of repeatedly restrained rats to those experiencing a first exposure to the stimulus shows that in the site of the motor output of the HPA axis, the hypothalamic paraventricular nuclei (PVN), all indices of activity are diminished after repetition. Corticotropin-releasing factor (CRF) and vasopressin(AVP) synthesis is decreased as is consequent ACTH and corticosterone secretion (6). This is reflected by the finding that a measure of activation of the CRF neurons, c-Fos staining, shows a reduced number of excited cells, and that the responsive CRF neurons are more ventrally located in the nuclei (20).…”

mentioning

confidence: 99%

Modulation of stress responses: How we cope with excess glucocorticoids

Dallman

2007

Experimental Neurology

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We are admirably equipped to respond to survive the acute slings and arrows of outrageous fortune. With acute challenges of sufficient magnitude, activity of the hypothalamo-pituitaryadrenal (HPA) axis is stimulated and the protean adrenocortical hormones, glucocorticoids, are secreted to do their job throughout all cell types in the body, most of which contain the appropriate receptors. The consequent actions of the glucocorticoids, together with the rapidly acting adrenomedullary catecholamines, alter metabolic, cardiovascular, immune and central neural responses to the ongoing condition so that we can effectively sustain life at the moment. Circulating glucose is increased with an abundant supply for the potential need for fighting or fleeing, as is arterial blood pressure; the immune system is prevented from over-responding to acute bacterial threats; contextual brain-generated behaviors are enhanced by both increased attention and drive (13). Thus, the glucocorticoids engage many of the body systems for optimal responses to acute challenge. These responses enable and sustain life.However, many of life's challenges cannot be escaped, or otherwise be behaviorally modified, this then entails recruitment of the brain chronic stress response network, with potential persistent elevations in glucocorticoid secretion. It seems abundantly clear that mechanisms have evolved to reduce activity in the brain chronic response network so that individuals undergoing inescapable challenge do not become debilitated, as occurs by definition with individuals with Cushings syndrome, who have unregulated glucocorticoid exposure. High glucocorticoid concentrations that persist, may rapidly curtail life through marked shifts in energy stores from the periphery to the center of the body, hypertension, muzzling the immune system and carving the brain into an alert and anxious, but insensible mess of responsivity that no longer can use learning and memories appropriately. Thus, persistently elevated glucocorticoid concentrations are far too much of a once good thing (12).Given this down-side of chronic exposure to persistently high glucocorticoids, it is not surprising that mechanisms have been selected for that damp their secretion in chronically stressed individuals. These mechanisms have been explored in many organisms, primarily rodents, exposed repeatedly or chronically to challenge. It turns out, again unsurprisingly, that there appears to be a host of mechanisms that allow strong damping of the HPA responses. However, with persistent life-threatening stimuli that may be unanticipated, it is also of key importance to maintain full responsivity of the system, even under conditions of chronic challenge. How does this happen?

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Habituation to repeated restraint stress is associated with lack of stress-induced c-fos expression in primary sensory processing areas of the rat brain

Cited by 210 publications

References 68 publications

Differential Activation of the Periaqueductal Gray by Mild Anxiogenic Stress at Different Stages of the Estrous Cycle in Female Rats

Differential Activation of the Periaqueductal Gray by Mild Anxiogenic Stress at Different Stages of the Estrous Cycle in Female Rats

Struggling behavior during restraint is regulated by stress experience

Modulation of stress responses: How we cope with excess glucocorticoids

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