Rapid stress-induced elevations in corticotropin-releasing hormone mRNA in rat central amygdala nucleus and hypothalamic paraventricular nucleus: An in situ hybridization analysis

Hsu, David T.; Chen, Fengling; Takahashi, Lorey K.; Kalin, Ned H.

doi:10.1016/s0006-8993(98)00032-8

Cited by 153 publications

(84 citation statements)

References 24 publications

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“…Previous studies by our lab have shown an increase in CRF mRNA in the CeA following restraint stress (Hsu et al, 1998) and work by others have reported a similar increase following rat exposure to a cat (Figueiredo et al, 2003). In addition, exposure of sheep to dogs has been shown to increase CRF release from the CeA by in vivo microdialysis (Cook, 2002).…”

Section: Discussionsupporting

confidence: 65%

Predator threat induces behavioral inhibition, pituitary-adrenal activation and changes in amygdala CRF-binding protein gene expression

Roseboom

Nanda

Bakshi

et al. 2007

Psychoneuroendocrinology

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SummaryBehavioral inhibition (BI) is an adaptive defensive response to threat; however, extreme BI is associated with anxiety-related psychopathology. When rats are exposed to a natural predator they display stress-and anxiety-related behavioral alterations and physiological activation. To develop a preclinical rodent model to study mechanisms underlying human BI and anxiety, we examined the extent to which ferret exposure elicits anxiety-related BI and HPA and amygdala activation of the CRF system. In the first experiment, BI and other behaviors were assessed in the presence or absence of a ferret. In the second experiment, ferret-induced corticosterone release and changes in brain cfos expression were assessed. In the final experiment, gene chip and quantitative real time-PCR analyses were performed on amygdala tissue from control and ferret-exposed rats. Ferret exposure increased BI and submissive posturing, as well as plasma corticosterone and the number of Fospositive cells in several brain regions including the amygdala. Gene expression analysis revealed increased amygdalar mRNA for CRF-binding protein, but not the CRF 1 receptor, CRF 2 receptor or CRF. In rodents, ferret exposure can be used to elicit anxiety-related BI, which is associated with HPA and amygdala activation. Since the amygdala and the CRF system have been implicated in adaptive and maladaptive anxiety responses in humans, these data support use of our rodent model to further investigate mechanisms underlying anxiety-related psychopathology in humans.

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Section: Discussionsupporting

confidence: 65%

Predator threat induces behavioral inhibition, pituitary-adrenal activation and changes in amygdala CRF-binding protein gene expression

Roseboom

Nanda

Bakshi

et al. 2007

Psychoneuroendocrinology

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“…Studies on molecular mechanisms through which CRH is stimulated in these areas lag behind compared to that of PVH. It has been shown that psychosocial stress increases CRH mRNA levels in the CeA (Hsu et al 1998, Kalin et al 1994 and laterodorsal (oval) subnucleus of BNST (Makino et al 1999) and in the Barrington's nucleus (Wood et al 2009). Although CRH mRNA is elevated in both of…”

Section: Regulation and Function Of Central (Extrahypophyseotropic) Crhmentioning

confidence: 99%

CRH: The link between hormonal-, metabolic- and behavioral responses to stress

Kovács

2013

Journal of Chemical Neuroanatomy

108

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Two major and mutually interconnected brain systems are recruited during stress reaction. One is the hypothalamic paraventricular nucleus (PVH) and the second is the extended amygdala. PVH governs the neuroendocrine stress response while CeA regulates most of the autonomic and behavioral stress reactions. The common neurohormonal mediator of these responses is the corticotropin-releasing hormone, CRH, which is expressed in both centers. CRH belongs to a larger family of neuropeptides that also includes urocortins 1, 2, and 3 all have different affinity towards the two types of CRHR receptors and have been implicated in regulation of stress and HPA axis activity. One functionally relevant aspect of CRH systems is their differential regulation by glucocorticoids. While corticosterone inhibits CRH transcription in the PVH, stress-induced glucocorticoids stimulate CRH expression in the extended amygdala. This review summarizes past and recent findings related to CRH gene regulation and its involvement in the neuroendocrine, autonomic and behavioral stress reaction.Key words: Corticotropin-releasing hormone, paraventricular nucleus, central amygdala, bed nucleus of stria terminalis, corticosterone, cAMP-response element.

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“…The differences in the types of stressors, the opioid dependence paradigms, and interval between exposure to stress/ withdrawal and tissue collection probably contributed to these discrepancies. Furthermore, acute stress produces only transient increases in CRF mRNA expression in the CeA (Helmreich et al, 1999;Hsu et al, 1998) so that evaluating CRF expression 4 h after stress may have prevented us from observing earlier changes that may have occurred in CRF activity in this region in response to acute restraint.…”

Section: Hpa Activitymentioning

confidence: 99%

Intermittent Morphine Administration Induces Dependence and is a Chronic Stressor in Rats

Houshyar

Gómez

Manalo

et al. 2003

Neuropsychopharmacol

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Although constant treatment with morphine (implanted pellets) does not activate the hypothalamic-pituitary-adrenal (HPA) axis, intermittent injections of morphine may constitute a chronic stressor in rats. To test this hypothesis, we compared the effects of morphine in escalating doses (10-40 mg/kg, s.c.) or saline injected twice daily for 4 days on energy balance, hormones, HPA responses to novel restraint and central corticotropin-releasing factor (CRF) mRNA 12 h and 8 days after the last morphine injection in adult male Sprague-Dawley rats. Weight gain stopped at the onset of morphine, weight loss was marked 36 h postmorphine; thereafter, body weight gain paralleled saline controls. At 12 h, insulin, leptin, and testosterone concentrations were reduced but normalized by 8 days. Restraint and tail nicks caused facilitated ACTH responses at 12 h, under-responsiveness at 8 days. CRF mRNA, measured only at 12 h, was increased in the paraventricular (PVN) and Barrington's nuclei (BAR), decreased in the bed nuclei of the stria terminalis (BNST) and unchanged in the amygdala (CeA) in morphine-treated rats. After stress, CRF mRNA increased in PVN in both groups, increased in BAR and decreased in BNST in saline but not morphine groups, and was unchanged in CeA in both groups. Results from all variables characterize intermittent morphine injections as a chronic stressor. In contrast to constant treatment, injected morphine probably allows some withdrawal during each 12 h interval, causing repeated stress. Drug addicts treat themselves intermittently, and stress causes relapse after withdrawal. Thus, intermittent morphine, itself, may promote relapse.

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Rapid stress-induced elevations in corticotropin-releasing hormone mRNA in rat central amygdala nucleus and hypothalamic paraventricular nucleus: An in situ hybridization analysis

Cited by 153 publications

References 24 publications

Predator threat induces behavioral inhibition, pituitary-adrenal activation and changes in amygdala CRF-binding protein gene expression

Predator threat induces behavioral inhibition, pituitary-adrenal activation and changes in amygdala CRF-binding protein gene expression

CRH: The link between hormonal-, metabolic- and behavioral responses to stress

Intermittent Morphine Administration Induces Dependence and is a Chronic Stressor in Rats

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