Restraint stress increases corticotropin-releasing hormone mRNA content in the amygdala and paraventricular nucleus

Kalin, Ned H.; Takahashi, Lorey K.; Chen, Fengling

doi:10.1016/0006-8993(94)91382-x

Cited by 203 publications

(106 citation statements)

References 16 publications

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“…29,65 In addition, acute stress in the adult results in CRH release as well as upregulation of CRH mRNA expression in ACe. This upregulation is thought to be mediated by stress-induced glucocorticoids, [66][67][68] and a facilitatory action of glucocorticoids on CRH expression has also been shown in the 10-dayold rat. 69 These data suggest that a single acute stress activates CRH-expressing neurons in ACe, leading to a facilitatory input into CRH-expressing PVN neurons and resulting in enhanced CRH expression in this latter region.…”

Section: Differential Effects Of Single and Recurrent Stress On Hypotmentioning

confidence: 86%

“…66,67,69 This effect is more apparent following repeated stress and cumulatively more glucocorticoid production. Concurrently, upon repeated stress, enhanced glucocorticoid levels may act via local and/or hippocampal receptors to suppress CRH mRNA in the PVN of the more glucocorticoid-sensitive immature rat.…”

Section: Differential Effects Of Single and Recurrent Stress On Hypotmentioning

confidence: 99%

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Neurobiology of the stress response early in life: evolution of a concept and the role of corticotropin releasing hormone

et al. 2001

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Over the last few decades, concepts regarding the presence of hormonal and molecular responses to stress during the first postnatal weeks in the rat and the role of the neuropeptide corticotropin releasing hormone (CRH) in these processes, have been evolving. CRH has been shown to contribute critically to molecular and neuroendocrine responses to stress during development. In turn the expression of this neuropeptide in both hypothalamus and amygdala is differentially modulated by single and recurrent stress, and is determined also by the type of stress (eg, psychological or physiological). A likely transcriptional regulatory factor for modulating CRH gene expression, the cAMP responsive element binding protein CREB, is phosphorylated (activated) in the developing hypothalamus within seconds of stress onset, preceding the transcription of the CRH gene and initiating the activation of stress-induced cellular and neuroendocrine cascades. Finally, early life stress may permanently modify the hypothalamic pituitary adrenal axis and the response to further stressful stimuli, and recent data suggest that CRH may play an integral role in the mechanisms of these long-term changes. Molecular Psychiatry (2001) 6, 647-656.

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Section: Differential Effects Of Single and Recurrent Stress On Hypotmentioning

confidence: 86%

Section: Differential Effects Of Single and Recurrent Stress On Hypotmentioning

confidence: 99%

Neurobiology of the stress response early in life: evolution of a concept and the role of corticotropin releasing hormone

et al. 2001

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Section: Discussionmentioning

confidence: 99%

“…40,54 Consistent with the functional role of hypothalamic and amygdala CRH in modulating stress responses, up-regulation of CRH expression in these two regions by challenges that activate the neuroendocrine stress response has been documented. 23,29 Teleologically, this mechanism for regulation of CRH levels should be advantageous, resulting in larger releasable pools of CRH upon subsequent challenges.In the hippocampus, the presence of CRH-expressing inter-neurons has been documented in both the mature and developing rat, 41,48,53,59 but the physiological functions of the peptide and the regulation of CRH levels at hippocampal synapses have not been fully established. Specifically, whether hippocampal CRH participates in the neuroendocrine stress response has been questioned.…”

mentioning

confidence: 99%

Neuronal activity and stress differentially regulate hippocampal and hypothalamic corticotropin-releasing hormone expression in the immature rat

et al. 2000

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Corticotropin-releasing hormone, a major neuromodulator of the neuroendocrine stress response, is expressed in the immature hippocampus, where it enhances glutamate receptor-mediated excitation of principal cells. Since the peptide influences hippocampal synaptic efficacy, its secretion from peptidergic interneuronal terminals may augment hippocampal-mediated functions such as learning and memory. However, whereas information regarding the regulation of corticotropin-releasing hormone's abundance in CNS regions involved with the neuroendocrine responses to stress has been forthcoming, the mechanisms regulating the peptide's levels in the hippocampus have not yet been determined. Here we tested the hypothesis that, in the immature rat hippocampus, neuronal stimulation, rather than neuroendocrine challenge, influences the peptide's expression. Messenger RNA levels of corticotropin-releasing hormone in hippocampal CA1, CA3 and the dentate gyrus, as well as in the hypothalamic paraventricular nucleus, were determined after cold, a physiological challenge that activates the hypothalamic pituitary adrenal system in immature rats, and after activation of hippocampal neurons by hyperthermia. These studies demonstrated that, while cold challenge enhanced corticotropin-releasing hormone messenger RNA levels in the hypothalamus, hippocampal expression of this neuropeptide was unchanged. Secondly, hyperthermia stimulated expression of hippocampal immediate-early genes, as well as of corticotropin-releasing hormone. Finally, the mechanism of hippocampal corticotropin-releasing hormone induction required neuronal stimulation and was abolished by barbiturate administration.Taken together, these results indicate that neuronal stimulation may regulate hippocampal corticotropin-releasing hormone expression in the immature rat, whereas the peptide's expression in the hypothalamus is influenced by neuroendocrine challenges. Keywordshippocampus; corticotropin-releasing factor; c-fos; rat; hypothalamus; stress Corticotropin-releasing hormone (CRH) is a peptide with both neuroendocrine and neurotransmitter properties. 57 The neuroendocrine effects of CRH, the key mediator of the stress response, originate from clusters of peptidergic cells in the hypothalamic paraventricular nucleus (PVN). 24,34 CRH also functions as a neuromodulator in a number of NIH Public Access Author ManuscriptNeuroscience. Author manuscript; available in PMC 2011 July 5. NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript limbic and autonomic brain circuits. 21,22,24,43 CRH-producing neurons are widely but specifically distributed in the brain, 49 including a substantial CRH-expressing neuronal population located in the central nucleus of the amygdala (ACe), 22,53 a region considered as a major source for extra-endocrine CRH-mediated neurotransmission. 24 Abundant target neurons for CRH, expressing cognate receptors, have been demonstrated in the hippocampus. 2,13,15 In addition, physiological effects of CRH on hippocampal neuron...

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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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Restraint stress increases corticotropin-releasing hormone mRNA content in the amygdala and paraventricular nucleus

Cited by 203 publications

References 16 publications

Neurobiology of the stress response early in life: evolution of a concept and the role of corticotropin releasing hormone

Neurobiology of the stress response early in life: evolution of a concept and the role of corticotropin releasing hormone

Neuronal activity and stress differentially regulate hippocampal and hypothalamic corticotropin-releasing hormone expression in the immature rat

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

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