Limbic system mechanisms of stress regulation: Hypothalamo-pituitary-adrenocortical axis

Herman, James P.; Ostrander, Michelle M.; Mueller, Nancy K.; Figueiredo, Helmer F.

doi:10.1016/j.pnpbp.2005.08.006

Cited by 1,156 publications

(903 citation statements)

References 129 publications

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“…Although most studies suggest that heightened emotional reactivity causes hippocampal simplification and amygdalar elaboration at the neuronal level (59), there is evidence from human (61) and animal (62,63) studies that smaller hippocampal volume at baseline and laboratory-induced hippocampal lesions can precede the behavioral manifestations of hyperemotionality. Rats with hippocampal lesions, for example, exhibit behavioral changes suggestive of hyper-reactivity; are more responsive to mild stressors, including foot-shock (63) and cage relocation (62); and have increased glucocorticoid responding to aversive events (64,65). In humans harboring an underlying AD process, heightened emotional reactivity may exacerbate disease progression Mini-Mental State Examination total scores, IRI Personal Distress subscale scores, and GDS total scores are presented for each diagnostic group.…”

Section: Discussionmentioning

confidence: 99%

Heightened emotional contagion in mild cognitive impairment and Alzheimer’s disease is associated with temporal lobe degeneration

Sturm

Yokoyama

Seeley

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

145

133

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Emotional changes are common in mild cognitive impairment (MCI) and Alzheimer's disease (AD). Intrinsic connectivity imaging studies suggest that default mode network degradation in AD is accompanied by the release of an emotion-relevant salience network. We investigated whether emotional contagion, an evolutionarily conserved affect-sharing mechanism, is higher in MCI and AD secondary to biological alterations in neural networks that support emotion. We measured emotional contagion in 237 participants (111 healthy controls, 62 patients with MCI, and 64 patients with AD) with the Interpersonal Reactivity Index Personal Distress subscale. Depressive symptoms were evaluated with the Geriatric Depression Scale. Participants underwent structural MRI, and voxel-based morphometry was used to relate whole-brain maps to emotional contagion. Analyses of covariance found significantly higher emotional contagion at each stage of disease progression [controls < MCI (P < 0.01) and MCI < AD (P < 0.001)]. Depressive symptoms were also higher in patients compared with controls [controls < MCI (P < 0.01) and controls < AD (P < 0.0001)]. Higher emotional contagion (but not depressive symptoms) was associated with smaller volume in right inferior, middle, and superior temporal gyri (P FWE < 0.05); right temporal pole, anterior hippocampus, parahippocampal gyrus; and left middle temporal gyrus (all P < 0.001, uncorrected). These findings suggest that in MCI and AD, neurodegeneration of temporal lobe structures important for affective signal detection and emotion inhibition are associated with up-regulation of emotion-generating mechanisms. Emotional contagion, a quantifiable index of empathic reactivity that is present in other species, may be a useful tool with which to study emotional alterations in animal models of AD.empathy | social behavior | simulation | affective resonance P rogressive deterioration of memory and other cognitive functions characterizes Alzheimer's disease (AD) (1) and its prodromal stage, mild cognitive impairment (MCI) (2). Deposition of beta-amyloid plaques and neurofibrillary tangles, the hallmark pathological changes in AD (3), is hypothesized to begin decades before the emergence of cognitive symptoms and subsequent functional decline (4). Emotional symptoms are also common and have been found in 35-85% of patients with MCI (5-7) and up to 75% of patients with AD (8), with depression and anxiety the most frequent symptoms seen. Individuals with MCI who have comorbid emotional complaints are more likely to progress to dementia than those without such symptoms (9-13). Taken together, these studies suggest that a clinical presentation that includes both cognitive decline and emotion dysregulation may point to an underlying AD process and that emotional symptoms themselves may portend or even exacerbate disease progression (9,11,14).The medial temporal lobe is among the earliest sites of disease in MCI and AD (2, 15), and hippocampal atrophy is associated with worse episodic memory performance on standardi...

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Section: Discussionmentioning

confidence: 99%

Heightened emotional contagion in mild cognitive impairment and Alzheimer’s disease is associated with temporal lobe degeneration

Sturm

Yokoyama

Seeley

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

145

133

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“…The amygdala is involved in a wide range of emotional behavior, including social cognition 66 and the stress response, 67 which appears to be modulated by progesterone. For example, the modulation of the preference for faces during the menstrual cycle appears to be mediated by progesterone, 68,69 as well as the enhancement of the hypothalamus-pituitaryadrenal (HPA) axis response to stressors during the luteal phase.…”

Section: Discussionmentioning

confidence: 99%

Progesterone selectively increases amygdala reactivity in women

et al. 2007

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The acute neural effects of progesterone are mediated by its neuroactive metabolites allopregnanolone and pregnanolone. These neurosteroids potentiate the inhibitory actions of c-aminobutyric acid (GABA). Progesterone is known to produce anxiolytic effects in animals, but recent animal studies suggest that pregnanolone increases anxiety after a period of low allopregnanolone concentration. This effect is potentially mediated by the amygdala and related to the negative mood symptoms in humans that are observed during increased allopregnanolone levels. Therefore, we investigated with functional magnetic resonance imaging (MRI) whether a single progesterone administration to healthy young women in their follicular phase modulates the amygdala response to salient, biologically relevant stimuli. The progesterone administration increased the plasma concentrations of progesterone and allopregnanolone to levels that are reached during the luteal phase and early pregnancy. The imaging results show that progesterone selectively increased amygdala reactivity. Furthermore, functional connectivity analyses indicate that progesterone modulated functional coupling of the amygdala with distant brain regions. These results reveal a neural mechanism by which progesterone may mediate adverse effects on anxiety and mood.

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“…Most of the somatosensory and viscerosensory information is directly mediated by catecholaminergic pathways (Liposits et al 1986, Liposits et al 1987, while cortical and limbic inputs are processed through gamma-aminobutyric acid (GABA) and/or glutamatergic local circuits (Herman et al 2002, Herman et al 2005, Roland & Sawchenko 1993). …”

Section: Regulation Of Hypothalamic Crh Transcriptionmentioning

confidence: 99%

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

Kovács

2013

Journal of Chemical Neuroanatomy

105

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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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Limbic system mechanisms of stress regulation: Hypothalamo-pituitary-adrenocortical axis

Cited by 1,156 publications

References 129 publications

Heightened emotional contagion in mild cognitive impairment and Alzheimer’s disease is associated with temporal lobe degeneration

Heightened emotional contagion in mild cognitive impairment and Alzheimer’s disease is associated with temporal lobe degeneration

Progesterone selectively increases amygdala reactivity in women

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

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