From Malthus to motive: How the HPA axis engineers the phenotype, yoking needs to wants

Pecoraro, Norman C.; Dallman, Mary F.; Warne, James P.; Ginsberg, Abigail B.; Laugero, Kevin D.; Fleur, Susanne E. la; Houshyar, Hani; Gómez, Francisca; Bhargava, Aditi; Akana, Susan F.

doi:10.1016/j.pneurobio.2006.07.004

Cited by 110 publications

(88 citation statements)

References 1,055 publications

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“…The autonomic response involves stimulation of sympathetic motor and hormonal outputs via descending neural circuits originating in hypothalamic preautonomic control centers and results in the release of catecholamines within the brain and circulation. The neuroendocrine stress response is mediated by activation of the hypothalamic-pituitary-adrenal (HPA) axis, which results in an increase in circulating corticosteroids that target multiple organ systems (Pecoraro et al, 2006). Stress exposure also provokes a shift in many neurobehavioral processes, such as anxiety/vigilance, memory, reward salience, pain sensitivity, and coping behaviors (McEwen, 2012a).…”

Section: Basic Primer On Stressmentioning

confidence: 99%

Neurobiological Interactions Between Stress and the Endocannabinoid System

Morena

Patel

Bains

et al. 2015

Neuropsychopharmacol

492

496

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Stress affects a constellation of physiological systems in the body and evokes a rapid shift in many neurobehavioral processes. A growing body of work indicates that the endocannabinoid (eCB) system is an integral regulator of the stress response. In the current review, we discuss the evidence to date that demonstrates stress-induced regulation of eCB signaling and the consequential role changes in eCB signaling have with respect to many of the effects of stress. Across a wide array of stress paradigms, studies have generally shown that stress evokes bidirectional changes in the two eCB molecules, anandamide (AEA) and 2-arachidonoyl glycerol (2-AG), with stress exposure reducing AEA levels and increasing 2-AG levels. Additionally, in almost every brain region examined, exposure to chronic stress reliably causes a downregulation or loss of cannabinoid type 1 (CB1) receptors. With respect to the functional role of changes in eCB signaling during stress, studies have demonstrated that the decline in AEA appears to contribute to the manifestation of the stress response, including activation of the hypothalamic-pituitary-adrenal (HPA) axis and increases in anxiety behavior, while the increased 2-AG signaling contributes to termination and adaptation of the HPA axis, as well as potentially contributing to changes in pain perception, memory and synaptic plasticity. More so, translational studies have shown that eCB signaling in humans regulates many of the same domains and appears to be a critical component of stress regulation, and impairments in this system may be involved in the vulnerability to stress-related psychiatric conditions, such as depression and posttraumatic stress disorder. Collectively, these data create a compelling argument that eCB signaling is an important regulatory system in the brain that largely functions to buffer against many of the effects of stress and that dynamic changes in this system contribute to different aspects of the stress response.

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Section: Basic Primer On Stressmentioning

confidence: 99%

Neurobiological Interactions Between Stress and the Endocannabinoid System

Morena

Patel

Bains

et al. 2015

Neuropsychopharmacol

492

496

View full text Add to dashboard Cite

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“…When food becomes restricted to certain times of the day, the animals display an increase in activity prior to the feeding time, which continues also in the absence of food on consecutive days and is therefore generated endogenously. The presence of an independent FEO was suggested based on the observation that on such a time restricted feeding scheme, the rhythms of food anticipatory behaviour and physiology, including corticosterone secretion (Krieger et al 1977), occur even in SCN-lesioned animals (reviewed in Hiroshige et al (1991), Mistlberger (1994), Stephan (2002), Pecoraro et al (2006) and Mendoza (2007)). Some studies claim that the DMH, which we have already encountered as a major relay station for SCN input into the PVN (Fig.…”

Section: The 'Food-entrainable Oscillator' Clockmentioning

confidence: 99%

Glucocorticoids and the circadian clock

Dickmeis¹

2008

Journal of Endocrinology

412

292

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Glucocorticoids, hormones produced by the adrenal gland cortex, perform numerous functions in body homeostasis and the response of the organism to external stressors. One striking feature of their regulation is a diurnal release pattern, with peak levels linked to the start of the activity phase. This release is under control of the circadian clock, an endogenous biological timekeeper that acts to prepare the organism for daily changes in its environment. Circadian control of glucocorticoid production and secretion involves a central pacemaker in the hypothalamus, the suprachiasmatic nucleus, as well as a circadian clock in the adrenal gland itself. Central circadian regulation is mediated via the hypothalamic-pituitary-adrenal axis and the autonomic nervous system, while the adrenal gland clock appears to control sensitivity of the gland to the adrenocorticopic hormone (ACTH). The rhythmically released glucocorticoids in turn might contribute to synchronisation of the cell-autonomous clocks in the body and interact with them to time physiological dynamics in their target tissues around the day.

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“…Loss of eCB-mediated synaptic inhibition at GABA synapses after repeated immobilization stress HPA responses exhibit remarkable plasticity in response to chronic homotypic and heterotypic stress paradigms (Pecoraro et al, 2006). Although these may result from changes in eCB signaling at higher brain centers, the importance of eCBs in directly affecting synaptic function in the PVN (Di et al, 2003) led us to investigate the effects of stress on retrograde eCB signaling in PNCs.…”

Section: Activity-dependent Ecb Signaling At Gaba Synapses On Pncsmentioning

confidence: 99%

“…An acute and adaptive endocrine response to stress, through comprehensive actions of glucocorticoids (GCs), is necessary for survival and, accordingly, is widely conserved across all mammalian species (Pecoraro et al, 2006;Ulrich-Lai and Herman, 2009). The cessation of this response depends, in part, on the central actions of circulating corticosteroids (CORTs) at brain structures such as the hippocampus (Sapolsky et al, 1990;De Kloet et al, 1998), limbic forebrain (Furay et al, 2008), and the hypothalamus (Keller-Wood and Dallman, 1984).…”

Section: Introductionmentioning

confidence: 99%

Repeated Stress Impairs Endocannabinoid Signaling in the Paraventricular Nucleus of the Hypothalamus

Wamsteeker¹,

Kuzmiski²,

Bains³

2010

J. Neurosci.

130

140

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Endocannabinoids (eCBs) are ubiquitous retrograde signaling molecules in the nervous system that are recruited in response to robust neuronal activity or the activation of postsynaptic G-protein-coupled receptors. Physiologically, eCBs have been implicated as important mediators of the stress axis and they may contribute to the rapid feedback inhibition of the hypothalamic-pituitary-adrenal axis (HPA) by circulating corticosteroids (CORTs). Understanding the relationship between stress and eCBs, however, is complicated by observations that eCB signaling is itself sensitive to stress. The mechanisms that link stress to changes in synaptic eCB signaling and the impact of these changes on CORT-mediated negative feedback have not been resolved. Here, we show that repetitive immobilization stress, in juvenile male rats, causes a functional downregulation of CB 1 receptors in the paraventricular nucleus of the hypothalamus (PVN). This loss of CB 1 receptor signaling, which requires the activation of genomic glucocorticoid receptors, impairs both activity and receptordependent eCB signaling at GABA and glutamate synapses on parvocellular neuroendocrine cells in PVN. Our results provide a plausible mechanism for how stress can lead to alterations in CORT-mediated negative feedback and may contribute to the development of plasticity of HPA responses.

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From Malthus to motive: How the HPA axis engineers the phenotype, yoking needs to wants

Cited by 110 publications

References 1,055 publications

Neurobiological Interactions Between Stress and the Endocannabinoid System

Neurobiological Interactions Between Stress and the Endocannabinoid System

Glucocorticoids and the circadian clock

Repeated Stress Impairs Endocannabinoid Signaling in the Paraventricular Nucleus of the Hypothalamus

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