Chronic corticosterone treatment increases the endocannabinoid 2-arachidonylglycerol in the rat amygdala

Hill, Matthew N.; Ho, W-S Vanessa; Meier, Sarah E.; Gorzalka, Boris B.; Hillard, Cecilia J.

doi:10.1016/j.ejphar.2005.10.058

Cited by 38 publications

(30 citation statements)

References 19 publications

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“…Chronic homotypic stress, including restraint and social defeat, reliably elevates 2-AG content in the amygdala (Hill et al, 2010b;Patel et al, 2005bPatel et al, , 2009Rademacher et al, 2008), mPFC (Dubreucq et al, 2012;Patel et al, 2005b;Rademacher et al, 2008), hypothalamus (Dubreucq et al, 2012;Patel et al, 2004), and hippocampus (Dubreucq et al, 2012). Consistent with what was seen with AEA, the increased 2-AG content observed following chronic homotypic stress is largely recapitulated by exposure to chronic corticosterone in the hippocampus (Bowles et al, 2012), amygdala (Hill et al, 2005a;Gray et al, unpublished data), and mPFC (Gray et al, unpublished data). One report has demonstrated that chronic stress results in a reduction of MAGL expression at the membrane within the amygdala (where it would most efficiently metabolize 2-AG), suggesting that reduced hydrolysis may account for the increased 2-AG contents seen following chronic homotypic stress (Sumislawski et al, 2011).…”

Section: Effects Of Chronic Stress On 2-ag Brain Levelssupporting

confidence: 67%

Neurobiological Interactions Between Stress and the Endocannabinoid System

Morena

Patel

Bains

et al. 2015

Neuropsychopharmacol

514

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: Effects Of Chronic Stress On 2-ag Brain Levelssupporting

confidence: 67%

Neurobiological Interactions Between Stress and the Endocannabinoid System

Morena

Patel

Bains

et al. 2015

Neuropsychopharmacol

514

496

View full text Add to dashboard Cite

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“…Furthermore, we have found that exposure of male mice to 21 days of chronic, unpredictable stress produces a significant decrease in CB 1 receptor mRNA in the hippocampus (Hillard et al, 2006). However, it should be noted that glucocorticoid regulation of CB 1 receptor expression is not ubiquitous throughout the CNS; we have recently demonstrated that the same corticosteroid regimen employed in this study does not affect CB 1 receptor density in the amygdala (Hill et al, 2005a) and a recent study has suggested that glucocorticoids increase CB 1 receptor density in the spinal cord (Wang et al, 2007). Repeated corticosterone treatment did not affect hippocampal content of the endocannabinoids AEA and 2-AG.…”

Section: Discussionmentioning

confidence: 82%

“…However, in vitro studies have demonstrated that bath perfusion of glucocorticoids increases contents of both 2-AG and AEA in hypothalamic slices (Di et al, 2005). The only in vivo data to date examining the effect of glucocorticoid administration on endocannabinoid content has been a recent study from our group demonstrating that repeated administration of corticosterone results in an increase in 2-AG content in the amygdala (Hill et al, 2005a). The aim of the current study was to characterize the effects of acute and prolonged corticosteroid treatment on the hippocampal endocannabinoid system.…”

Section: Introductionmentioning

confidence: 95%

Prolonged glucocorticoid treatment decreases cannabinoid CB₁ receptor density in the hippocampus

Hill

Carrier

et al. 2007

Hippocampus

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Experimental studies indicate a bidirectional, functional relationship between glucocorticoids and the endocannabinoid system; however, the effects of repeated glucocorticoid treatment on the endocannabinoid system have not been examined. In this study, we treated male rats with either a single dose or a 21-day course of treatment with corticosterone (20 mg/kg) and measured hippocampal cannabinoid CB(1) receptor expression and endocannabinoid content. The 21-day, but not the single, administration of corticosterone significantly reduced both the binding site density and amount of protein of the hippocampal cannabinoid CB(1) receptor without affecting affinity for the CB(1) receptor agonist, [(3)H]CP55940. With regard to hippocampal endocannabinoid content, acute corticosterone treatment resulted in a significant reduction in anandamide but did not affect 2-arachidonylglycerol, while repeated corticosterone treatment did not alter content of either anandamide or 2-arachidonylglycerol. These data support the hypothesis that the cannabinoid CB(1) receptor is under negative regulation by glucocorticoids in the hippocampus, and suggest that hippocampal cannabinoid CB(1) receptor signaling could be reduced under conditions associated with hypersecretion of glucocorticoids, such as chronic stress.

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“…Glucocorticoids, in turn, secreted in response to stressful experiences, rapidly increase endocannabinoid release in the hypothalamic supraoptic nucleus and paraventricular nucleus (23,60). Hill et al (24) have further shown that chronic corticosterone treatment increases the levels of the endocannabinoid 2-AG in the rat amygdala. Such findings suggest that glucocorticoids might enhance memory consolidation at least in part by stimulating endocannabinoid neurotransmission.…”

Section: Discussionmentioning

confidence: 96%

“…In particular, it has been shown that within minutes after their administration, glucocorticoids facilitate endocannabinoid production and release in specific hypothalamic regions regulating hypothalamic-pituitary-adrenocortical axis activity (23,24). Such interactions are of interest in light of growing evidence that glucocorticoids, in addition to inducing slow effects on gene transcription, also have a variety of rapid physiological actions (25).…”

mentioning

confidence: 99%

Endocannabinoids in the rat basolateral amygdala enhance memory consolidation and enable glucocorticoid modulation of memory

Campolongo

Roozendaal

Trezza

et al. 2009

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

266

209

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Chronic corticosterone treatment increases the endocannabinoid 2-arachidonylglycerol in the rat amygdala

Cited by 38 publications

References 19 publications

Neurobiological Interactions Between Stress and the Endocannabinoid System

Neurobiological Interactions Between Stress and the Endocannabinoid System

Prolonged glucocorticoid treatment decreases cannabinoid CB₁ receptor density in the hippocampus

Endocannabinoids in the rat basolateral amygdala enhance memory consolidation and enable glucocorticoid modulation of memory

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Chronic corticosterone treatment increases the endocannabinoid 2-arachidonylglycerol in the rat amygdala

Cited by 38 publications

References 19 publications

Neurobiological Interactions Between Stress and the Endocannabinoid System

Neurobiological Interactions Between Stress and the Endocannabinoid System

Prolonged glucocorticoid treatment decreases cannabinoid CB1 receptor density in the hippocampus

Endocannabinoids in the rat basolateral amygdala enhance memory consolidation and enable glucocorticoid modulation of memory

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Product

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Prolonged glucocorticoid treatment decreases cannabinoid CB₁ receptor density in the hippocampus