Role of the basolateral amygdala in mediating the effects of the fatty acid amide hydrolase inhibitor URB597 on HPA axis response to stress

Bedse, Gaurav; Colangeli, Roberto; Lavecchia, Angelo Michele; Romano, Adele; Altieri, Fabio; Cifani, Carlo; Cassano, Tommaso; Gaetani, Silvana

doi:10.1016/j.euroneuro.2014.07.005

Cited by 45 publications

(31 citation statements)

References 58 publications

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“…Consistent with this hypothesis, acute administration of a CB1 receptor antagonist evokes a limited and specific pattern of neuronal activation in the brain, of which the BLA is one of the most prominent sites of activity, in addition to the PVN (Newsom et al, 2012;Patel et al, 2005a;Singh et al, 2004). More so, global or intra-BLA inhibition of AEA-hydrolysis dampens stress-induced activation of the HPA axis (Bedse et al, 2014;Hill et al, 2009c;Patel et al, 2004). In fact, the ability of systemic administration of a FAAH inhibitor to dampen neuronal activation within the PVN is completely reversible by local CB1 receptor antagonism within the BLA (Bedse et al, 2014), indicating that elevations of AEA signaling within the BLA are capable of attenuating stress-induced activation of the HPA axis, likely through a trans-synaptic relay from the BLA to the PVN.…”

Section: Functional Role Of Ecb Signaling In the Neurobiological Effementioning

confidence: 52%

“…Interestingly, at least with respect to consolidation, the role of eCB signaling, while downstream of glucocorticoids, is upstream of norepinephrine, as modulation of eCB signaling did not block the effects of beta-adrenoreceptor activation on enhancing memory consolidation (Atsak et al, 2014). More so, FAAH inhibition has been found to increase norepinephrine levels within the amygdala in response to stress (Bedse et al, 2014), suggesting that the effects of eCB signaling are upstream of norepinephrine release. Collectively, these findings suggest that glucocorticoids rapidly recruit eCBs in the BLA to increase the sensitivity of pyramidal neurons to the memory-enhancing effects of norepinephrine (McIntyre et al, 2002;Quirarte et al, 1997).…”

Section: Functional Role Of Ecb Signaling In the Neurobiological Effementioning

confidence: 99%

“…More so, global or intra-BLA inhibition of AEA-hydrolysis dampens stress-induced activation of the HPA axis (Bedse et al, 2014;Hill et al, 2009c;Patel et al, 2004). In fact, the ability of systemic administration of a FAAH inhibitor to dampen neuronal activation within the PVN is completely reversible by local CB1 receptor antagonism within the BLA (Bedse et al, 2014), indicating that elevations of AEA signaling within the BLA are capable of attenuating stress-induced activation of the HPA axis, likely through a trans-synaptic relay from the BLA to the PVN. As such, these data would indicate that AEA is a regulatory signal within the BLA that suppresses activation of the HPA axis by gating BLA to PVN communication.…”

Section: Functional Role Of Ecb Signaling In the Neurobiological Effementioning

confidence: 99%

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Neurobiological Interactions Between Stress and the Endocannabinoid System

Morena

Patel

Bains

et al. 2015

Neuropsychopharmacol

510

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: Functional Role Of Ecb Signaling In the Neurobiological Effementioning

confidence: 52%

Section: Functional Role Of Ecb Signaling In the Neurobiological Effementioning

confidence: 99%

Section: Functional Role Of Ecb Signaling In the Neurobiological Effementioning

confidence: 99%

See 1 more Smart Citation

Neurobiological Interactions Between Stress and the Endocannabinoid System

Morena

Patel

Bains

et al. 2015

Neuropsychopharmacol

510

496

View full text Add to dashboard Cite

show abstract

“…1) due to a rapid induction of the AEA degradative enzyme fatty acid amide hydrolase (FAAH) and FAAH-mediated AEA hydrolysis, which suggests that the tonic eCB inhibition of the BLA is exerted by AEA (Hill et al, 2009). Intra-BLA administration of a FAAH inhibitor attenuates activation of the HPA axis via increased CB 1 receptor activation, since it was blocked by inhibiting CB 1 receptors (Bedse et al, 2014). It was recently shown that this rapid induction of FAAH in the BLA is mediated by a stress-induced increase in CRH levels (Gray et al, 2015).…”

Section: Acute Stress Regulation Of Endocannabinoids and The Hpa Axismentioning

confidence: 98%

Endocannabinoid Regulation of Neuroendocrine Systems

Tasker

Chen

Fisher

et al. 2015

International Review of Neurobiology

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“…It is possible that amygdala 2-AG is regulating physiological and behavioral variables sensitive to adaptation other than the HPA axis. Second, the apparently discrepant results sometimes obtained when studying the role of eCBs under non-stress versus stress conditions (Bedse et al, 2014;Ganon-Elazar and Akirav, 2009;Campos et al, 2010) suggest a complex role of eCBs that needs to be fully explored.…”

Section: Discussionmentioning

confidence: 95%