Emotional, endocrine and brain anandamide response to social challenge in infant male rats

Marco, Eva M.; Scattoni, María Luisa; Rapino, Cinzia; Ceci, Chiara; Chaves, Nicole; Macrı̀, Simone; Maccarrone, Mauro; Laviola, Giovanni

doi:10.1016/j.psyneuen.2013.04.004

Cited by 20 publications

(17 citation statements)

References 68 publications

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“…Similarly, in the hippocampus, acute restraint stress increases FAAH protein levels 24 h after the stress exposure (Navarria et al, 2014). Interestingly, this effect appears to be conserved throughout the lifespan as early life stress in the form of maternal separation has also been shown to reduce AEA content within the hippocampus (Marco et al, 2013). Unlike the consistency seen in the amygdala and hippocampus, the mPFC seems to be somewhat of a more complex structure as exposure to swim stress has been found to produce a robust reduction of AEA content (McLaughlin et al, 2012), but neither acute restraint (Gray et al, 2015;Hill et al, 2011b;Rademacher et al, 2008) nor acute social defeat (Dubreucq et al, 2012) were found to have any effect on AEA content in the mPFC.…”

Section: Effects Of Acute Stress On Aea Brain Levelsmentioning

confidence: 95%

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: Effects Of Acute Stress On Aea Brain Levelsmentioning

confidence: 95%

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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“…Thus, eCBs critically modulate both the hypothalamic-pituitary-adrenal axis and the monoamine transmission, as demonstrated through numerous anatomical, electrophysiological and in vivo behavioral studies (for reviews see [58,[60][61][62][63][64][65]). Several preclinical and clinical data strongly suggest that emotional behaviors are associated with altered levels of AEA, PEA and 2-AG, which have distinct roles in the emotion arousal, social behavior and emotionality [66][67][68][69][70][71], with their receptors and metabolic enzymes being potential targets for preventing and treating mood-related and anxiety-related disorders, particularly posttraumatic stress disorder. In particular, inhibition of AEA-degrading enzyme FAAH reduces anxiety-like behaviors [72] and facilitates long-term fear extinction and rescues deficient fear extinction in rodent models by enhancing CB 1 signaling and synaptic plasticity in the basolateral amygdala [64], whereas genetic deletion of 2-AG-degrading enzyme MAGL leads to impaired CB 1 signaling and anxiety-like behavior [73 ].…”

Section: Do Bioactive Lipids Affect Emotions?mentioning

confidence: 99%

Bioactive lipids as modulators of immunity, inflammation and emotions

Chiurchiù

Maccarrone

2016

Current Opinion in Pharmacology

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“…It is now clear that eCB system is altered in several neurodegenerative diseases and, very interestingly, that distinct elements of the eCB system in peripheral blood mirror these perturbations, providing novel and noninvasive diagnostic tools for several neuroinflammatory diseases [92,93]. In addition, the eCB system controls emotional responses [94], behavioral reactivity to context [95], and social interaction [96]. Thus, it can be hypothesized that alterations in this endogenous circuitry may contribute to the autistic phenotype.…”

Section: Alterations Of the Ecb System In Autismmentioning

confidence: 99%

Endocannabinoid Signaling in Autism

et al. 2015

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Autism spectrum disorder (ASD) is a complex behavioral condition with onset during early childhood and a lifelong course in the vast majority of cases. To date, no behavioral, genetic, brain imaging, or electrophysiological test can specifically validate a clinical diagnosis of ASD. However, these medical procedures are often implemented in order to screen for syndromic forms of the disorder (i.e., autism comorbid with known medical conditions). In the last 25 years a good deal of information has been accumulated on the main components of the Bendocannabinoid (eCB) system^, a rather complex ensemble of lipid signals (Bendocannabinoids^), their target receptors, purported transporters, and metabolic enzymes. It has been clearly documented that eCB signaling plays a key role in many human health and disease conditions of the central nervous system, thus opening the avenue to the therapeutic exploitation of eCB-oriented drugs for the treatment of psychiatric, neurodegenerative, and neuroinflammatory disorders. Here we present a modern view of the eCB system, and alterations of its main components in human patients and animal models relevant to ASD. This review will thus provide a critical perspective necessary to explore the potential exploitation of distinct elements of eCB system as targets of innovative therapeutics against ASD.Key Words Autism spectrum disorder . endocannabinoid system . fragile X syndrome . metabolic regulation . reward system The Endocannabinoid SystemTwenty-five years after the cloning and expression of a complementary DNA that encoded a G protein-coupled receptor, named type-1 cannabinoid (CB 1 ) receptor [1], there is a good deal of information on the main components of the so-called Bendocannabinoid (eCB) system^, as well as on its role in controlling cannabinergic signaling in human health and disease [2][3][4]. Anandamide (AEA) and 2-arachidonoylglycerol (2-AG) are the most active eCBs as yet identified, although this family of bioactive lipids includes other arachidonic acid (AA) derivatives with cannabimimetic properties (i.e., noladin ether, virodhamine, N-arachidonoyldopamine, to name but a few). The classical dogma that eCBs are synthesized and released Bon demand^upon (patho)physiological stimuli has been recently revisited on the basis of unexpected evidence for intracellular reservoirs and transporters of eCBs. These new entities have been shown to drive intracellular trafficking of eCBs, adding a new dimension to the regulation of their biological activity [5]. To date, several metabolic routes have B. Chakrabarti, A. Persico and N. Battista are equal first authors.

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Emotional, endocrine and brain anandamide response to social challenge in infant male rats

Cited by 20 publications

References 68 publications

Neurobiological Interactions Between Stress and the Endocannabinoid System

Neurobiological Interactions Between Stress and the Endocannabinoid System

Bioactive lipids as modulators of immunity, inflammation and emotions

Endocannabinoid Signaling in Autism

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