ePoster · Neuroscience
Francis Bambico, Andrew MacPherson, Tadhg Strand, Gavin Afonso, Courtney Clarke, Shannon Waye, Nageeb Hasan, Caio Oliveira, Matheus Cravatti, Jose Nobrega · FENS Forum 2024
A cognitive model of stress posits that psycho-affective disorders can arise from a perceived lack of stress control. Uncontrollability is linked to perturbed prefrontocortical (PFC)-limbic signalling of endocannabinoids (anandamide) and altered hormonal activity (prolactin and glucocorticoids). Behavioural therapies such as cognitive-behavioural/remediation therapies ameliorate symptoms by enhancing perceived controllability. There is also evidence that augmenting endocannabinoid and hormonal levels results in antidepressant/anti-stress action. Based on a modified version of the rodent Morris
ePoster · Neuroscience
Anna Portugalov, Irit Akirav · FENS Forum 2024
Introduction: Early life stress (ELS) significantly increases predisposition to depression. Here, we examined whether the restoring effects of treatment with the fatty acid amide hydrolase (FAAH) inhibitor URB597, which elevates anandamide levels, are associated with alterations in microRNAs (miRNAs) related with depression and whether specific miRNAs have a crucial role in the antidepressant-like effect of URB597. Methods: In experiment 1, male rats were exposed to ELS using the "Limited Bedding and Nesting" paradigm from postnatal day (P)7 to P14. During P45 to P60 (late-adolescence), URB59
ePoster · Neuroscience
Kwang-Mook Jung, Erica Squire, Hye-Lim Lee, Daniele Piomelli, Vipan Parihar · FENS Forum 2024
An estimated one-third of American veterans of the 1991 Gulf War continue to experience multiple unexplained health problems known as Gulf War Illness (GWI). GWI is a chronic disorder that is characterized by persistent and heterogeneous symptoms including but not limited to anxiety, pain, fatigue, and cognitive impairment. In the current study, we hypothesized that exposure to toxic chemicals during the Gulf War (GW) may produce a long-lasting disruption in the endocannabinoid (ECB) system, one of the brain’s endogenous anti-inflammatory mechanisms, leading to dysregulated microglial activati