Skip to contentSkip to filters

We use cookies for analytics.

Topic: fatty acid amide hydrolase

ePoster
3 ePosters

In Neuroscience

Autism spectrum disorder (ASD) is associated with immune alterations and neuroinflammation. Increasing endocannabinoid tone attenuates ASD-related behavioural changes in rodent models and modulates Toll-like receptor (TLR)-induced neuro-immune responses. This study examined the effect of TLR3 activation, in the presence or absence of a fatty acid amide hydrolase (FAAH) inhibitor, on neuroinflammatory gene expression and endocannabinoid levels, in a preclinical rodent model of ASD. Female Sprague-Dawley rats prenatally exposed to either saline or valproic acid (VPA) received 1) the TLR3 agonist

ePoster · Neuroscience

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

Targeting the dysfunctional endocannabinoid system in Gulf War Illness

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

ePoster · Neuroscience