Endocannabinoidsenhance hK(V)7.1/KCNE1 channel function and shorten the cardiac action potential and QT interval. Genotype-positive patients who suffer from the cardiac channelopathy Long QT Syndrome (LQTS) may display a spectrum of clinical phenotypes, with often unknown causes. Therefore, there is a need to identify factors influencing disease severity to move towards an individualized
Endocannabinoid-Enhanced “Liking†in Nucleus Accumbens Shell Hedonic Hotspot Requires Endogenous Opioid Signals Stimulating either endogenous cannabinoids or opioids within a restricted dorsomedial "hedonic hotspot" in nucleus accumbens (NAc) shell enhances hedonic impact, or "liking" reactions to sweet tastes. In this study, we probed within this hotspot the relationship between
Distinct neuronal activation patterns are associated with PCP-induced social withdrawal and its reversal by the endocannabinoid-enhancing drug URB597 The fatty acid amide hydrolase inhibitor, URB597, an endocannabinoidenhancing drug, reverses social withdrawal in the sub-chronic PCP rat model of schizophrenia, but reduces social interaction (SI) in controls. To identify the anatomical substrates
that inducible nitric oxide synthase activity and mRNA are significantly upregulated in the rat hippocampus following just 4 hours of restraint stress. Similar to nitric oxide, endocannabinoids are synthesized on demand, with preclinical observations suggesting that cannabinoid receptor agonists and endocannabinoidenhancers inhibit nitrergic activity. Specifically, previous work has shown that enhancement
. Both endocannabinoidsenhanced responses to non-nociceptive stimuli and reduced responses to nociceptive stimuli. These pro- and anti-nociceptive effects were blocked by co-injection of a TRPV channel inhibitor, which are thought to function as an endocannabinoid receptor. In experiments to determine the effects of endocannabinoids on animals that had undergone injury-induced sensitization, 2-AG
is a key aspect of social functioning that is thought to be disrupted in ASD. Therefore, as a proof of principle for the core component of ASD-social impairment-we tested an endocannabinoid-enhancing compound on two widely studied mouse models of ASD, the BTBR and (model of Syndrome). We used the established three-chambered social approach test. We specifically increased the activity of anandamide
considered to be eligible for the review if they were original articles, they reported a quantitative or qualitative relation between cannabinoid ligands, their receptors, and immune system, and they were carried out in vitro or in mammals, included humans. All the information was systematically extracted and evaluated. We identified 122 articles from 446 references. Overall, endocannabinoidsenhanced
this gap, the purpose of this study is to explore the impact of oral PEA, a non-psychoactive endocannabinoidenhancer with little to no side effects, to alter pain related biomarkers. Our central hypothesis is that PEA will alter pain related protein signatures, inflammatory markers, and neurophysiological changes in adults with KOA pain.The investigators propose a crossover clinical trial of 20 adults
perception of bitter stimuli.Other physiological factors such as, hypothalamic and mesolimbic endocannabinoids, enhance appetite by stimulating neurochemical pathways underlying both homeostatic and rewarding aspects of food intake. Endocannabinoids are involved in food-related reward mechanisms, and there are increasing evidence that these mechanisms are dysregulated in AN patients. Moreover, functional