Pharmacological inhibition of endocannabinoid degradation modulates the expression of inflammatory mediators in the hypothalamus following an immunological stressor

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

“…All the effects observed were not paralleled by significant changes in circulating CORT levels, which were however sensitive to the stress procedure, as previously reported in the literature . This result is in agreement with several previous findings showing that acute systemic administration of URB597 ( Figure 1B) does not affect stress-induced CORT levels in plasma (Hill et al, 2010b;Kerr et al, 2012;Roberts et al, 2014;. However, to our knowledge, there is only one paper reporting a decrease of CORT secretion in mice subjected to restraint-stress (Patel et al, 2004).…”

“…The discrepancy with more recent studies was in part justified by some authors as a consequence of the different time points for blood sampling (Kerr et al, 2012). We hypothesize that it might be due to different types of stress used in the experiments.…”

Minocycline modulates neuropathic pain behaviour and cortical M1–M2 microglial gene expression in a rat model of depression

“…TaqMan gene expression assays (Applied Biosystems, UK) were used to quantify the genes of interest: cluster of differentiation molecule 11b (CD11b; Rn00709342_m1), CD68 (Rn01495634_g1), MRC2 (mannose receptor, Rn01456616_m1), Interleukin-1β (IL-1β; Rn00580432_m1), tumour necrosis factor-α (TNFα, Rn99999017_m1), IL-6 (Rn00561420_m1), IL-10 (Rn00563409_m1), SOCS3 (Rn00585674_s1) and IL-1 receptor antagonist (IL-1ra, Rn00573488_m1). RT-PCR was performed using an ABI Prism 7500 instrument (Applied Biosystems, UK), as previously described (Burke et al, 2013a, Kerr et al, 2013, Kerr et al, 2012, Burke et al, 2013b. β-actin (Rn00667869_m1) was used as an endogenous control and to normalise gene expression data.…”

Protective Action of Anandamide and Its COX-2 Metabolite against L-Homocysteine-Induced NLRP3 Inflammasome Activation and Injury in Podocytes

“…Several laboratories have reported inhibitory effects on inflammation and associated diseases and pathologic phenomena by elevating endogenous AEA levels through different approaches, including fatty acid amide hydrolase gene KO (Naidu et al, 2010;Kinsey et al, 2011;Wang et al, 2015), fatty acid amide hydrolase inhibitors (Kinsey et al, 2011;Schuelert et al, 2011;Booker et al, 2012;Caprioli et al, 2012;Kerr et al, 2012;Murphy et al, 2012;Sasso et al, 2012;Krustev et al, 2014;Sałaga et al, 2014;Tchantchou et al, 2014), and AEA reuptake inhibitors (Mestre et al, 2005;D'Argenio et al, 2006). Further studies are needed to address whether such approaches are also protective in glomerular injury associated with hHcys.…”