Neurochemical effects of the endocannabinoid uptake inhibitor UCM707 in various rat brain regions

Cannabinoid CB1 and Cholecystokinin CCK2 Receptors Modulate, in an Opposing Way, Electrically Evoked [3H]GABA Efflux from Rat Cerebral Cortex Cell Cultures: Possible Relevance for Cortical GABA Transmission and Anxiety

“…In view of this, it can be hypothesized that under the present experimental conditions, eCB efflux is quite independent from the eCB transporter, thus explaining the effect of UCM707. In line with this, several reports reported an increase of anandamide effects after the treatments with eCB transporter inhibitors (Ortega-Gutiérrez et al, 2005;de Lago et al, 2007;Hasanein and Javanmardi, 2008).…”

Mechanisms of TNFα-induced cardiac dysfunction in cholestatic bile duct-ligated mice: Interaction between TNFα and endocannabinoids

“…Cardiomyocytes were incubated in storage solution (Tyrode solution containing 1.1 mM CaCl2 and bovine serum albumin 50 mg/ml, pH 7.4, at 30 °C) with vehicle (mouse IgG), TNFα (200 pg/ml), UCM707 (3 × 10 −6 M), AM251 (10 −6 M). In sham-V mice, cell contraction, and relaxation were measured after acute incubation with TNFα, TNFα + UCM707, AM251, and TNFα + AM251 for 30 min [18,19]. …”

“…Protein expression of cardiac NFκBp65, JNK, p38MAPK, iNOS, and Cu/Zn-SOD were quantified as previously described [15,18,20]. G3PDH (glyceraldehydes-3-phosphate dehydrogenase) expression was used as an internal control.…”

“…Cardiac TNF α, NFκB p65 , p38MAPK β, p38MAPK α, and ERK1 mRNA transcription was measured by semi-quantitative RT-PCR as in previous studies [15,18,20]. G3PDH served as an internal control.…”

In it together? The case for endocannabinoid–noradrenergic interactions in fear extinction

“…Acute AEA or WIN55,212–2 treatment increased NA levels in the DH ex vivo, and the latter effect was CB1R‐dependent (Hao et al., 2000; Moranta et al., 2004, 2006). Another study found that subchronic treatment with the eCB transport inhibitor UCM707 had no effect on ex vivo NA levels in the DH or amygdala (de Lago et al, 2007). URB597 alone had no effect on NA efflux from the BLA in vivo, but it did potentiate stress‐induced NA release in this area (Bedse et al., 2015).…”