Indeed, relative to bLRs, bHRs also had a greater proportion of dopamine D2(high) receptors, the functionally active form of the receptor, in the striatum, in spite of lower D2 mRNA levels and comparable total D2 binding. In addition, fast-scan cyclic voltammetry revealed that bHRs had more spontaneous dopamine ‘release events’ in the core of the nucleus accumbens than bLRs. Thus, bHRs exhibit
parallels to ‘externalizing disorders’ in humans, representing a genetic animal model of addiction vulnerability associated with a propensity to attribute incentive salience to reward-related cues, behavioral disinhibition, Akt activator and increased dopaminergic ‘tone.’ Neuropsychopharmacology (2010) 35, 388-400; doi: 10.1038/npp.2009.142; published online 30 September 2009″
“Objective: Although anoxia/reoxygenation of cultured cells has been used to model lung ischemia-reperfusion injury, this does not accurately mimic events experienced by lung cells while a lung is retrieved from a donor, stored, and transplanted. We developed an in vitro model of nonhypoxic ischemia-reperfusion injury to simulate these events.
Methods: Human umbilical vein endothelial cells underwent simulated cold ischemia by replacing 37 degrees C culture media with 4 degrees C Perfadex (Vitrolife,
Kungsbacka, Sweden) solution for 5 hours in 100% O(2). Culture dishes were allowed to warm to room temperature for 1 hour (implantation), and then Perfadex solution was replaced with 37 degrees C culture media (reperfusion).
Results: During cold ischemia, the selleck chemical human umbilical vein endothelial cell filamentous actin cytoskeleton quickly became rearranged, and gaps developed in the previously confluent monolayer occupying 20% of
the surface area. Simulated reperfusion resulted in reorganization to a confluent monolayer. Development of gaps was not due to enhanced necrosis based on lactate dehydrogenase Tariquidar nmr retention assay. Endothelial cytoskeletal rearrangement could account for early edema caused by ischemia-reperfusion injury with reperfusion. Mitogen-activated protein kinase and nuclear factor kappa B activation occurred with simulated reperfusion despite normoxia. Levels of the proinflammatory cytokines interleukin 6 and interleukin 8 were significantly increased in media at the end of reperfusion.
Conclusions: Exposing human umbilical vein endothelial cells to simulated cold ischemia without hypoxia causes reversible cytoskeletal alterations, activation of inflammatory pathways, and elaboration of cytokines. Because this model accurately depicts events occurring during lung transplantation, it will be useful to explore mechanisms regulating lung cell response to this unique form of ischemia-reperfusion injury.”
“A single exposure to psychostimulants or morphine is sufficient to induce persistent locomotor sensitization, as well as neurochemical and electrophysiological changes in rodents.