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There were no statistical differences seen in body mass, BMI, or lean body mass (LBM). This information has led to an increased interest as to whether or not CLA would have the same effects in humans . The primary emphasis was on pertinent articles based on human trials involving overweight subjects that were performed in a randomized and placebo-controlled process. In addition, patients often do not perceive a need to seek the assistance of a healthcare professional with these alternative therapies, and they also may be an alternative to previously failed attempts with conventional approaches . To date, there is little clinical evidence to support their use. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. 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To test whether disrupting endocannabinoid signaling decreases drug-induced phasic dopamine events, Cheer et al. (2007) monitored drug-induced increases in phasic dopamine release events in the nucleus accumbens shell using fast-scan cyclic voltammetry. All drugs of abuse increase phasic dopamine events, which theoretically promote drug seeking (Cheer et al. 2007; Aragona et al. 2008). Endocannabinoids binding to presynaptic cannabinoid CB1 receptors is known to result in the suppression of GABA-mediated inhibition (Wilson and Nicoll 2001), a form of synaptic plasticity known as depolarization-induced suppression of inhibition (Alger and Kim 2011). Once synthesized, endocannabinoids traverse the plasma membrane into the extra-synaptic space, where they retrogradely activate cannabinoid CB1 receptors on presynaptic terminals (Wilson and Nicoll 2001). 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