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Regardless, based on previous findings of increased cytosolic Ca 2+ by nicotine, it is possible to hypothesize that such increases in [Ca 2+ ] i trigger mitochondrial Ca 2+ uptake, especially if with chronic nicotine exposure, mitochondrial localization toward the plasma membrane or the ER would allow for rapid uptake of Ca 2+ influx or intracellular release, respectively

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You might remember that the Prefrontal Cortex is the place in the brain that the reward pathway terminates (see Figure 1.9)

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