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Drug Addiction Brain

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The definition of a drug addiction is the loss of control over the intense urges to take the drug even at the expense of adverse consequences (Volkow & Li, 2005). The drugs are used multiple mechanisms like positive reward, inhibitory control, and executive function to modulate the brain functions. In this paper, I am going to examine how addictive drugs alter the brain function and result in mediating our behaviors.
The primary function of the brain is to monitor the external and internal environment of the individual, then respond to an unconscious and/or conscious level. However, our body requires more complex works for a living. What are the fundamental concepts of how the nervous system mediates behavior? The brain does not work independently …show more content…
The main question about the drug addiction is that how chronic drug use affects the function of the brain and how this leads to the aberrant behavioral manifestations of addiction (Volkow & Li, 2005). Surprisingly, a desire of drug-intake is motivated with drug reward like needs of water when thirsty except that the natural reward does not have the characteristic of compulsiveness, persistent, and loss of control (Stewart and Wise, 1992). Given with the reward hypothesis, most of the recent studies of addictive behavior in neurobiology examined the circuits of the reward system.
Goldstein and Volkow (2002) conducted the study about the underlying neurobiological basis of drug addiction with the method of neuroimaging. They found that the anatomical core of the reward system is dopaminergic neurons of the ventral tegmentum area (VTA) that project to the nucleus accumbens (NAc), amygdala, prefrontal cortex (PFC) and other forebrain structures. Several of those structures may be specifically involved in the reward produced by different substances which means that not only the dopamine is the conductor but the other monoamines and acetylcholine may also …show more content…
The recent discovery of CART peptides may importantly expand our knowledge about the neurochemistry of reward. Natural rewarding activities and artificial chemical rewarding stimuli act at the same locations, but while natural activities are controlled by feedback mechanisms that activate aversive centers, no such restrictions bind the responses to artificial stimuli (Vetulani, 2001). Endocannabinoids are synthesized postsynaptically and act as retrograde signals to regulate presynaptic transmitter release. The receptors, targets for THC, play an important role in use/abuse of marijuana (Everitt & Heberlein, 2013). Addictive drugs alter synaptic plasticity in the VTA through a common mechanism. Addictive drugs such as cocaine induce synaptic plasticity in the ventral tegmental area and its projection areas, which may represent the cellular correlate of an addiction trace. Cocaine induces changes in excitatory transmission primarily in the VTA. Specific synaptic and cellular changes in the NAc persist following prolonged exposure to cocaine, and this remodeling may contribute to altered behavior (Creed & Lüscher,

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