Mechanisms of addiction The<unk>  and a specific set of the pathway's output neurons (e.g. D1-type medium spiny neurons within the nucleus accumbens) play a central role in the neurobiology of addiction. Drug addiction is an illness caused by habitual substance use that induces chemical changes in the brain's circuitry. Common addictive substances such as cocaine, alcohol, and nicotine have been shown to increase extracellular levels of dopamine within the<unk> , preferentially within the nucleus accumbens. The mechanisms by which these drugs do so vary depending on the drug prototype. For example, cocaine precludes the re-uptake of synaptic dopamine through blocking the presynaptic dopamine transporter. Another stimulant, amphetamine, promotes increased dopamine from the synaptic vesicles. Non-stimulant drugs typically bind with ligand-gated channels or G protein-coupled receptors. Such drugs include alcohol, nicotine, and tetrahydrocannabinol (THC). These dopaminergic activations of the<unk>  are accompanied by the perception of reward. This stimulus-reward association shows a resistance to extinction and creates an increased motivation to repeat that same behavior that caused it. In relation, a 2017 study found that abusive (emotional, physical, and sexual) and adverse life events were associated with a heightened limbic response to cocaine. In other words, individuals who had previously suffered abuse were more likely to have a brain pathway primed for cocaine or drug use. Relation to neurological and psychological disorders The<unk>  is implicated in schizophrenia, depression, and Parkinson's disease. It is also theorized to be implicated in overuse of digital media, although it could simply be a consequence of a sedentary lifestyle. Each involves distinct structural changes within the<unk> .
Mesolimbic pathway
Tuberoinfundibular pathway
Amygdalofugal pathway
Mesocortical pathway
Hypothalamotegmental tract
Limbic system
Endocannabinoid system
Ciliospinal center