The dopamine neurons projecting from the VTA to the nucleus accumbens are believed to play an important role in "reward". Some investigators believe that when you experience pleasurable events, you can thank dopamine release in the nucleus accumbens for the reward experience. Cocaine and amphetamine both elevate dopamine levels in the nucleus accumbens and other dopamine target regions in the brain. It is believed that the powerfully-reinforcing and rewarding properties of cocaine and amphetamine are due to this increase in brain dopamine activity. Of course, dopamine neurons did not evolve to mediate cocaine reward, but presumably evolved to mediate the reinforcing effects of natural rewards, such as food, water and sex. Drugs like cocaine and amphetamine presumably produce their reward effects by artificially tapping into this neuronal system that evolved to mediate natural reward processes.
Other investigators are more conservative, and point out that most of our knowledge about dopamine function comes from studies in rats. Since the rat cannot directly tell us when he/she is experiencing pleasure, we know only that when dopamine activity is disrupted, normally rewarding events (food, water, sex, cocaine, amphetamine) seem to lose their reinforcing properties (that is, the ability to cause a repetition in the behavior that preceded their occurrence). For example, teach a rat to press a lever in order to receive food. Later, administer a drug that blocks dopamine receptors in the brain (a dopamine antagonist). After initially pressing the lever for food, the rat soon gives up pressing, as if the food were no longer reinforcing.
Dopamine neurons projecting to the striatum are implicated in motor functions. A loss of these "nigrostriatal" dopamine neurons is the cause of Parkinson's disease (tremors, rigid movements, difficulty initiating movements). As you might imagine, a rat under the influence of a dopamine antagonist drug is likely to show some impairment in its ability to perform operant responses, like lever-pressing. Therefore, if the rat under the influence of a dopamine-blocking drug stops lever-pressing for food, it is difficult to determine whether this is because the food has lost its reinforcing propertes or whether it is because it is now more difficult to perform the operant response. For an experimental methodology to disentangle these reward and motor explanations see Representative Publications: Horvitz and Ettenberg (1989)
Dopamine and Schizophrenia Another issue in the dopamine story is that dopamine is implicated in schizophrenia. Almost all "antipsychotic" drugs prescribed for schizophrenics are dopamine antagonist drugs. Individuals who overdose on amphetamine and cocaine (dopamine agonistdrugs) often develop psychotic symptoms (hallucinations/delusions) which are indistinguishable from those of schizophrenics. Given dopamine's role in motor and reinforcement functions, why would dopamine overactivity produce schizophrenic symptoms? One strong possibility is that dopamine release to certain brain regions occurs when you are "attending" to salient events. Representative Publications: Horvitz, Stewart, and Jacobs (1997); Horvitz (2000)
An overactivity of dopamine at these sites may produce attentional abnormalities, so that stimuli which would normally be ignored are instead considered to be relevant. This is exactly what many schizophrenia researchers believe occurs in schizophrenics. Stimuli that you would normally ignore (for instance background sounds that you are ignoring as you read this discussion, or were ignoring) are not filtered-out in schizophrenics. These "irrelevant" events enter consciousness as salient events, and delusional schemes are developed to "explain" the significance of these events.
If you were to start from the bridge of your nose, and move backwards into the brain, you would find the two neighboring sites where most brain dopamine neurons originate, the substantia nigra (SN) and the ventral tegmental area (VTA). The dopamine neurons originating in the VTA send their axons to the prefrontal cortex (an area implicated in attention and working memory) and to the nucleus accumbens (associated with motivational functions). The dopamine neurons in the SN project to the striatum (associated with motor function).