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Role in pleasure and motivation
Dopamine is commonly associated with the pleasure system of the brain, providing feelings of enjoyment and reinforcement to motivate us to do certain activities. Dopamine is released (particularly in areas such as the nucleus accumbens and striatum) by naturally-rewarding experiences such as food, sex, use of certain drugs and neutral stimuli that become associated with them. This theory is often discussed in terms of drugs (such as cocaine and amphetamines), which seem to be directly or indirectly related to the increase of dopamine in these areas, and in relation to neurobiological theories of chemical addiction, which argue that these dopamine pathways are pathologically altered in addicted persons. However, cocaine and amphetamine have different mechanisms of action. Cocaine is a dopamine transporter blocker: it competitively inhibits dopamine uptake to increase the lifetime of dopamine. On the other hand, amphetamines act as dopamine transporter substrates to competitively inhibit dopamine uptake and increase dopamine efflux via a dopamine transporter.
However, the idea that dopamine is the 'reward chemical' of the brain, a view held by many during early stages of its research, now seems too simple. Dopamine is released when unpleasant or aversive stimuli are encountered, so it is not associated only with 'rewards' or pleasure. Recent research has begun to examine whether or not the firing of dopamine neurons might function as a reward-prediction error signal, based on evidence that, when a reward is greater than expected, there is an increase in the firing of certain dopamine neurons (in contrast to when there is a lesser-than-expected reward, and there is a marked decrease in the firing of the same neurons). Some argue that dopamine may be involved in desire rather than pleasure.
Confusion of dopamine's role in pleasure comes from studies performed on animals. It has been shown experimentally that when the dopaminergic system of a rat is selectively abolished it will stop eating. However when the rat is force fed food it will still display the proper facial expressions which indicate whether they like or dislike it. Conversely mutant hyperdopaminergic mice show higher wanting of food but not liking.1 This research was taken to mean that dopamine mediated desire and incentive salience instead of pleasure. In humans, though, drugs that reduce dopamine activity (e.g., antipsychotics) have been shown to induce both amotivation (lack of desire) as well as anhedonia (inability to experience pleasure).2 The selective D2/D3 agonists pramipexole and ropinirole have anti-anhedonic and pro-motivational properties as measured by the Snaith-Hamilton Pleasure Scale.3 Opioid and cannabinoid transmission instead of dopamine is believed to be what modulates food reward and palatability (liking).4 This explains why animals would still have the same liking of food independent of brain dopamine concentrations. Other pleasures are likely dependent on dopamine. Libido can be increased by drugs that enhance dopaminergic functioning but not by ones that affect opioid peptides or other neurotransmitters. Sociability is also closely tied to dopamine neurotransmission. Low D2 receptor binding is found in people with social anxiety. Traits common to negative schizophrenia (social withdrawal, apathy, anhedonia) are thought to be related to a hypodopaminergic state in certain areas of the brain. In instances of bipolar mania subjects can become hypersocial as well as hypersexual. This is also believed to be due to an increase in dopamine, because it can be alleviated with dopamine blocking antipsychotics.
Other theories suggest that the crucial role of dopamine may be in predicting pleasurable activity. Related theories argue that dopamine function may be involved in the salience ('noticeableness') of perceived objects and events, with potentially important stimuli such as: 1) rewarding things or 2) dangerous or threatening things ~ seeming more noticeable or important. This hypothesis argues that dopamine assists decision-making by influencing the priority of such stimuli to the person concerned.
However, these theories are based on correlational, rather than causal, experimental evidence. The available evidence that examined causal relationships between dopamine and motivation does not seem to agree with any of the above-stated theories. For example, pharmacological blockade of brain dopamine receptors increases rather than decreases drug-taking behavior. The theories viewing dopamine as the mediator of 'desire/wanting,' 'predicting pleasurable activity,' 'noticeableness' or 'decision-making' cannot adequately explain this experimental evidence. Thus, the functional role of dopamine in motivation remains controversial.
Deficits in dopamine levels have also been implicated as one of several possible causes for Adult attention-deficit disorder (AADD), and some types of medications used to treat Attention-deficit hyperactivity disorder (ADHD/ADD) will help to stimulate dopaminergic systems, leading to potentially heightened, but preferably not distorted, sensation, for those who may be afflicted by it and be receiving treatment for it.[/b]
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