Dopamine - Wikipedia, the free encyclopedia
Motivation and pleasure
Dopamine is commonly associated with the pleasure system of the brain, providing feelings of enjoyment and reinforcement to motivate a person proactively to perform certain activities. Dopamine is released (particularly in areas such as the nucleus accumbens and striatum) by naturally rewarding experiences such as food, sex[4][5], 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, arguing that these dopamine pathways are pathologically altered in addicted persons. However, cocaine and amphetamine influence separate mechanisms of action.
Cocaine is a dopamine transporter blocker that competitively inhibits dopamine uptake to increase the lifetime of dopamine and augments an overabundance of dopamine (an increase of up to 150%) within the parameters of the dopamine neurotransmitters. Like cocaine, amphetamines increase the concentration of dopamine in the synaptic gap, but by a different mechanism. Amphetamines are similar in structure to dopamine, and so can enter the terminal button of the presynaptic neuron via its dopamine transporters as well as by diffusing through the neural membrane directly. When entering inside the presynaptic neuron, amphetamines force the dopamine molecules out of their storage vesicles and expel them into the synaptic gap by making the dopamine transporters work in reverse. Dopamine's role in experiencing pleasure has been questioned by several researchers. It has been argued that dopamine is more associated with anticipatory desire and motivation (commonly referred to as "wanting") as opposed to actual consummatory pleasure (commonly referred to as "liking"). Dopamine is not released when unpleasant or aversive stimuli are encountered, and so motivates towards the pleasure of avoiding or removing the unpleasant stimuli.
Recent research suggests that the firing of dopamine neurons is a motivational chemical as a result of reward-anticipation. This is based on evidence[citation needed] that, when a reward is perceived to be greater than expected, the firing of certain dopamine neurons increases, which correspondingly increases desire or motivation toward the reward.
Clues to dopamine's role in motivation, desire, and pleasure have come from studies performed on animals. In one such study rats were depleted of dopamine by up to 99% in the nucleus accumbens and neostriatum using 6-hydroxydopamine.[6] With this large reduction in dopamine, the rats would no longer eat by their own volition. The researchers then force fed the rats food and noted whether they had the proper facial expressions indicating whether they liked or disliked it. The researchers of this study concluded that the reduction in dopamine did not reduce the rat's consummatory pleasure, only the desire to actually eat. In another study, mutant hyperdopaminergic (increased dopamine) mice show higher "wanting" but not "liking" of sweet rewards.[7]
In humans, though, drugs that reduce dopamine activity (neuroleptics, [eg. some antipsychotics) have been shown to reduce motivation as well as cause anhedonia (the inability to experience pleasure).[8] Conversely the selective D2/D3 agonists pramipexole and ropinirole have anti-anhedonic properties as measured by the Snaith-Hamilton Pleasure Scale.[9] (The Snaith-Hamilton-Pleasure-Scale (SHAPS), introduced in English in 1995, assesses self-reported anhedonia in psychiatric patients.)
Opioid and cannabinoid transmission instead of dopamine may modulate consummatory pleasure and food palatability(liking).[10] This could explain why animals "liking" of food is independent of brain dopamine concentration. Other consummatory pleasures, however, may be more associated with dopamine. One study found that both anticipatory and consummatory measures of sexual behavior (male rats) were disrupted by DA receptor antagonists.[11] Libido can be increased by drugs that affect dopamine but not by drugs 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, manic subjects can become hypersocial as well as hypersexual. This is also credited to an increase in dopamine, because mania alleviates from dopamine blocking antipsychotics.
Research suggests a crucial role of dopamine in reward systems and anticipation of pleasure. Dopamine may also have a role 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. [12] This hypothesis argues that dopamine assists decision-making by influencing the priority, or level of desire, of such stimuli to the person concerned.
Pharmacological blockade of brain dopamine receptors increases rather than decreases drug-taking behavior. Since blocking dopamine decreases desire, the increase in drug taking behavior may be seen as not a chemical desire but as a deeply psychological desire to just 'feel something'.
Deficits in dopamine levels are implicated in Attention-deficit hyperactivity disorder(ADHD), and stimulant medications used to successfully treat the disorder increase dopamine neurotransmitter levels, leading to decreased symptoms.
Motivation and pleasure
Dopamine is commonly associated with the pleasure system of the brain, providing feelings of enjoyment and reinforcement to motivate a person proactively to perform certain activities. Dopamine is released (particularly in areas such as the nucleus accumbens and striatum) by naturally rewarding experiences such as food, sex[4][5], 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, arguing that these dopamine pathways are pathologically altered in addicted persons. However, cocaine and amphetamine influence separate mechanisms of action.
Cocaine is a dopamine transporter blocker that competitively inhibits dopamine uptake to increase the lifetime of dopamine and augments an overabundance of dopamine (an increase of up to 150%) within the parameters of the dopamine neurotransmitters. Like cocaine, amphetamines increase the concentration of dopamine in the synaptic gap, but by a different mechanism. Amphetamines are similar in structure to dopamine, and so can enter the terminal button of the presynaptic neuron via its dopamine transporters as well as by diffusing through the neural membrane directly. When entering inside the presynaptic neuron, amphetamines force the dopamine molecules out of their storage vesicles and expel them into the synaptic gap by making the dopamine transporters work in reverse. Dopamine's role in experiencing pleasure has been questioned by several researchers. It has been argued that dopamine is more associated with anticipatory desire and motivation (commonly referred to as "wanting") as opposed to actual consummatory pleasure (commonly referred to as "liking"). Dopamine is not released when unpleasant or aversive stimuli are encountered, and so motivates towards the pleasure of avoiding or removing the unpleasant stimuli.
Recent research suggests that the firing of dopamine neurons is a motivational chemical as a result of reward-anticipation. This is based on evidence[citation needed] that, when a reward is perceived to be greater than expected, the firing of certain dopamine neurons increases, which correspondingly increases desire or motivation toward the reward.
Clues to dopamine's role in motivation, desire, and pleasure have come from studies performed on animals. In one such study rats were depleted of dopamine by up to 99% in the nucleus accumbens and neostriatum using 6-hydroxydopamine.[6] With this large reduction in dopamine, the rats would no longer eat by their own volition. The researchers then force fed the rats food and noted whether they had the proper facial expressions indicating whether they liked or disliked it. The researchers of this study concluded that the reduction in dopamine did not reduce the rat's consummatory pleasure, only the desire to actually eat. In another study, mutant hyperdopaminergic (increased dopamine) mice show higher "wanting" but not "liking" of sweet rewards.[7]
In humans, though, drugs that reduce dopamine activity (neuroleptics, [eg. some antipsychotics) have been shown to reduce motivation as well as cause anhedonia (the inability to experience pleasure).[8] Conversely the selective D2/D3 agonists pramipexole and ropinirole have anti-anhedonic properties as measured by the Snaith-Hamilton Pleasure Scale.[9] (The Snaith-Hamilton-Pleasure-Scale (SHAPS), introduced in English in 1995, assesses self-reported anhedonia in psychiatric patients.)
Opioid and cannabinoid transmission instead of dopamine may modulate consummatory pleasure and food palatability(liking).[10] This could explain why animals "liking" of food is independent of brain dopamine concentration. Other consummatory pleasures, however, may be more associated with dopamine. One study found that both anticipatory and consummatory measures of sexual behavior (male rats) were disrupted by DA receptor antagonists.[11] Libido can be increased by drugs that affect dopamine but not by drugs 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, manic subjects can become hypersocial as well as hypersexual. This is also credited to an increase in dopamine, because mania alleviates from dopamine blocking antipsychotics.
Research suggests a crucial role of dopamine in reward systems and anticipation of pleasure. Dopamine may also have a role 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. [12] This hypothesis argues that dopamine assists decision-making by influencing the priority, or level of desire, of such stimuli to the person concerned.
Pharmacological blockade of brain dopamine receptors increases rather than decreases drug-taking behavior. Since blocking dopamine decreases desire, the increase in drug taking behavior may be seen as not a chemical desire but as a deeply psychological desire to just 'feel something'.
Deficits in dopamine levels are implicated in Attention-deficit hyperactivity disorder(ADHD), and stimulant medications used to successfully treat the disorder increase dopamine neurotransmitter levels, leading to decreased symptoms.
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