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Dopamine, Dopamine

In the brain, this phenethylamine functions as a neurotransmitter, activating the five types of dopamine receptors D 1 , D 2 , D 3 , D 4 , and D 5 , and their variants. Dopamine is produced in several areas of the brain, including the substantia nigra and the ventral tegmental area. http://www.encyclopedia.com/doc/1O87-ventraltegmentalarea.html Reference for VTA.

It was named dopamine because it was a monoamine, and its synthetic precursor was 3,4- d ihydr o xy p henyl a lanine (L-DOPA).

In some neurons, dopamine is further processed into norepinephrine by dopamine beta-hydroxylase.

Dopamine that is not broken down by enzymes is repackaged into vesicles for reuse.

According to this hypothesis, the phasic responses of dopamine neurons are observed when an unexpected reward is presented. These responses transfer to the onset of a conditioned stimulus after repeated pairings with the reward. Further, dopamine neurons are depressed when the expected reward is omitted. Thus, dopamine neurons seem to encode the prediction error of rewarding outcomes. In nature, we learn to repeat behaviors that lead to maximize rewards. Dopamine is therefore believed to provide a teaching signal to parts of the brain responsible for acquiring new behavior. Temporal difference learning provides a computational model describing how the prediction error of dopamine neurons is used as a teaching signal.

It has been found that D1 receptors are responsible for the cognitive-enhancing effects of dopamine.

The lactotrope cells that produce prolactin, in the absence of dopamine, secrete prolactin continuously; dopamine inhibits this secretion. Thus, in the context of regulating prolactin secretion, dopamine is occasionally called prolactin-inhibiting factor ( PIF ), prolactin-inhibiting hormone ( PIH ), or prolactostatin . Prolactin also seems to inhibit dopamine release, such as after orgasm, and is chiefly responsible for the refractory period.

Dopamine is released (particularly in areas such as the nucleus accumbens and prefrontal cortex) by naturally rewarding experiences such as food, sex, drugs, and neutral stimuli that become associated with them. Recent studies indicate that aggression may also stimulate the release of dopamine in this way. This theory is often discussed in terms of drugs such as cocaine, nicotine, and amphetamines, which directly or indirectly lead to an increase of dopamine in the mesolimbic reward pathway of the brain, and in relation to neurobiological theories of chemical addiction, arguing that this dopamine pathway is pathologically altered in addicted persons. Vanderbilt University (2008, January 15). Aggression As Rewarding As Sex, Food And Drugs, New Research Shows. ScienceDaily.

By entering the presynaptic neuron, amphetamines force dopamine molecules out of their storage vesicles and expel them into the synaptic gap by making the dopamine transporters work in reverse.

This hypothesis is based on the evidence that, when a reward is greater than expected, the firing of certain dopaminergic neurons increases, which consequently increases desire or motivation towards the reward.

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.

Evidence comes partly from the discovery of a class of drugs called the phenothiazines (which block D 2 dopamine receptors) that can reduce psychotic symptoms, and partly from the finding that drugs such as amphetamine and cocaine (which are known to greatly increase dopamine levels) can cause psychosis.

It is typically co-administered with an inhibitor of peripheral decarboxylation (DDC, dopa decarboxylase), such as carbidopa or benserazide. Inhibitors of alternative metabolic route for dopamine by catechol-O-methyl transferase are also used. These include entacapone and tolcapone.

These enzymes use molecular oxygen (O 2 ) to oxidise various 1,2-diphenols to their corresponding quinones. The natural substrate for PPOs in bananas is dopamine. The product of their oxidation, dopamine quinone, spontaneously oxidises to other quinones. The quinones then polymerise and condense with amino acids and proteins to form brown pigments known as melanins. The quinones and melanins derived from dopamine may help protect damaged fruit and vegetables against growth of bacteria and fungi.

Source: Wikipedia > Dopamine



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