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Is digoxin a generic drug. This drug is also known as digoxin. Its effects on dopamine release were not studied well, however, results showed that the drug increased striatal serotonin concentrations.[40] Moreover, D-amphetamine was found to affect dopamine release in the nucleus accumbens.[40,41] These findings suggest that D-amphetamine and digoxin enhance dopamine transmission in the ventral tegmental area, possibly increasing locomotor activity. Dopamine is also released into the nucleus accumbens and prefrontal cortex, two brain areas (the most significant structures in dopamine) that have been related to drug addiction. Dopamine in the mid-frontal valacyclovir generic for sale cortex may affect motivation and motivation-related behaviors. In humans, administration of cocaine produces a marked increase in dopamine multiple brain regions including the frontal and parietal cortices.[42] In addition, dopamine release the caudate nucleus, a brain region that is important for motivation and reward,[43] has been found to be increased with chronic cocaine use. Interestingly, is not metabolized to dopamine in the liver. This suggests that cocaine is synthesized in the brain, and may ultimately be converted to dopamine by another mechanism. Another compound, liraglutide, has been reported to significantly increase striatal dopamine release in rats. It works by blocking tyrosine hydroxylase, which converts tryptophan to the biologically active form of amino acid tyrosine. Liraglutide was well tolerated and produces immediate effects. It is often prescribed for ADHD, depression and certain other neurological conditions. The mechanism of action digoxin may involve an increase in dopamine release or possibly a of dopamine from DAT. DAT is an intracellular storage compartment for dopamine. DAT is the transporter protein responsible for dopamine delivery inside of cells. The ability digoxin to increase dopamine release in striatal areas may be due to the effect it has on dopamine receptors. Dopamine is involved in learning and motivation the brain. It is believed that decreased dopamine levels over time lead to deficits in emotional behavior and cognition. Dopamine is also involved in impulse control. As a result of chronic stimulant abuse, the dopamine receptor can become overactive. This increases dopamine secretion and impairs proper impulse control. Furthermore, excessive dopamine release causes the striatum to be overexcited, which results in the dopamine releasing neurons, called VMAT-dependent D1 receptors, to become overactivated.[44] Therefore, the D1 receptors become "bottomed out" and have difficulty signaling with more D2 receptors, which allows for dopamine release, a critical component of learning and motivation. In the striatum, D2 receptors are main type of dopamine receptors. D2 receptors are the primary type located at synapses, where they interact with.

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