polymath
Bluelight Crew
There are several kinds of drugs that have dopaminergic effects... There are DA releasers/reuptake inhibitors(amphetamine, cocaine), direct DA agonists(bromocriptine, apomorphine), substances that increase DA production in cells(L-dopa) and then there are MAO-B inhibitors that inhibit the breakdown of DA.
The effects of these are not similar at all. For example, large doses of bromocriptine, apomorphine and L-dopa cause nausea because of activation of DA receptors in the chemoreceptor trigger zone in fourth ventricle. Cocaine, amphetamine or selegiline don't have this effect even in large doses, even though you would expect that these drugs would increase synaptic DA in the CTZ, too.
Also, direct agonists and L-dopa only rarely cause euphoria similar to amphetamines or cocaine... It seems like the effect of dopaminergic stimulants is more specific to the mesolimbic area of the brain, while the direct agonists and L-dopa cause dopaminergic effects indiscriminately in all areas of the brain.
The only similarity between the drugs seems to be that both amphetamine and L-dopa cause paranoid psychosis if given in large doses.
What causes these differences between different dopaminergics? Or is this something that no one currently knows the answer to?
With cholinergic drugs, for example, the situation is a lot simpler. The effects of ACh overactivity are the same, whether they be caused by a mixture of nicotine/muscarine agonists or by a cholinesterase inhibitor.
The effects of these are not similar at all. For example, large doses of bromocriptine, apomorphine and L-dopa cause nausea because of activation of DA receptors in the chemoreceptor trigger zone in fourth ventricle. Cocaine, amphetamine or selegiline don't have this effect even in large doses, even though you would expect that these drugs would increase synaptic DA in the CTZ, too.
Also, direct agonists and L-dopa only rarely cause euphoria similar to amphetamines or cocaine... It seems like the effect of dopaminergic stimulants is more specific to the mesolimbic area of the brain, while the direct agonists and L-dopa cause dopaminergic effects indiscriminately in all areas of the brain.
The only similarity between the drugs seems to be that both amphetamine and L-dopa cause paranoid psychosis if given in large doses.
What causes these differences between different dopaminergics? Or is this something that no one currently knows the answer to?
With cholinergic drugs, for example, the situation is a lot simpler. The effects of ACh overactivity are the same, whether they be caused by a mixture of nicotine/muscarine agonists or by a cholinesterase inhibitor.