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Re: GBR 12909 causes sedation

Posted by linkadge on November 2, 2007, at 22:49:09

In reply to Re: GBR 12909 causes sedation » linkadge, posted by Astounder on November 2, 2007, at 17:31:56

>That selective DRIs are not psychostimulants can >be explained in that NET blockade is necessary >to increase DA levels in the frontal cortex, as >NET plays a greater role in clearing away >extracellular DA in this area than does DAT.

Who says that increases frontal cortex dopamine is necessary and sufficant to make a stimulant?
5-ht2a antagonists increase dopamine in the frontal cortex, but are not stimulants. The stimulating effects in my opinion are due to enhancement of noradrenergic function in more primitive brain structures.

>Furthermore, cortical glial uptake of DA depends >more on NET than DAT.

Arguing that the norepinephrine transporter has greater involvement in the uptake of dopamine than does the dopamine transporter (in certain brain regions) does not disprove my theory that norepinephrine is more involved in energy levels / alertness.

NET only takes up dopamine in certain brain regions under certain conditions. Increasing dopamine in the frontal cortex is likely to produce enhanced attention, but not necessarily psychomotor activation. Caffine for instance, increases dopamine release in the frontal cortex, in doses somewhat less than what are generally required for psychomotor activation.


>I believe dopamine is essential to the >alertfulness-promoting effects of >psychostimulants.

It might be essential, but that doesn't mean it plays a greater role in alertness than does norepinephrine.

>Solely noradrenergic drugs do not reduce daytime >sleepiness in narcolepsy,

Says who? Drugs like endronax can work very well in narcolepsy, probably due to high noradrenergic innervation in the reticular formation, unless you are going to argue that their effect is due to dopamine. Besides, I don't think dopamine agonists would help narcoleptics. Narcoleptics aren't lacking motivation or the ability to coordinate smooth muscle movement (ie dopamine).

>though they can be used to treat other symptoms, >like cataplexy. Selective D2 antagonists like >Haldol reverse the arousal from psychostimulants >without affecting NE

This is not a good example as haloperidol has potent antagonism at several serotonergic and noradrenergic receptors. For instance, according to http://pdsp.cwru.edu/pdsp.php, antagonism at alhpa-1 for instance, is almost as strong as its d2 antagonism.

Regardless, if a potent and selective d2 angatonist were to decrease spontanious locomotor activity it is impossble to prove that it has indeed directly reduced energy/alertness, or simply elimated the *motivation* to move/think.

Linkadge



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poster:linkadge thread:791344
URL: http://www.dr-bob.org/babble/20071027/msgs/793082.html