What increase dopamine in frontal cortex and decrease dopamine in mesolimbics pathway
I think about supplements, drugs.
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dopamine in frontal cortex and mesolimbic area
Started by
scibor1
, Oct 17 2013 04:35 PM
frontal cortex dopamine
3 replies to this topic
#2
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Posted 18 October 2013 - 04:20 PM
I couldn't think of any reason why you would want to do this as you are effectively counteracting each others effects.
Unfortunately its also impossible to target both separately and along with the mesocortical pathway it is the main pathway that projects into the pre-frontal cortex.
The primary target receptor in the pre-frontal cortex is D1. However there are very few receptors and the best way to increase activity here is by increasing adrenergic function (which feed into the dopaminergic neurons). NRIs like atomoxetine will have this effect but will also increase activity in the mesolimbic pathway. Alpha 2 receptor (Alpha 2a) agonists are the best choice with little to no effect on mesolimbic activity. Clonidine is an option but Guanfacine is selective for Alpha 2a receptors and is your best bet.
To decrease activity in the mesolimbic pathway you are looking at dopamine antagonists as the only real option - with a primary interest at D2 receptors and to a lesser extent d3. Antipsychotics are one possibility but come with serotonergic antagonistic effects (although antagonism of 5HT2c (and less extent all 5HT2 receptors) increase activity in the pre-frontal cortex) and one hell of a lot of side effects. They will also decrease activity in the pre-frontal region. A lot of the atypical antipsychotics are selective to autoreceptors at lower doses and so will actually increase activity until the dose is high enough. Eticlopride is a research drug but a highly selective D2 anatagonist.
What are you trying to achieve?
Unfortunately its also impossible to target both separately and along with the mesocortical pathway it is the main pathway that projects into the pre-frontal cortex.
The primary target receptor in the pre-frontal cortex is D1. However there are very few receptors and the best way to increase activity here is by increasing adrenergic function (which feed into the dopaminergic neurons). NRIs like atomoxetine will have this effect but will also increase activity in the mesolimbic pathway. Alpha 2 receptor (Alpha 2a) agonists are the best choice with little to no effect on mesolimbic activity. Clonidine is an option but Guanfacine is selective for Alpha 2a receptors and is your best bet.
To decrease activity in the mesolimbic pathway you are looking at dopamine antagonists as the only real option - with a primary interest at D2 receptors and to a lesser extent d3. Antipsychotics are one possibility but come with serotonergic antagonistic effects (although antagonism of 5HT2c (and less extent all 5HT2 receptors) increase activity in the pre-frontal cortex) and one hell of a lot of side effects. They will also decrease activity in the pre-frontal region. A lot of the atypical antipsychotics are selective to autoreceptors at lower doses and so will actually increase activity until the dose is high enough. Eticlopride is a research drug but a highly selective D2 anatagonist.
What are you trying to achieve?
#4
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Posted 29 June 2015 - 08:46 AM
Yes, give us more information - mental disorders, neuropsychiatric conditions, etc.
Regarding Atrw55's suggestion - I would say, DON'T try Cannabidiol (CBD) but try CannaBIGerol! 
CBG is a potent Alpha-2 agonist as well as a powerful anti-inflammatory, so it should be quite beneficial.
It's damn hard to come by tho', so be prepared to pay waaay out of your pocket to get it in pure form.
Otherwise, Guanfacine as Tom_ mentioned - Intuniv is pretty great stuff.
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