Posted by TheOutsider on October 7, 2004, at 14:25:23
In reply to Re: Monoamine advice please, posted by zuzu80 on October 7, 2004, at 12:52:45
> Good question and the answer can cover pages and pages even books ! I have read whole book chapteres about each one and their roles, but looks like that even a modest understand exist, scientists still have a long way to go.
>
> SE, NA and DA are main transmitters in the brain (and body) and they are involved in amny aspects of our mental functioning. SE is involved in mood, and hypofunction here can lead to excessive sadness and helplessness. NA is excitatory, it's involved in alertness, energy and along with DA in motivation, drive, interest and capacity for reward (pleasure). However, all these neurotransmitters act in harmony and interdependently (all have effects on each other), eg the same neuron can be affected by both SE and NA, or a SE neuron output (serotonin) gets mediated by other presynaptic NA neurons and so on..
>
> Antidepressants usually affect a given neurotransmitter's transmition all over the nervous system non selctively, and hence the side effects. The active machanism of action whether it's: reuptake inhibition, degenerative enzyme inhibition, receptor agonism/antagonism happens rapidly (after 1st or the very first days of treatment), however, the antidepressant effect will apear only after weeks. This is due to the fact that the actual increase in SE/NA/ or DA doesn't in and on itself lead to the antidepressant effect. Rather the AD effect is due to receptor change ( eg down regulation) that occurs in response to the treatment only after couple of weeks.
>
> Affecting one chemical, say SE by a SSRI, will affect in long term also NE and DA transmission. The same applies to a Noradrenaline reuptake inhibitors ....
>
> Theoretically and actually (from experience):
>
> Targeting SE: leads to improved mood, and reduced anxiety (after some time).
>
> Targeting NE: improves energy, concentration, alertness, interest and possibly pleasure and reward (ie combat anhedonia). A pro noradrenaline drug will usually worsen anxiety and it boosts emotions ( happy to be more happy and depressed to be even more depressed!!).
>
> DA is a bit tricky. Drugs that affect it are usually specific in their site of action. DA has three main tracts in the brain. One involved in movement and problems here lead to Paskinsons. Second in cognition, interest, delusions, paranoia, sociability, problems here are part of Schizophrenia. A third one is almost purely pleasure and reward, acte hyperfunction here is the job Cocaine.
>
> DA enhancing drugs can cause a variety of things: pleasure, euphoria, paranoia, increased sociablity illusions (mainly controlled substances: stimulants and cocaine), others some AD effect, others movement disorders.... Increased anxiety is typical with such drugs. Some antipsychotics at low doses can enhance DA transmission (rather than blocking it) and there're some studies that suggest their AD effect. But almost all of them have the risk of iducing extrapyramidal symptoms (parkinsonism and even non reversible movement disorders).
>
> I will try to post here a link to an arcticle I read that reviews the monoamine system and it's involvement in affective disorders.
>
> Don't hesitate to ask if you wonder about something.
>
> Christine
Thats a really interesting explination.I don't mean to be critical but the dopamine system issen't as simple as clearly divided up as your explination suggests. For example Parkinsons patients usually suffer from depression 'I think', so they do kind of shade into each other.
poster:TheOutsider
thread:399934
URL: http://www.dr-bob.org/babble/20041007/msgs/400019.html