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Dopamine. It binds selectively to dopamine D(2) and D(3) receptors in the limbic system of the brain. Low doses preferentially block presynaptic D(2)/D(3) receptors, enhancing dopaminergic transmission. Higher doses block postsynaptic receptors, inhibiting dopaminergic hyperactivity.
So it is clinically effective on the negative symptoms of acute schizophrenia exacerbations at low dosages (50-300 mg/day), and also on the positive symptoms of the disease at high dosages (400-800 mg/day).
So, it is not effective for treating MDD?
Amisulpride has also been demonstrated to be an antidepressant for patients with major depression in many clinical trials. In part because of the selective D2/D3 receptor antagonist properties of amisulpride, it has long been widely assumed that dopaminergic modulation is the property responsible for mediating its antidepressant and antipsychotic properties.
I am back now,
but after severe depression with mind blackening, thought blockage, and extreme sentitiveness to black light, and perceiving any negative word as too black, which brings the mood extremely down
is it correct to treat this symptoms with Amisulpride 400mg for almost 1 year, with no signs of improvement by only regular deterioration?
Especially as before this the previous medicine was Olanzapine, which blocks Dopamine and Serotonine, taken for 1 year at high dosages?
1 year is plenty of time to see if a drug is going to be effective or not. If not, I would suggest you try something new. Work with your doctors on this. Treatment for these conditions is often "hit-or-miss" and several agents typically need to be tried before an effective one is found.
yes, but it isnt true that to treat depression Dopamine must not be BLOCKED but RELEASED?
yes, but blocking reuptake in the synaptic cleft is equivalent to increased release.
in general, ISNT FIRST TRYING TO INCREASE/ UNBLOCK THE FLOW OF SEROTONIN AND DOPAMINE
because I read that atypical antypsychotics block receptors in the brain's dopamine and serotonin pathways
therefore they are good for schizofrenia and psychosis, originated by excess levels of these chemical
the action of these meds is not simple and is dose dependent...by decreasing degredation of the neurotramsmitters in the preynaptic region (i.e "blocking" reuptake), they prolong their presence in the synaptic cleft so that they can work harder and longer...increasing dopaminergic and/or serotoninergic activity. At higher doses they block excessive stimulation of the post-synaptic receptors .
but depression treatment means not good mood. Good mood chemicals are ser and dop. So logically I guess you must try to unblock them...increase ser. and dop.
but blocking their elimination is equivalent to unblocking their production...