Psychiatric Drugs - Educational thread

[Szegedist]

True dat, yo.

On a more serious note I don't see much of a difference between professionals that prescribe psychiatric drugs and street dealers in that their goal is to have a returning customer to make a profit. Mood altering drugs shouldn't be promoted. Only a small minority of the population needs psychiatric drugs to function in society.

And often the people who are prescribed them dont really need them. Feeling a bit sad? Why work on your issues when you can just take a pill?
ADHD is another one, not so long ago it was just "children being children", but now you have pills for it.

[Petros Agapetos]

I take 150 mg of Bupropion to reverse the sexual side effects caused by Trintelix, an SSRI antidepressant I take to increase serotonin levels to make me relaxed, less anxious, increase my mood and make me feel happy. Bupriopion increases dopamine concentrations

I take 40 mg of Dexedrine to increase my dopamine and norepinephrine levels during the day,, and by that I mean. I have been diagnosed with ADHD, and so I am eligible for psychostimulants, I take them to help me study better - they make me alert, lively, and happy during the day, while at night I take Abilify, a neuroleptic (which reverses the effect of Dexedrine). Abilify is a partial dopamine agonist, it only partially activates dopamine receptors compared to the extent that dopamine does. Dopamine is responsible for feelings of pleasure, euphoria, sexual gratification/orgasm.

Dexedrine causes dopamine and norepinephrine release. It causes a feeling of light ecstasy, makes me alert, helps me concentrate.

Dopamine D1 receptor: The D1 subtype is the most abundant dopamine receptor in the central nervous system. The DRD1 gene expresses primarily in the caudate putamen in humans.
D1 receptors regulate neuronal growth and development, mediate some behavioral responses, and modulate dopamine receptor D2-mediated events.

Dihydrexidine is a moderately selective full agonist at the dopamine D1 and D5 receptors.[1] It has approximately 10-fold selectivity for D1 and D5 over the D2 receptor.[2] Although dihydrexidine has some affinity for the D2 receptor, it has functionally selective D1 signaling, thereby explaining why it lacks D2 agonist behavioral qualities.

Dihydrexidine has shown impressive antiparkinson effects in the MPTP-primate model, and has been investigated for the treatment of Parkinson's disease.The drug was resurrected when it was shown that smaller subcutaneous doses were safe. This led to a pilot study in schizophrenia and current clinical trials to assess its efficacy in improving the cognitive and working memory deficits in schizophrenia and schizotypal disorder.

SKF-81,297 is a synthetic drug of the benzazepine chemical class that acts as a selective dopamine D1/D5 receptor full agonist, and produces a characteristic stimulant-like pattern of anorexia, hyperactivity and self-administration in animals. This profile is shared with several related drugs such as 6-Br-APB and SKF-82,958, but not with certain other D1 full agonists such as A-77,636, reflecting functional selectivity of D1 activation. Newer findings reveal that SKF-81,297 additionally acts as a partial agonist at D1-D2 receptor heteromers.

Rotigotine is a dopamine agonist of the non-ergoline class of medications indicated for the treatment of Parkinson's disease (PD) and restless legs syndrome. Like other dopamine agonists, rotigotine has been shown to possess antidepressant effects and may be useful in the treatment of depression as well. Rotigotine acts as a non-selective agonist of the dopamine D1, D2, D3, and, to a lesser extent, D4 and D5 receptors, with highest affinity for the D3 receptor. In terms of affinity, rotigotine has 10-fold selectivity for the D3 receptor over the D2, D4, and D5 receptors and 100-fold selectivity for the D3 receptor over the D1 receptor. In functional studies however, rotigotine behaves as a full agonist of D1, D2, and D3 with similar potencies (EC50). Its ability to activate both D1-like and D2-like receptors is similar to the case of apomorphine (which notably has greater efficacy in the treatment of Parkinson's disease than D2-like-selective agonists but has suboptimal pharmacokinetic properties) and pergolide but unlike pramipexole and ropinirole.
Rotigotine possesses the following in vitro receptor binding profile:

D1 receptor (Ki = 83 nM)
D2 receptor (Ki = 13.5 nM)
D3 receptor (Ki = 0.71 nM)
D4.2 receptor (Ki = 3.9 nM)
D4.4 receptor (Ki = 15 nM)
D4.7 receptor (Ki = 5.9 nM)
D5 receptor (Ki = 5.4 nM)
α1A-adrenergic receptor (Ki = 176 nM)
α1B-adrenergic receptor (Ki = 273 nM)
α2A-adrenergic receptor (Ki = 338 nM)
α2B-adrenergic receptor (Ki = 27 nM)
α2C-adrenergic receptor (Ki = 135 nM)
5-HT1A receptor (Ki = 30 nM)
5-HT7 receptor (Ki = 86 nM)
H1 receptor (Ki = 330 nM)

All affinities listed were assayed using human materials except that for α2B-adrenergic which was done with NG 108–15 cells. Rotigotine behaves as a partial or full agonist (depending on the assay) at all dopamine receptors listed, as an antagonist at the α2B-adrenergic receptor, and as a partial agonist at the 5-HT1A receptor. Though it has affinity for a large number of sites as shown above, at clinical doses rotigotine behaves mostly as a selective D1-like (D1, D5) and D2-like (D2, D3, D4) receptor agonist, with its α2B-adrenergic and 5-HT1A activity also possibly having some low relevance.

[RenaRyuguu]

Trintellix is an atypical antidepressant, a serotonin modulator and stimulator.

Pharmacodynamics
Trintelix is a so-called "serotonin modulator and stimulator". It has been shown to possess the following pharmacological actions:

SERT*[Serotonin transporter] Inhibition
NET*[Norepinephrine transporter] Inhibition
5-HT1A*Agonist
5-HT1B* Partial agonist
5-HT1D*Antagonist
5-HT3*Antagonist
5-HT7*Antagonist

Note: 5HT stands for serotonin; the above are serotonin receptors that Trintelix targets in the brain. An increase in serotonin receptor activity is associated with relief of depressive symptoms.

A serotonin modulator and stimulator (SMS), sometimes referred to more simply as a serotonin modulator, is a type of drug with a multimodal action specific to the serotonin neurotransmitter system. To be precise, SMSs simultaneously modulate one or more serotonin receptors and inhibit the reuptake of serotonin. The term was created to describe the mechanism of action of the serotonergic antidepressant Trintellix, which acts as a serotonin reuptake inhibitor (SRI), partial agonist of the 5-HT1A receptor, and antagonist of the 5-HT3 and 5-HT7 receptors.

SMSs were developed because there are many different subtypes of serotonin receptors (at least 15 in total are currently known) and not all of these receptors appear to be involved in the antidepressant effects of SRIs. Some serotonin receptors seem to play a relatively neutral or insignificant role in the regulation of mood, but others, such as 5-HT1A autoreceptors and 5-HT7 receptors, appear to play an oppositional role in the efficacy of SRIs in treating depression. As such, a drug which combines the actions of, say, an SRI, 5-HT1A partial agonism, and 5-HT7 receptor antagonism, could, in theory, have the potential to prove more effective than pure SRIs.

An alternative term is serotonin partial agonist/reuptake inhibitor (SPARI).

All fake drugs are shit stick to natural or at least that's how I roll lololol