• N&PD Moderators: Skorpio | thegreenhand

  • Neuroscience & Pharmacology Discussion Welcome Guest
    Posting Rules Bluelight Rules
    Recent Journal Articles Chemistry Mega-Thread
    FREE Chemistry Databases! Self-Education Guide

The Big and Bangin' Pseudo-Advanced Drug Chemistry, Pharmacology and More Thread, V.2

Status
Not open for further replies.
Incredibly trivial question. What is the best way to pronounce "moiety"?

I've usually heard MOY-e-tee (sounds like "boy Eddie" but with stress on the first syllable). But today I heard moo-EYE-e-tee and I like that better.
 
Anyone familiar with sodium valproate care to take a guess at how much of its effects are related to sodium channel/Neurotrophic effects vs. GABA? I'm hoping most of its efficacy (for mania) is stemming from sodium channel/neurotrophic factor mediated effects and not GABA...
 
Last edited:
The 2 other major bipolar drugs--lithium and carbamazepine--owe their efficacies to some type of fuckery with sodium. I would imagine Depakote to be the same.

I certainly didn't feel any baseline anxiolysis from Depakote. I would expect that from a gabaergic drug.
 
^I don't remember it being sedating. It was fairly side-effect free for me. TBPH it had such a faint presence that I suspected it was placebo. But I didn't really have hypomanic episodes while on it, so I suppose it worked as intended.

Lamotrigine was added a few months later and my mood was very stable. I think lamotrigine is an excellent prophylaxis for bipolar depression.
 
Depakote--placebo. Lamictal--worthelss for me. I now take benadryl, cogentin, haldol, trazodone, and gabapentin at bedtime for my bipolar, and that combination seems to work pretty well for me. I used to take Restoril too, which was nice, but one time I got my prescription for it filled, took five or so, went to sleep, woke up, blacked out, ended up taking all 30 x 30mg capsules, ended up in the psych ward for a week, and was lucky I didn't die. I stopped getting scripts for benzodiazepines after that, for obvious reasons.
 
^Haldol can be bad news, even with Cogentin on board. Have you tried any atypicals, or even lithium?
 
Yes, I've been on all the atypicals pretty much. Risperdal was largely without effect for me, though is good for stopping an unwanted trip I found. Abilify did fuck all nothing for me. Thorazine (not an atypical, I know) caused akasthisia a lot, but was at least somewhat sedating/helpful under the right circumstances. Zyprexa was quite good; I took it for years. However, when the generic came out, I tried it again, and this time it did almost nothing. Seroquel had a tendency to cause dry mouth, and a steadily building tolerance to its therapeutic effects caused me to have to go off of it. Geodon does NOT control my schizoaffective delusionsal thoughts and behavior effectively at all. Latuda, I hate; it puts me in a dysphoric mood. Stelazine (another typical) I can't remember much about. Idk, I may be forgetting a couple. I hate lithium; it makes me dumb and gives me flat affect. But Haldol works well for me. At 10mg per day, I don't get extrapyramidal symptoms, even without Cogentin, which I find largely worthless but take anyway for some reason. The weight gain for the two antipsychotics I respond best to, Zyprexa and Haldol, are equally horrific (about 50 lbs. consistent weight gain for either one for me), but it beats being psychotic and locked away in a psych ward or personal care home with the other unwanted, mentally ill derelicts.
 
fuck wow. I hope you can find a way to reverse the weight gain. Lorcaserin?
 
Lorcaserin in my experience is overrated
The weight gain operates on two levels
first, altering metabolism
second, altering appetite
it is really a matter of willpower and choices

to randomly reply to other posts

VPA does indeed have some effect on GABA but our understanding is limited
zyprexa is OK especially for schizoaffective type situations but metabolic effects suck
Geodon is crap although sometimes useful together with Ativan for acute agitation (i.m.)
some people don't take their Geodon with food though which renders it worthless
I prefer to stick to the tried and true, Haldol yes but I favor Prolixin
Cogentin shouldn't be the be all and end all to deal with side effects the are other options
Lamictal is a great drug for bipolar (II) especially those with a tendency towards depression
it is a good augmentation for depression but not only that for clozapine & other antipsychotics as well
but for real bipolar (I) pts who tend towards psychotic mania it is often not enough
good thing about Lamictal is it is very transparent subjectively
there are of course really nasty potential side effects but they are quite rare
VPA has added benefits in that it helps control impulsivity and stuff
but has a higher side effect burden but is better in bipolar(I) with a tendency towards mania IM(C)E
but actually it turns out the research support for all that is less objectively factual than we think
but really
psychiatry is about finding empircally the best choice to manage symptoms
more art than science vs what some would have you believe
and yes I do this for a living
but no nothing here is medical advice
 
did they change the name of "noradrenaline" to "norepinephrine" for marketing reasons?
 
ad + renus = ἐπί + νεφρός

Latin and Greek for the same thing, above the kidney
don't think it is a marketing thing
Epinephrine is the more American term
Adrenaline is more British
but they are the same
 
Oh yeah, the worst extrapyramidal symptoms that I've ever had were caused by Serentil, an old typical antipsychotic. Don't ever let them give you that shit! Atypicals don't work any better than typicals. But yeah, prescribing psych medicine is more of an art than a science and needs to be tinkered with to tailor the right drug regimen to the individual patient because, well, people have different brains and everything.
 
Why don't dopamine receptor agonists have the same effect as dopamine releasing agents or reuptake inhibitors?


Not recommending this at all, but hypothetically if one were to take a MAOb inhibitor along with phenethylamine, what would happen?
 
Can you give some examples? My intuition is to say that there are other factors that go into whether or not a drug produces euphoria. Are you talking about anti-parkinsonian medications versus something like methylphenidate? I think that's a good question, but again things like what brain region a drug targets, how fast it's absorbed, what other mechanisms other than dopaminergic agonism may be at play, and how long it lasts all play a decent role.

As for your second question, likely that would result in a hypertensive crisis, and possibly a stroke and death. A warning sign is a powerful headache in the back of the head. I was stupid enough to do it anyway. The feeling is just too powerful and transient to be worth it. Of course I'm drawing on anecdotes here, but when you read about people taking MAOIs with phenethylamine for a period, you read about a very high degree of addiction, as in at least on par to that of amphetamine. Eventually when the person decides to stop for whatever reason, they go through a long-ass time, we're talking months or years, before they start to feel more normal.

I didn't find it good for concentration even.
 
My question also applies to serotonin releasers and agonists. Why do agonists of serotonin receptors (like DMT) differ in subjective effects from serotonin releasers? Obviously DMT is selective for certain receptors, but what if one were to administer a load of agonists such that all types and subtypes of 5HT receptors were agonised; would this produce a response akin to serotonin releasers?
 
Hmmm correct me if I'm mistaken but seeing as I think releasers usually reverse the transporter it might possibly have something to do with variability of transporter density across different serotonin types? Is there variability of SERT density across different neurons or brain regions?

I know MDMA is kind of a weird one because it's a 5-HT2B agonist as well and 5-HT2B is necessary for both its serotonin and dopamine effects (I guess due to 2B being necessary for the function of SERT). Apparently most SSRIs are 5-HT2B agonists as well.

On that note does anybody know why these things that have affinity for SERT also have affinity for 5-HT2B? Do they somehow access the SERT through 2B or is there a similar binding site between the two?
 
Last edited:
aced126 said:
My question also applies to serotonin releasers and agonists. Why do agonists of serotonin receptors (like DMT) differ in subjective effects from serotonin releasers? Obviously DMT is selective for certain receptors, but what if one were to administer a load of agonists such that all types and subtypes of 5HT receptors were agonised; would this produce a response akin to serotonin releasers?
Click to expand...

if i'm understanding right, i've asked myself the same question. i remember one claim that agonists like DMT and other psychedelics agonized the 5HT2a receptor in a different manner than serotonin or lisuride (stimulated PLA2 vs. PLC, or both to different degrees), though this doesn't match the data from one study where they measured efficacy of different psychedelics and serotonin to stimulate these pathways (this review on hallucinogens from Nichols has a nice section on functional selectivity on page 13 / 143)

i think the current model doesn't cut it, or i'm missing something... :\
 
Status
Not open for further replies.
Top