Co-Administration of Prescription Serotonin Ant/agonists - The Implications?

[Vaya]

Hey all,

It has recently come to my attention how utterly potent a 5HT2 antagonist risperidone really is; in another thread, I'd made the comment that 0.25mg was enough to nullify at least ninety percent of a 500ug LSD experience.

Desoxyn (dextro-methamphetamine HCl) is a fairly potent serotongergic (as well as DA/NE) agent, and I take 10mg Desoxyn and 0.25mg Risperdal (remember, enough to abort a 500ug psychedelic experience entirely) at precisely the same time each morning.

I am purely speculating, but would the fact that Risperdal is competing for control over the release of serotonin in my brain against dex-methamp nullify the serotonergic effect of Desoxyn? My line of inquiry stems from the fact that I do indeed feel the serotonergic effect of d-methamp when I take it, in addition to the obvious DA/NE effects, despite the fact that such a powerful 5HT2 antagonist (e.g. Risperdal) is being co-administered with it every morning.

I also know from an enlightened member of these lovely boards, that 5HT2 agonists are cross-tolerant with 5HT2 antagonists.
Would it therefore be an effective (or, dare I say it, reasonable) assumption to make that my response to the pharmacological mechanisms peculiar to each compound regarding serotonin are in-line to be greatly diminished, if not cancelled out by one another?

If my doctor spaced on her medical training the day she prescribed me Risperdal which not only antagonizes but creates a cross-tolerance with the powerful serotonergic DA/NE d-methamphetamine, would someone with a slightly (or entirely) more refined knowledge of neuropharmacology and psychiatry explain to me what, if any, potential dangers, side effects and/or long-term consequences I may be facing by routinely co-administering these compounds?

One example of a "long-term consequence" I have contrived in order to illustrate the type of speculation I need from you other members is as follows:
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Vaya, per doctors' orders, continues to co-administer the 5HT agonist d-methamp and 5HT antagonist risperdal for a period of time (for our purposes, let us say one year). Due to the aforementioned cross-tolerance, Vaya's beneficial reaction to the specific effects of each compound diminishes as time goes by, leaving him with an antipsychotic that does not antagonize as it should and a prescription stimulant that can no longer agonize as it should unless I were, God forbid, to increase the dosage that I am at already.
----------------------------------------------------------------------------------------------------------------------------------------------------------------------
I am eagerly anticipating even speculative answers on what may happen; I would, of course, address this issue with my M.D., but she happens to be on extended leave from her office right now and Advanced Drug Discussion has ubiquitously proven to be more invaluable in terms of real information than my M.D. has been in the past.

Bottom line: Am I set up for pharmacological failure right now?

Much obliged,

~ vaya

 

[basement_shaman]

You seem to forget the rest of the serotonin receptors. Yes, you are antagonizing 2a, but you are still having agonist effects on, for example, 1a, which would be anxiolytic. It seems you may be on risperdal in order to block the psychotic symptoms that can arise from methamp use.

 

[Vaya]

You seem to forget the rest of the serotonin receptors. Yes, you are antagonizing 2a, but you are still having agonist effects on, for example, 1a, which would be anxiolytic. It seems you may be on risperdal in order to block the psychotic symptoms that can arise from methamp use.

Fantastic point, I hadn't forgotten about the others, but neglected do search about to see if methamphetamine is more selective for, say, 1a over 2a. But your last statement is incorrect - I was put on risperdal to help curb mild irritability (hence why the dosage is so low - I'm not using it as an anti-psychotic, clinically speaking); additionally, I was placed on risperdal prior to being scripted methamp, although I have been scripted stimulant meds for about fifteen years now.

However, one would think that, even accounting for 5-HT selectivity with regards to methamphetamine's pharmacological profile, its concievable that risperdal would block some of the serotonergic properties of the methamp. Or am I just missing the forest for the trees here? Methamphetamine impairs the function of 5-hydroxy tryptylase, the precursor to 5HT itself - so I'm not sure how accounting for selectivity under the umbrella of 5-HT would change anything.

Seriously, though, this is an area from which I have no background and I welcome any and all thoughts and criticisms because I am worried about what is occurring at my 5HT receptor sites!
When I went to look up whether or not anyone had published anything regarding METH's specificity for certain sub-types of 5HT, I was also alarmed to discover that a well-known endogenous antioxidant - Melatonin, which I take every night for sleep - in combination with methamphetamine actually exacerbates methamphetamine-induced clinical neurotoxicity!

Here's a link to *that* article... Really am worried for my health at this point, from both ends of the equation.

Exacerbation of Methamphetamine-Induced Neurochemical Deficits by Melatonin

At any rate, thanks for the response and opening my eyes to the possibility that I overlooked something fundamental there. Must be all the melatonin and meth, eh? 8(

~ vaya

 

[Amu]

Vaya, the brain is highly complex, and the scare of low-dose dextromethamphetamine-induced neurotoxicity is unwarranted in most cases, if desoxyn is helping you, stick with it, if you notice specific side effects that are harmful, simply switch over at that time to Dexedrine. Your point about melatonin is exactly why I'm not so sure of slapping on a "neuroprotection stack" when taking stimulants, it probably just reduces our constant stress about toxicity and that in of itself will reduce neurotoxicity, I've considered at times adding memantine, magnesium, NAC, R-ALA, selenium, melatonin, vitamins, etc... but we probably need a lot more time before we can figure out how exactly they interact with stimulants. Of course, we know meth ABUSE is neurotoxic from obvious evidence. We unfortunately have no clue what is occuring at your 5-HT receptor sites, have you considered trying just the Desoxyn for a month and seeing the difference?

 

[Vaya]

Vaya, the brain is highly complex

Hmmm... I guess you do learn something new everyday...

if desoxyn is helping you, stick with it, if you notice specific side effects that are harmful, simply switch over at that time to Dexedrine.

Well put, Amu. You're right - a recreational dose of "ice" (the legal terminology for a substance, sold as meth, thats is at least 80% dextro-Methamphetamine) is in the ball park of 75-125mg (0.075-0.125g) with no tolerance. Usually, it is consumed in such a way that it absolutely spikes your system (insufflation, plugging, subliming/smoking and intravenous) whereas the oral consumption twice daily of 0.005-0.010g has a far less war-like effect on your DAT and SERT. That, and a good portion of the sought-after compound is rendered ineffective by means of first-pass GI metabolism. The two variations on consumption style and circumstances render the two virtually incomparable - which, unfortunately, is what I was trying to do. Compare 'em.

Your point about melatonin is exactly why I'm not so sure of slapping on a "neuroprotection stack" when taking stimulants, it probably just reduces our constant stress about toxicity and that in of itself will reduce neurotoxicity

The article even quotes Vitamin C (absorbic acid) as a potential pro-oxidant when in tandem with methamphetamine administration.
However
That particular article goes on to relate the following:

It is true that the doses of both METH and melatonin used in this investigation exceed those used by the naive abuser; however, as tolerance develops the dose of METH is markedly escalated and may approach the high doses used in these studies.

For me this is where it gets trickier and trickier to decipher (and I imagine so for the researchers, too!). Questions begin bubbling out of nothing as though carbonation from a soda such as, per pound or kg of body weight, what is a sufficiently high dose of melatonin that the combination renders melatonin pro-oxidative??

I can't see further investigation into this line of query happening anytime very soon, with the possible exception being the hypothetical (but not too far out these days) situation in which someone contrives a sensationalist 'epidemic' of intelligent speed freaks that simply begs further investigation 8) someone may read this very article, decide for themselves that the average John Q. Public uses lots of meth, is knowledgable about general pharmacology, and so uses melatonin to find reprieve after a binge which ends up dovetailing and then killing him. This scenario is based off of some of the parting words by the authors of the melatonin study:

Melatonin is currently promoted in some countries as an over-the-counter “natural” medication for insomnia and other sleep disorders (UC Berkeley Wellness Letter, 1995). Because insomnia is one of the sequelae experienced by METH abusers, it is conceivable that they may perceive melatonin as a safe sleep-aid (UC Berkeley Wellness Letter, 1996) to overcome the insomnia associated with the “high” experienced during the METH “rush.” Moreover, because those who abuse METH are often knowledgeable about the potential neurotoxic effects of METH and its congeners, it is conceivable that they might use melatonin to protect against the possible oxidative neurotoxicity associated with the use of these central nervous system stimulants.

In fact, irregardless of how it gets done, I'd still like to see it done so that people like us (those that really DO fit my aforementioned portrait of a drug user) can make truly informed decisions as to whether or not we ought purchase expensive vitamins, supplements, elemental metals and the like to minimize the potential damage we do to ourselves given the nature of that which we consume. I can tooootally relate to what you wrote above, which I've decided to be obnoxious about and quote below:

I've considered at times adding memantine, magnesium, NAC, R-ALA, selenium, melatonin, vitamins, etc... but we probably need a lot more time before we can figure out how exactly they interact with stimulants.

(as an aside, what is NAC?) I already have a regiment that, amongst several others, includes B-vitamins (-3, -5, -6, -12), melatonin, selenium, R-ALA, cheleated magnesium, copper, the spectrum of omega fatty acids, DHEA (occasionally), L-tyrosine and folic acid. But in attempting to expensively help myself, am I really expensively harming myself?!? Time may tell....

and regarding memantine, it was my (perhaps misinformed) impression that it was A.) not commercially available (available by prescription only) and B.) predominately a UK thing. I could be wrong, but I've *never* seen it for sale in the United States with my own two eyes. Doesn't mean it doesn't happen, just means I was surprised by that one.

We unfortunately have no clue what is occuring at your 5-HT receptor sites, have you considered trying just the Desoxyn for a month and seeing the difference?

We actually do have a vague (albeit completely inconclusive) idea of how DAT reversal consequently aids in damaging 5-HT receptor sites, but I - for the life of me - cannot locate the article where the research was outlined and presented. I'll do an exhaustive look around my library of bookmarked scholarly journal articles and see if I can't come up with it, because I'd love to show you. As for your last question, I hadn't really thought about it. I've been on Risperdal for two months and stimulants for fifteen years but Desoxyn specifically only the last 1 1/2 months, so I haven't gotten much of a chance to tinker with things. I have noticed, though, absolutely no difference in Desoxyn performance when I get a case of the fuckits and neglect to take my risperdal for two, maybe three days straight. And as I've posted recently in a thread whose title had something to do with shrooms, my miniscule risperdal dose is still enough to nearly mute the effects of 500ug of LSD, so that lends even more credence to basement_shaman's thought that desoxyephedrine HCl acts serotonergically by means of other subreceptors of 5-HT, not just (if at all) 5-HT2a.

Your thoughts are really appreciated, my friend. Thank you for putting a little bit of time and effort into helping me debug my inquiries, no matter how obscure

~ vaya

 

[Amu]

Interesting Vaya, melatonin is supposed to be "safe" since it doesn't undergo redox cycling and shouldn't turn pro-oxidant. NAC is N-Acetyl-Cysteine, a fairly good anti-oxidant and anti-OCD agent. It's a bit shocking that risperdal doesn't change your experience with desoxyn, then again it does depend on the dose and the person's particular brain structure. Indeed DAT reversal can damage 5-HT receptor sites if excess dopamine acts as an agonist at the 5-HT receptor sites, and then is metabolized into pro-oxidant agents, effecting 5-HT receptor mitochondria and a host of other things. Also, a lot of damage is also a result of excess glutamate, but that also means there should be a threshold dose below which neurotoxicity should not occur, it is when the brain's supply of endogenous anti-oxidants is depleted, and this depends on far too many variables. All those studies do use huge doses for both meth and other agents, and are usually on rats that don't mimic human ADHD patients on desoxyn. Nonetheless, you would expect to see the results of severe toxicity if it was occuring in the several decades desoxyn has been around. Memantine is indeed a prescription drug and it is around the US but it is quite expensive, a lot of nootropic lovers do find ways to get it though, and it has caused quite a lot of online discussion in the past few years about use with stimulants to reduce tolerance and prevent neurotoxicity.

 

[negrogesic]

I have not the time to address these questions at the moment. I apologize if I missed it in the above posts, but I must ask:

For what indication was the risperdal prescribed ? Or to be frank; what are your current (and mutually agreed upon) psychiatric Dx's? Also, while it may not seem relevant, can you give an approximate age and sex (not approximated; generally speaking)?

 

[Roger&Me]

Fantastic point, I hadn't forgotten about the others, but neglected do search about to see if methamphetamine is more selective for, say, 1a over 2a. But your last statement is incorrect - I was put on risperdal to help curb mild irritability (hence why the dosage is so low - I'm not using it as an anti-psychotic, clinically speaking); additionally, I was placed on risperdal prior to being scripted methamp, although I have been scripted stimulant meds for about fifteen years now.

...and you wonder why you're irritable?

It's clear as day that the xanax, halcion, and risperdal are only there to control the side effects from overuse of stimulants.

 

[negrogesic]

^^^I suppose I missed that. It answers my question as to the risperdal use indication. Also (in answer to my other questions), I am lead to conjecture that the patient is likely a female in her late ~30's. As to the Dx's, I am going to go out on a limb and say "various-NOS" (joke).

As to the concern of 'pharmacological failure' and 'long-term' consequences resulting from 20mg/day po desoxyn and .5mg risperdal; I see no major issues other than efficacy concerns. Even at .5mg of risperdal, it is still possible for patients to experience EPS manifestations. On a purely personal note, .5mg is subjectively not an insignificant dose; I have taken .5mg experimentally, and found it sufficient to produce a rather unpleasant 'meat-head' effect. Yet, I am hesitant to disagree with a physicians off-label use of the medicine.

In any case, the concerns expressed may be valid, but I feel like this case may involve a number of extreme or extraordinary factors. For instance, two of the medications listed are generally speaking 'last-line' treatments (desoxyn for ADHD, halcion as a hypnotic). Furthermore, while not unheard of, risperdal is generally not used for uncomplicated irritability.

 

[Charles Ferdinand]

5-HT2A and 5HT2C receptors tend to downregulate to both agonists and antagonists.
It's psychopharmacology if you are interested on how will you behave and neuropharmacology if you are interested in how your neurons will behave.

 

[Vaya]

I appreciate the thought, Roger&Me. Irritation as a primary symptom of ADD was the reason I was given Adderall at age 10 - a decision made for me. Had I then had an understanding of neurological development and drug-induced neurotoxicity, I would have opted out and let my being develop thoroughly before choosing to take stims. I believe that to be put on such powerful medications during one of the most significant cruxes of the aging process may forever alter the neurological evolution of the brain. I recognize the probability that stimulants may have been the fulcrum upon which unrelated problems I have encountered in my life originally found leverage, though.

I need to disagree with your conclusion based on the reality that my irritable temperament pre-dates stimulant use - as I've mentioned, I have struggled to control it since birth (though obviously I myself do not remember the first few years of being discontented all the time).
As I began to learn the nuances of the pharmacology of amphetamines at 15, my cognitive rebellion against the idea of taking stimulants at a young age became reality & I stopped taking them for the better part of two years.
Those two years... I shall never forget them. Riddled with inner anger and agitation. I resumed stimulant therapy at age 17, never exceeding 10mg of Adderall daily, and the evidence began to emerge; the irritability disappeared, was erased as though lead by rubber. At 21 I again re-evaluated the stimulants. Could the re-emergence of an irritable temperament have been due to the fact that puberty was in effect when my irritable affect re-emerged without a bit of amphetamine salts? Again, for a year I ceased taking stimulant medications. The results were indisputably identical, and equally as disheartening. I have missed taking it occasionally over the years but it only takes 2-2 1/2 days to be right back where I was. It's really quite surreal, Dr. Jekyll/Mr. Hyde shit. I'm not a monster without 'em but I could definitely stand to be less pissy

Through trial and re-trial I have learned that there is also an absolute & positive correlation between taking low-dose stimulants and a sense of serenity, and this complies with the diagnostic criteria for AD(H)D.
I no longer wonder why I am irritable. Stimulants quiet my mind and adjust the prism through which my mind interprets and responds to the world around me. Without them I have been and would be in the depths of significant suffrage. I no longer wonder why I'm irritable because I'm not irritable on 15mg 2x/day Dexedrine or 10mg Desoxyn 2x/day, which doesn't constitute "overuse of stimulants." At least, not in my mind.
Without what I just shared with you, your logic is reasonable. To be honest I thought it very sound of you to have pointed out the absurdity of using a triad of sedatives to combat the presumed side effect of a fourth medication. It just doesn't apply here.

-------------------------------------------------------------------------------------------------
The Halcion I am no longer prescribed; it was an acute four-week intervention against insomnia related to a traumatic incident I went through not long ago, and I would rather I not need to make the essence of that experience explicit. The "mild irritability" for which Risperdal is prescribed has been a bi-product of depression resulting from the aforementioned trauma. Risperdal is also helping fight that depression.

As to the concern of 'pharmacological failure' and 'long-term' consequences resulting from 20mg/day po desoxyn and .5mg risperdal; I see no major issues other than efficacy concerns. Even at .5mg of risperdal, it is still possible for patients to experience EPS manifestations.

Thank you for this input, it seems I've worked myself up over something insignificant. Referring to "halcion as a hypnotic" and "uncomplicated irritability," please refer to what I've written above. Thank you for your time and insight.

I am lead to conjecture that the patient is likely a female in her late ~30's.

...and then there's THIS. I have no idea how to respond to it, let alone what to think of it!! (kidding around, really, but it makes me introspect to hear that. I'm male and 25 years old.)

~ vaya

 

[ebola?]

My line of inquiry stems from the fact that I do indeed feel the serotonergic effect of d-methamp when I take it

How do you know?

eboal

 

[Hammilton]

^ Bingo!

Probably true though. Risperidone is a strong antidopaminergic as well, and actually blocks more or less of everything methamphetamine aims at (well, targets of recreational value). So if he or she is having desirable effects from the drug, he or she is probably experiencing said desirable effects from all of the receptor targets. Still, having a dopaminergic effect, which is fairly easy to recognize, but trying to discern effects from 5HT release from DA and NA release is more or less impossible. Would be interesting to see how well humans can discern various stimulants from each other when they're given various highly selective antagonists. That's probably the sort of thing you'd have to do in rats, though. Not easy to find a suitable number of people to have a sufficient number of trials with four drugs and eight or more antagonists. I bet similar research has been done in rodents already looking at single drugs.

kind of lost me when I read "irregardless" though....

 

[Vaya]

How do you know?

I don't know for sure, ebola. Conceptually, I tend to think of each neurotransmitter as having a distinct, often unmistakable 'flavor' about it that I can usually identify based on a number of Central- and Peripheral Nervous System reactions I have to them.
Hear me out and then decide if my thinking is just bogus.

As I've indicated in this thread I have an extensive history with therapeutic doses of stimulant medications, primarily of the amphetamine class. This habituation has helped me to identify factors like cognitive motivation, increased sociability and heightened executive function. Norepinephrine I can identify due to its very specific effects on my heart and sympathetic nervous system. The way I can tell these two apart, being that both are stimulatory, is that I have moved from, let's say Adderall to Dexedrine; d-amp has less effect on NE, and so I am able to assess the "flavor" of NE due to its absence in Dexedrine vs. Adderall. By the same token, I can strengthen my ideation of the "flavor" of DA because of the pronunciation of its aforementioned effects the stronger the dopaminergic drug I take.

The same goes with serotonin. There are bodily sensations and visual phenomena (with Desoxyn, lack of stimulant-induced insomnia, better regulation of body temperature than with amphetamine alone, and minor color saturation being the most pronounced), and behavioral symptoms such as an improved ability to sleep post-Desoxyn though I've just taken a more potent DA agonist than I would have with Dexedrine. And while DA agonism deters depression, Serotonin agonism deters it in a less 'rigid' fashion - that is, I can regulate my mood more precisely on a serotonergic compound as opposed to a strictly dopaminergic one. And since I am able to do this on Desoxyn - along with familiar perceptual disturbances vaguely akin to MDMA - and knowing how d-methamp is an agonist to both DA and SE receptors - I make the assumption that the SE-esque properties of d-methamp are, in fact, due to 5-HT receptor agonism. The visual phenomena (most likely stimulated by 5HT2a agonism specifically, like MDMA and your classical psychedelic drugs) disappears from the Desoxyn experience when I take it concomitantly with Risperdal.

Anyhow, this is a poor explanation. And has turned into a poor thread (not anyone else's fault but my own ineptitude at explaining what I really mean). Unless I can verbally conceptualize it more satisfactorily, I'm satisfied, based on my own knowledge of your superior intellect for these types of conversations, that you can decide for yourself whether or not I am disillusioned.
Very thought-provocative question, though. I'd always taken the 'feelings' and 'knowing' to which neurotransmitters they were attributable for granted.

~ vaya

 

[ebola?]

The problems here are multiple:

1. The effects of varied monoamine release are multiple and synergistic: the 'feel' of an agent that releases multiple monoamines will not resemble a thought experiment where one adds up the effects of multiple selective agents. For example, a selective serotonin releaser does not feel like a less focused, energetic, and stimulant-euphoric MDMA; there is something about wide-spectrum monoamine release that induces empathetic opening. One couldn't predict this by looking at amphetamine and a SSRA alone.

It also follows that one can't get an accurate picture of the overall spectra of possible effects by holding the level of release of one monoamine constant and varying the release of another, as you do with your comparison between dexedrine and adderall.

2. Other pharmacological qualities matter. These include direct adrenergic agonism, BBB penetration, direct agonism at monoamine receptors, VMAT2 affinity and efficacy, time course of concentration of the drug in the blood, and other mechanisms of action. For example, 4FA's EC50 values alone wouldn't suggest it more entactogenic than meth.

3. We don't even have very clear pictures of what specific types of monoamine release feel like. For example, no monoamine releaser is highly specific for dopamine. Relatedly, n-ethyl-cathinone, a high selective norepinephrine releaser, is vastly more reinforcing and euphoric than one would have thought.

Your reasoning isn't bad, though. just somewhat speculative.

ebola

 

[Vaya]

just somewhat speculative

Shit, i'll hastily admit they're almost entirely speculative!
One of my tendencies is to let my mind run with speculations. I appreciated the layout of your response; it quite concisely summed up the errors in which I have approached this topic. Esp. loved the 4FA EC50 vs. MDMA example. thanks a lot

~ vaya

 

[SNR]

Answering the "Antagonist/Agonist interaction" question, I would assume that nothing dangerous would occur. The ligand with the stronger binding affinity would bind more readily than the other molecule. Depending on dose, you may have some of the weaker ligand binding to some receptors, but for the most part, only the stronger one would occupy those receptors.

 

[negrogesic]

I appreciate the thought, Roger&Me. Irritation as a primary symptom of ADD was the reason I was given Adderall at age 10 - a decision made for me. Had I then had an understanding of neurological development and drug-induced neurotoxicity, I would have opted out and let my being develop thoroughly before choosing to take stims. I believe that to be put on such powerful medications during one of the most significant cruxes of the aging process may forever alter the neurological evolution of the brain. I recognize the probability that stimulants may have been the fulcrum upon which unrelated problems I have encountered in my life originally found leverage, though.

I need to disagree with your conclusion based on the reality that my irritable temperament pre-dates stimulant use - as I've mentioned, I have struggled to control it since birth (though obviously I myself do not remember the first few years of being discontented all the time).
As I began to learn the nuances of the pharmacology of amphetamines at 15, my cognitive rebellion against the idea of taking stimulants at a young age became reality & I stopped taking them for the better part of two years.
Those two years... I shall never forget them. Riddled with inner anger and agitation. I resumed stimulant therapy at age 17, never exceeding 10mg of Adderall daily, and the evidence began to emerge; the irritability disappeared, was erased as though lead by rubber. At 21 I again re-evaluated the stimulants. Could the re-emergence of an irritable temperament have been due to the fact that puberty was in effect when my irritable affect re-emerged without a bit of amphetamine salts? Again, for a year I ceased taking stimulant medications. The results were indisputably identical, and equally as disheartening. I have missed taking it occasionally over the years but it only takes 2-2 1/2 days to be right back where I was. It's really quite surreal, Dr. Jekyll/Mr. Hyde shit. I'm not a monster without 'em but I could definitely stand to be less pissy

Through trial and re-trial I have learned that there is also an absolute & positive correlation between taking low-dose stimulants and a sense of serenity, and this complies with the diagnostic criteria for AD(H)D.
I no longer wonder why I am irritable. Stimulants quiet my mind and adjust the prism through which my mind interprets and responds to the world around me. Without them I have been and would be in the depths of significant suffrage. I no longer wonder why I'm irritable because I'm not irritable on 15mg 2x/day Dexedrine or 10mg Desoxyn 2x/day, which doesn't constitute "overuse of stimulants." At least, not in my mind.
Without what I just shared with you, your logic is reasonable. To be honest I thought it very sound of you to have pointed out the absurdity of using a triad of sedatives to combat the presumed side effect of a fourth medication. It just doesn't apply here.

-------------------------------------------------------------------------------------------------
The Halcion I am no longer prescribed; it was an acute four-week intervention against insomnia related to a traumatic incident I went through not long ago, and I would rather I not need to make the essence of that experience explicit. The "mild irritability" for which Risperdal is prescribed has been a bi-product of depression resulting from the aforementioned trauma. Risperdal is also helping fight that depression.



Thank you for this input, it seems I've worked myself up over something insignificant. Referring to "halcion as a hypnotic" and "uncomplicated irritability," please refer to what I've written above. Thank you for your time and insight.

...and then there's THIS. I have no idea how to respond to it, let alone what to think of it!! (kidding around, really, but it makes me introspect to hear that. I'm male and 25 years old.)

~ vaya

My apologies; your polite and verbose replies had a 'feminine air', and along with your colorful signature, I assumed you were female in sex.

I am on the run right now so I will more less reiterate my primary concern in your case: At your age, I would be very cautious with neuroleptic therapy unless its truly needed or no alternative exists. Mirtazapine comes to mind.

 

[Vaya]

Answering the "Antagonist/Agonist interaction" question, I would assume that nothing dangerous would occur. The ligand with the stronger binding affinity would bind more readily than the other molecule. Depending on dose, you may have some of the weaker ligand binding to some receptors, but for the most part, only the stronger one would occupy those receptors.

Any thoughts on which might have a higher binding affinity for 5HT2a? My initial speculation is risperidone, since it is among the strongest antagonists of this receptor of all AAP medications, but could be wrong

My apologies; your polite and verbose replies had a 'feminine air', and along with your colorful signature, I assumed you were female in sex.

None necessary man. It's happened countless times in 8+ years here. Plus, no shame in being female or in your late 30's, so it would be crazy to be offended by that assumption, right? hahah :D

found it sufficient to produce a rather unpleasant 'meat-head' effect.

that description is a bulls-eye way to put the feeling. Bingo. That's why I agree with

At your age, I would be very cautious with neuroleptic therapy unless its truly needed or no alternative exists.

~ vaya

 

[atrollappears]

I don't know what you mean when you say you feel the serotonergic aspect, but I don't think that any reasonable clinical dose would have a significant action on serotonin. The reason I say this is that a graph transporter activity by concentration looks like a sigmoid curve, so that below a certain dose and above a certain dose, it doesn't make much difference. The activity curve of meth for SERT is far enough away from the DA/NA ones that DA/NA can be affected while leaving SERT virtually unaffected.

A quick glance at the graph shows, looking at the relative concentration, that this should be the case for clinically relevant doses.
http://www.biomedcentral.com/1471-2210/6/6/figure/F1