81 replies to this topic

[YosefANaumovich]

This is a thread for people who experience schizophrenic symptoms whether having actually been diagnosed schizophrenic or not, and whether having been given a completely different diagnosis (e.g. autism) or not.

 

Wouldn't it be nice if we could share what has worked for our symptoms in order that we may be helped by others and so too help others? It's a win-win!

 

Obviously, the point is not to talk about the drugs already prescribed by psychiatrists but about nootropics and other non-psychiatric drugs that can be bought off-label, are experimental, etc.

 

According to Wikipedia, symptoms of schizophrenia are the following:

(Positive - symptoms that add)

1. Hallucinations (tactile, auditory, visual, olfactory, gustatory).

2. Delusions (false beliefs that are fixed and not subject to reasoning).

3. Paranoia (feeling of persecution, being watched, etc.).

4. Bizarre behaviors.

5. Disordered thoughts and/or speech (disorganized thoughts, word salads, thought blocking) 

6. Movement disorders (agitated movements or no movements at all).

 

(Negative/cognitive - symptoms that take away)

7. Flat affect (lack of facial expressions, face appears flat, monotone voice).

8. Lack of ability to experience pleasure.

9. Lack of ability to experience any emotions at all.

10. Lack of ability to plan and/or fulfill plans.

11. Lack of communication (subject uses very few words or none at all).

12. Poor executive functioning (ability to understand and use information in decision-making).

13. reduced focus or attention span.

14. Poor working memory (using information after learning it).

15. Sudden unexplainable mood changes (i.e. agitation, happiness, etc., not to be confused with bipolar disorder).

 

If there are any mistakes in the original post (i.e. this) then do mention them and I will correct them thereafter.

Edited by YosefANaumovich, 29 April 2015 - 10:53 AM.

[YosefANaumovich]

It needs to be said that I am not a diagnosed schizophrenic nor do I experience delusions or hallucinations (If I believed I did, they wouldn't be anyway). My symptoms are mainly cognitive deficits and negative symptoms.

 

Here are a list of things that have currently worked for me:

3: niacin (nicotinic acid 500mg+), l-theanine(400mg+ suntheanine), magnesium (3g+).

(I obviously do not consider myself paranoid but from a psychiatrist's perspective, it could be termed paranoia.)

 

7: St. John's Wort ("SJW," recommended dosage), choline (bitartate 500mg+) prior to bed, niacin (nicotinic acid 500mg+).

9: SJW, Choline (bititrate 500mg+) before bed, l-tyrosine + fasting (2g+), DL- phenynalaline + fasting (500mg+)

15: Increasing testosterone significantly, abstaining from sexual activities, doing thorough daily exercises.

 

 

The "new" theory about what causes schizophrenia's cognitive deficits (negative symptoms) and positive symptoms is an underfunctioning NMDA receptor. It's of course more complex than that but that's what you'd get from reading about it in popular-level journals.

Thus, any drug that works as an AGONIST (not ANTagonist) should improve schizophrenic symptoms, while anything that works as an ANTagonist should worsen schizophrenic symptoms significantly.

 

Agonists are chemicals like l-theanine, l-sarcosine, D-aspartic acid (especially when coupled with sarcosine), NAC (N-acetyl-cysteine) and others.

Antagonists are chemicals like ketamine, "angel dust, " etc.

 

Did sarcosine, D-aspartic acid and NAC work for my symptoms? Absolutely not. If there were any effect then such an effect was negligible and might as well just have been a placebo.

 

It needs to be noted that chemicalss that work too much on the NMDA receptor reportedly can cause neurotoxicity and thus any chemical that works on the NMDA receptor should only do so a little.

Edited by YosefANaumovich, 29 April 2015 - 11:09 AM.

[YoungSchizo]

Been taking Sarcosine for 5 years, it changed my life and/or drastically severity of some debilitating symptoms. Combined with DAA it's double effective but after 1/2 weeks adding DAA it's making me depressed, I guess the neurotoxicity.

 

SJW is a very tricky supplement to take for schizophrenics, read many anecdotes that there is a big chance it may worsen positives.

 

I've tried a shit load of meds, supplements and some nootropics. Mostly all failures, what has helped me:

Mirtazapine - damping my hyperactive (mania-like) thoughts.

Sarcosine - alleviated positive, cognitive and negative symptoms (mainly cognitive and negatives).

Clonazepam - Made my hallucinations go away. And there is proof that it normalizes brain waves and enhances cognition.

CBD - great drug to monitor my irregular/faulty thought-process and it normalized the function of my PFC. Mainly alleviated thought intrusions and normalized the disruptive brainwaves in the PFC region.

Pregnenolone - enhances mood and negatives (slightly). But it's a great supplement to normalize hormonal balance and/or regain muscle tissue when quitting antipsychotics (antipsychotics just kills the balance in my experience, even after quitting)

 

Nootropics I'm not sure if it helps yet, I have to revisit those one day.

 

My 2 cents

[YosefANaumovich]

Been taking Sarcosine for 5 years, it changed my life and/or drastically severity of some debilitating symptoms. Combined with DAA it's double effective but after 1/2 weeks adding DAA it's making me depressed, I guess the neurotoxicity.

 

SJW is a very tricky supplement to take for schizophrenics, read many anecdotes that there is a big chance it may worsen positives.

 

I've tried a shit load of meds, supplements and some nootropics. Mostly all failures, what has helped me:

Mirtazapine - damping my hyperactive (mania-like) thoughts.

Sarcosine - alleviated positive, cognitive and negative symptoms (mainly cognitive and negatives).

Clonazepam - Made my hallucinations go away. And there is proof that it normalizes brain waves and enhances cognition.

CBD - great drug to monitor my irregular/faulty thought-process and it normalized the function of my PFC. Mainly alleviated thought intrusions and normalized the disruptive brainwaves in the PFC region.

Pregnenolone - enhances mood and negatives (slightly). But it's a great supplement to normalize hormonal balance and/or regain muscle tissue when quitting antipsychotics (antipsychotics just kills the balance in my experience, even after quitting)

 

Nootropics I'm not sure if it helps yet, I have to revisit those one day.

 

My 2 cents

Sarcosine for 5 years? That's a very long time! What was your dosage and how long did it take until you noticed that it bettered your situation?

[YoungSchizo]

 

Been taking Sarcosine for 5 years, it changed my life and/or drastically severity of some debilitating symptoms. Combined with DAA it's double effective but after 1/2 weeks adding DAA it's making me depressed, I guess the neurotoxicity.

 

SJW is a very tricky supplement to take for schizophrenics, read many anecdotes that there is a big chance it may worsen positives.

 

I've tried a shit load of meds, supplements and some nootropics. Mostly all failures, what has helped me:

Mirtazapine - damping my hyperactive (mania-like) thoughts.

Sarcosine - alleviated positive, cognitive and negative symptoms (mainly cognitive and negatives).

Clonazepam - Made my hallucinations go away. And there is proof that it normalizes brain waves and enhances cognition.

CBD - great drug to monitor my irregular/faulty thought-process and it normalized the function of my PFC. Mainly alleviated thought intrusions and normalized the disruptive brainwaves in the PFC region.

Pregnenolone - enhances mood and negatives (slightly). But it's a great supplement to normalize hormonal balance and/or regain muscle tissue when quitting antipsychotics (antipsychotics just kills the balance in my experience, even after quitting)

 

Nootropics I'm not sure if it helps yet, I have to revisit those one day.

 

My 2 cents

Sarcosine for 5 years? That's a very long time! What was your dosage and how long did it take until you noticed that it bettered your situation?

 

 

My dosage is still 2g a day. The effect/improvement with Sarcosine was instantly. Some debilitating positive symptoms decreased 90% and till this day it remains that way. The improvement of negative symptoms also increased instantly, this hasn't change much till this day. Cognitive enhancement slowly increased over many months. Though, I have to add, Sarcosine is not a magic bullet for any of these symptoms. If your NMDA genetic make-up is "like mine" it can change some symptoms drastically, other people don't see any improvement at all, no matter which dosage they try, that's why Bitopertin has failed to pass the phase III clinical trials.

 

btw the combo NAC + Sarcosine seem to help some people. For me NAC does nothing, it even may have worsened my positive when I took it.

[AlexCanada]

How do you guys get the Niacin to work reliably? It would sometimes cause a strong flush where I feel lousy and dumb for 1-2 hours but then afterwards my mind is flowing so much more smoothly. I become more pro-social, animated, more lively, and mood is more positive.  But sometimes it feels like the flush can last for 20+ hours or I feel a strong dullness and bland feeling, very unreactive mood for extended period of time. It's very unpredictable. The regular non-time release Niacin.

 

Also would Glycine work similarly to Sarcosine? Sarcosine sounds amazing.  I assume glycine to be taken before bed?

 

How long usually for benefits?

 

I mainly have most the negative symptoms of schiz including emotional dullness, anhedonia and cognitive issues.   Magnesium Glycinate worked some wonders before but the dopamine antagonism from magnesium aspect made me feel apathetic at times.

[YosefANaumovich]

How do you guys get the Niacin to work reliably? It would sometimes cause a strong flush where I feel lousy and dumb for 1-2 hours but then afterwards my mind is flowing so much more smoothly. I become more pro-social, animated, more lively, and mood is more positive.  But sometimes it feels like the flush can last for 20+ hours or I feel a strong dullness and bland feeling, very unreactive mood for extended period of time. It's very unpredictable. The regular non-time release Niacin.

 

Also would Glycine work similarly to Sarcosine? Sarcosine sounds amazing.  I assume glycine to be taken before bed?

 

How long usually for benefits?

 

I mainly have most the negative symptoms of schiz including emotional dullness, anhedonia and cognitive issues.   Magnesium Glycinate worked some wonders before but the dopamine antagonism from magnesium aspect made me feel apathetic at times.

You are correct with niacin (nicotinic acid). Sometimes niacin works, sometimes it doesn't. Sometimes it causes a great euphoria and lessens some of the schizophrenic symptoms, sometimes it doesn't.

When it doesn't, it doesn't matter if you take 500mg or 10g, it just won't work. But when it does work, it can work with as little as 500mg, less or more.

 

I know that some drugs cease to work if other drugs are absent in the body, such as with racetams whose requirements are primarily choline, carnitine and sodium; if not enough sodium or carnitine or choline is available then headache and other symptoms can occur, or simply none at all, and racetams reduce these chemicals as well.

 

I know that niacin, from studies, slightly effects choline levels. Thus, I've taken niacin with choline but the only times I've noticed anything with this combination was if I took them prior to going to sleep and in such a case it most likely was just the choline at work and not the niacin, since choline produces this "wellness" feeling on its own after waking up.

 

Then, since niacin works in combination with fats, I've taken high amounts of coconut oil (around 80% saturated fat) slightly prior to administrating niacin. This also did not produce any noticeable effect.

 

Maybe niacin requires the presence of other B vitamins, or maybe fatty-acids, or proteins, or G-d knows what.

 

I think it would be great if one of us bought all the conceivable possible things that niacin could require, such as proteins, etc., and narrowed down what made niacin work and what didn't. That may be an experiment for me to do.

 

 

As for glycine and sarcosine, glycine according to what I've read has shown great effects on schizophrenics but the problem is that the absorption of it is poor and very high doses (many grams) need to be administrated daily to notice any effect at all. I think 40grams were mentioned and that's obviously not a route for any non-rich person to take. There may also have been mentioned the problem of glycine toxicity at so high doses.

Sarcosine, on the other hand, doesn't require that high doses and as YoungSchizo pointed out, causes good improvements.

Though, it may not work for you. Neither sarcosine nor D-aspartic acid in high amounts, even with NAC added (all 3 chemicals are NMDA agonists) made any difference whatsoever for me.

l-theanine, however, being another NMDA agonist, did very slightly alleviate some symptoms for me. The problem, though, is that it works on glutamate primarily and thus causes drowsiness as would be felt if one took high amounts of glutamate.

[YosefANaumovich]

I know that people have tried NAC (N-acetyl-Cysteine) which is a precursor for glutathione, and have done so without much improvement if any improvement at all, but has anyone tried glutathione itself?

Evidence supports that ketamine - being an nmda antagonist and inducing schizophrenia-like symptoms, blocks glutathione absorption. Evidence also supports that schizophrenics lack glutathione.

http://www.ncbi.nlm....pubmed/18703087

 

[Flex]

I believe that the mGlu2/3 agonism of NAC causes the flat affect, or at least to me.

Green tea extract is afaik a (mild) glutamate releaser. So from my theory, it should be thje opposite of NAC.

Keep in mind that its also a potent blood thinner.

[Area-1255]

I believe that the mGlu2/3 agonism of NAC causes the flat affect, or at least to me.

Green tea extract is afaik a (mild) glutamate releaser. So from my theory, it should be thje opposite of NAC.

Keep in mind that its also a potent blood thinner.

A 5-HT5A antagonist plus a 5-HT1A antagonist should be a novel, potent, and void of side-effect treatment for schizophrenia..unfortunately, no chemicals exist outside of scientific study...for this and other reasons , we need to rally to get companies to produce these chemicals. 

 

5-HT1A antagonists not only would help psychotic disorders, but would also improve.

 

• OCD (obsessive compulsive disorder)
• Depression
• The efficacy of SSRI's and reduce side-effects if coupled with a 5-HT2A antagonist.
• Dysautonomia and adrenaline deficiency. (perhaps improving stimulant dependence and addiction)

 

5-HT5A antagonists would help as well as psychosis.

 

• OCD 
• Anxiety
• Insomnia

 

http://www.sciencedi...924977X14002065    /  http://www.acnp.org/...0117/CH115.html

 

 

 

Abstract ASP5736, a novel 5-HT_5A receptor antagonist, ameliorates positive symptoms and cognitive impairment in animal models of schizophrenia

We recently identified ASP5736, (N-(diaminomethylene)-1-(3,5-difluoropyridin-4-yl)-4-fluoroisoquinoline-7-carboxamide (2E)-but-2-enedioate), a novel antagonist of 5-HT_5A receptor, and here describe the in vitro and in vivo characterization of this compound. ASP5736 exhibited a high affinity for the human 5-HT_5Areceptor (K_i=3.6±0.66 nM) and antagonized 5-carboxamidotryptamine (5-CT)-induced Ca²⁺ influx in human cells stably expressing the 5-HT_5A receptor with approximately 200-fold selectivity over other receptors, including other 5-HT receptor subtypes, enzymes, and channels except human 5-HT_2c receptor (Ki=286.8 nM) and 5-HT₇ receptor (Ki=122.9 nM). Further, ASP5736 dose-dependently antagonized the 5-CT-induced decrease in cAMP levels in HEK293 cells stably expressing the 5-HT_5A receptor. We then evaluated the effects of ASP5736 on cognitive impairments in several animal models of schizophrenia. Working memory deficit in MK-801-treated mice and visual learning deficit in neonatally phencyclidine (PCP)-treated mice were both ameliorated by ASP5736. In addition, ASP5736 also attenuated MK-801- and methamphetamine (MAP)-induced hyperactivity in mice without causing sedation, catalepsy, or plasma prolactin increase. The addition of olanzapine did not affect ASP5736-induced cognitive enhancement, and neither the sedative nor cataleptogenic effects of olanzapine were worsened by ASP5736. These results collectively suggest that ASP5736 is a novel and potent 5-HT_5A receptor antagonist that not only ameliorates positive-like symptoms but also cognitive impairments in animal models of schizophrenia, without adverse effects. Present studies also indicate that ASP5736 holds potential to satisfy currently unmet medical needs for the treatment of schizophrenia by either mono-therapy or co-administered with commercially available antipsychotics.

 

 

 

WAY 100135, an Antagonist of 5-HT1A Serotonin Receptors, Attenuates Psychotomimetic Effects of MK-801

Krzysztof Wdzony Ph.D¹, Marzena Maćkowiak Ph.D¹, Wojciech Zajczkowski Ph.D¹, Katarzyna Fijal MS¹, Agnieszka Chocyk MS¹ and Anna Czyrak Ph.D¹

¹Institute of Pharmacology, Polish Academy of Sciences, Kraków, Poland

Correspondence: Dr. Krzysztof Wedzony, Institute of Pharmacology, Polish Academy of Sciences; 31–343 Kraków, 12 Smtna Street, Poland

Received 11 February 2000; Revised 9 May 2000; Accepted 25 May 2000

Topof page Abstract

In the present study, we investigated whether the antagonist of 5-HT1A receptors, WAY 100135, was capable of modifying the psychostimulant and psychotomimetic effects of MK-801, a non-competitive antagonist of NMDA receptors. It was found that: 1) WAY 100135 (10 and 20 mg/kg, but not 1.25, 2.5, and 5 mg/kg) transiently, in a dose dependent manner, attenuated the locomotor stimulant effects of MK-801 (0.4 mg/kg). Given alone, WAY 100135 had no effect on the locomotor activity of rats; 2) WAY 100135 (1.25 and 2.5 mg/kg, but not 10 or 20 mg/kg), attenuated or abolished the disruptive effects of MK-801 on the sensorimotor gating measured in a prepulse-induced inhibition of the acoustic startle response paradigm. WAY 100135 in all tested doses had no effect on the sensorimotor gating or amplitude of the acoustic startle response; 3) WAY 100135 (1.25, 2.5 mg/kg, but not 5 mg/kg) attenuated the detrimental effects of MK-801 on working memory and selective attention, measured in a delayed alternation task. Again, given alone, WAY 100135 did not influence the behavior of rats in that experimental paradigm; and 4) MK-801 (0.4 mg/kg) had no effect on the 5-HT1A receptor mRNA level in rat hippocampus, measured 2 and 24 hours after MK-801 administration. These data indicate that 5-HT1A receptors might be involved in the psychotomimetic effects of non-competitive NMDA receptor antagonists. In addition, 5-HT1A serotonin receptor antagonists and partial agonists may have potential antipsychotic properties.

http://www.nature.co...l/1395558a.html

Edited by Area-1255, 01 May 2015 - 08:19 PM.

[Flex]

Forgott to mention Sodium Benzoate.

It worked seemingly only to me, but there are some research papers about it.

 

IIRC the effects were for 1 h subtle and ok but followed by confusion and foggish state which lasted 3-4 hours.

However I had an nice euphoric feeling aftewards which lasted 2-3 days.

 

I have to add that everything what I´ve taken the first time, had strong effects compared o the following times where I sometimes barely experienced the half of it or even lesser.

In addition, I´am and was on Mirtazapine (45mg) which increases cortical glutamate via adrenergic a2 inhibition

 

--> danger of glutamate toxicity when taking something glutamergic and inhibiting a2 !!!!

 

See:

Sodium benzoate a D-serine degradation inhibitor and PFC activator

http://www.longecity...-pfc-activator/

Edited by Flex, 01 May 2015 - 10:11 PM.

[YosefANaumovich]

I believe that the mGlu2/3 agonism of NAC causes the flat affect, or at least to me.

Green tea extract is afaik a (mild) glutamate releaser. So from my theory, it should be thje opposite of NAC.

Keep in mind that its also a potent blood thinner.

L-theanine (amino acid in Green Tea) is an NMDA agonist. I take it and it is sedating in high doses and relaxing in lower dosages. I do feel that it removes my flat affect.
NAC, however, has absolutely no effect on me from what I can tell and I take 1 gram of it in the morning, 1 gram prior to bed, and have been doing so for at least a month now (used to take it with multiple grams of sarcosine and D-aspartic acid daily and noticed no effect either).

 

Would glutathione itself cause flat affect, or work better than NAC?

The obvious thing would be to think that the reason that NAC was suggested instead of glutathione (while NAC is a precursor for glutathione) is because NAC is more effective.

But I've seen sources that claim that glutathione itself is more effective (although not credible ones).

[Flex]

This might be, though it had dulling efects to me. Some dont experience this effect and are satisfied.

Sry I was actually reffering to EGCG:

(-)-Epigallocatechin gallate, the most active polyphenolic catechin in green tea, presynaptically facilitates Ca2+-dependent glutamate release via activation of protein kinase C in rat cerebral cortex.

http://www.ncbi.nlm....pubmed/17663453

[YoungSchizo]

 

I believe that the mGlu2/3 agonism of NAC causes the flat affect, or at least to me.

Green tea extract is afaik a (mild) glutamate releaser. So from my theory, it should be thje opposite of NAC.

Keep in mind that its also a potent blood thinner.

A 5-HT5A antagonist plus a 5-HT1A antagonist should be a novel, potent, and void of side-effect treatment for schizophrenia..unfortunately, no chemicals exist outside of scientific study...for this and other reasons , we need to rally to get companies to produce these chemicals. 

 

5-HT1A antagonists not only would help psychotic disorders, but would also improve.

 

• OCD (obsessive compulsive disorder)
• Depression
• The efficacy of SSRI's and reduce side-effects if coupled with a 5-HT2A antagonist.
• Dysautonomia and adrenaline deficiency. (perhaps improving stimulant dependence and addiction)

 

5-HT5A antagonists would help as well as psychosis.

 

• OCD 
• Anxiety
• Insomnia

 

http://www.sciencedi...924977X14002065    /  http://www.acnp.org/...0117/CH115.html

 

 

 

Abstract ASP5736, a novel 5-HT_5A receptor antagonist, ameliorates positive symptoms and cognitive impairment in animal models of schizophrenia

We recently identified ASP5736, (N-(diaminomethylene)-1-(3,5-difluoropyridin-4-yl)-4-fluoroisoquinoline-7-carboxamide (2E)-but-2-enedioate), a novel antagonist of 5-HT_5A receptor, and here describe the in vitro and in vivo characterization of this compound. ASP5736 exhibited a high affinity for the human 5-HT_5Areceptor (K_i=3.6±0.66 nM) and antagonized 5-carboxamidotryptamine (5-CT)-induced Ca²⁺ influx in human cells stably expressing the 5-HT_5A receptor with approximately 200-fold selectivity over other receptors, including other 5-HT receptor subtypes, enzymes, and channels except human 5-HT_2c receptor (Ki=286.8 nM) and 5-HT₇ receptor (Ki=122.9 nM). Further, ASP5736 dose-dependently antagonized the 5-CT-induced decrease in cAMP levels in HEK293 cells stably expressing the 5-HT_5A receptor. We then evaluated the effects of ASP5736 on cognitive impairments in several animal models of schizophrenia. Working memory deficit in MK-801-treated mice and visual learning deficit in neonatally phencyclidine (PCP)-treated mice were both ameliorated by ASP5736. In addition, ASP5736 also attenuated MK-801- and methamphetamine (MAP)-induced hyperactivity in mice without causing sedation, catalepsy, or plasma prolactin increase. The addition of olanzapine did not affect ASP5736-induced cognitive enhancement, and neither the sedative nor cataleptogenic effects of olanzapine were worsened by ASP5736. These results collectively suggest that ASP5736 is a novel and potent 5-HT_5A receptor antagonist that not only ameliorates positive-like symptoms but also cognitive impairments in animal models of schizophrenia, without adverse effects. Present studies also indicate that ASP5736 holds potential to satisfy currently unmet medical needs for the treatment of schizophrenia by either mono-therapy or co-administered with commercially available antipsychotics.

 

 

 

WAY 100135, an Antagonist of 5-HT1A Serotonin Receptors, Attenuates Psychotomimetic Effects of MK-801

Krzysztof Wdzony Ph.D¹, Marzena Maćkowiak Ph.D¹, Wojciech Zajczkowski Ph.D¹, Katarzyna Fijal MS¹, Agnieszka Chocyk MS¹ and Anna Czyrak Ph.D¹

¹Institute of Pharmacology, Polish Academy of Sciences, Kraków, Poland

Correspondence: Dr. Krzysztof Wedzony, Institute of Pharmacology, Polish Academy of Sciences; 31–343 Kraków, 12 Smtna Street, Poland

Received 11 February 2000; Revised 9 May 2000; Accepted 25 May 2000

Topof page Abstract

In the present study, we investigated whether the antagonist of 5-HT1A receptors, WAY 100135, was capable of modifying the psychostimulant and psychotomimetic effects of MK-801, a non-competitive antagonist of NMDA receptors. It was found that: 1) WAY 100135 (10 and 20 mg/kg, but not 1.25, 2.5, and 5 mg/kg) transiently, in a dose dependent manner, attenuated the locomotor stimulant effects of MK-801 (0.4 mg/kg). Given alone, WAY 100135 had no effect on the locomotor activity of rats; 2) WAY 100135 (1.25 and 2.5 mg/kg, but not 10 or 20 mg/kg), attenuated or abolished the disruptive effects of MK-801 on the sensorimotor gating measured in a prepulse-induced inhibition of the acoustic startle response paradigm. WAY 100135 in all tested doses had no effect on the sensorimotor gating or amplitude of the acoustic startle response; 3) WAY 100135 (1.25, 2.5 mg/kg, but not 5 mg/kg) attenuated the detrimental effects of MK-801 on working memory and selective attention, measured in a delayed alternation task. Again, given alone, WAY 100135 did not influence the behavior of rats in that experimental paradigm; and 4) MK-801 (0.4 mg/kg) had no effect on the 5-HT1A receptor mRNA level in rat hippocampus, measured 2 and 24 hours after MK-801 administration. These data indicate that 5-HT1A receptors might be involved in the psychotomimetic effects of non-competitive NMDA receptor antagonists. In addition, 5-HT1A serotonin receptor antagonists and partial agonists may have potential antipsychotic properties.

http://www.nature.co...l/1395558a.html

 

 

 

Possibilities to obtain ASP5736..?

[Flex]

Found those two antipsychotics to be inverse agonist at 5-ht1a.

 

Spiperone

http://en.wikipedia.org/wiki/Spiperone

 

Methiothepin

http://en.wikipedia....wiki/Metitepine

 

but at least in the case of Spiperone, unfortunaetly at the presynaptic site:

 

Autoregulation of Serotonin Neurons: Role in Antidepressant Drug Action

1) different rank order in the effectiveness of 5-HT1A agonists to inhibit DRN (8-OH-DPAT, gepirone > LSD > 5-HT) versus hippocampus firing activity (5-HT > gepirone > 8-OH-DPAT; Blier and de Montigny, 1987,1990; Chaput and de Montigny, 1988); 2) preferential antagonistic effect of BMY 7378 at postsynaptic sites (Chaput and de Montigny, 1988) and of spiperone at presynaptic receptors (Lum and Piercey, 1988; Blier et al., 1989b, 1993a; Fornal et al., 1994a);

http://intl.pharmrev...t/51/3/533.full

 

 

You could look into Zinc which is a negative allsoteric modulator of post 5-ht1a.

The downside is its NMDA inhibition but afaik its weak.

From my experiences, I feel allready a vasoconstriction  at 10mg and (believe ) to have lesser hot flushes in my face when I´m nervous,

also I for my self dont experience any great dulling NMDA blockade effect at 10mg, though others might be more sensitive dont know.

See:

Allosteric modulation of 5-HT(1A) receptors by zinc: Binding studies.

http://www.ncbi.nlm....pubmed/18951909

 

posted in

 

http://www.longecity...e-2#entry723809

Edited by Flex, 02 May 2015 - 06:54 PM.

[Area-1255]

Oh if only it were That easy, problem is of course...they are both anti-psychotics..so they have dopamine affinity....

{sigh} if only tht.co would hurry up and get back online!!

Asenapine is an odd chemical.

Found those two antipsychotics to be inverse agonist at 5-ht1a.

 

Spiperone

http://en.wikipedia.org/wiki/Spiperone

 

Methiothepin

http://en.wikipedia....wiki/Metitepine

 

but at least in the case of Spiperone, unfortunaetly at the presynaptic site:

 

Autoregulation of Serotonin Neurons: Role in Antidepressant Drug Action

1) different rank order in the effectiveness of 5-HT1A agonists to inhibit DRN (8-OH-DPAT, gepirone > LSD > 5-HT) versus hippocampus firing activity (5-HT > gepirone > 8-OH-DPAT; Blier and de Montigny, 1987,1990; Chaput and de Montigny, 1988); 2) preferential antagonistic effect of BMY 7378 at postsynaptic sites (Chaput and de Montigny, 1988) and of spiperone at presynaptic receptors (Lum and Piercey, 1988; Blier et al., 1989b, 1993a; Fornal et al., 1994a);

http://intl.pharmrev...t/51/3/533.full

 

 

You could look into Zinc which is a negative allsoteric modulator of post 5-ht1a.

The downside is its NMDA inhibition but afaik its weak.

From my experiences, I feel allready a vasoconstriction  at 10mg and (believe ) to have lesser hot flushes in my face when I´m nervous,

also I for my self dont experience any great dulling NMDA blockade effect at 10mg, though others might be more sensitive dont know.

See:

Allosteric modulation of 5-HT(1A) receptors by zinc: Binding studies.

http://www.ncbi.nlm....pubmed/18951909

 

posted in

 

http://www.longecity...e-2#entry723809

 

[Flex]

I´ve intended it for YZ because hes using anyway Antipsychotics.

Sry forgott to mention it.

 

 

 

[Area-1255]

I´ve intended it for YZ because hes using anyway Antipsychotics.

Sry forgott to mention it.

Oh, no problemo, he's a little flustered right now. Read his profile. 

 

EDIT : Not if you mean Young Schizo, not him, he's cool..the other guys acting like a nut case though.

Edited by Area-1255, 02 May 2015 - 11:23 PM.

[Flex]

wow.

I guess there must be a common past or something. ála back then in kuwait or vietnam lol

Anyway, I know that I dont know

 

btw, I´ve meant Young Schizo.

[Area-1255]

wow.

I guess there must be a common past or something. ála back then in kuwait or vietnam lol

Anyway, I know that I dont know

 

btw, I´ve meant Young Schizo.

I figured, and as far as the other stuff - I'm sure you took a look at the other dude's lavish delirium. Nice little pedestal right on the front page to show how much of a lunatic can really surf onto LC, and crash within 72 hours. 

[YoungSchizo]

LOL wtf happened to that guy, did I miss something?

[YoungSchizo]

I've been on ZMA (zinc 30mg, magnesium and B6) for years. Can't really say that it negatively or positively effects my symptoms, don't feel much difference on or off it at all. 

 

As for typical antipsychotic, is it worth looking into it? I mean, aren't those much more evil than atypicals when it comes down to dopamine affinity and/or serious side-effects? 

[Area-1255]

I've been on ZMA (zinc 30mg, magnesium and B6) for years. Can't really say that it negatively or positively effects my symptoms, don't feel much difference on or off it at all. 

 

As for typical antipsychotic, is it worth looking into it? I mean, aren't those much more evil than atypicals when it comes down to dopamine affinity and/or serious side-effects? 

Abilify is like the only anti-psychotic with negligible / minimal side-effects , including neuro-endocrine but it can still cause anxiety for some people...amisulpride is relatively low on side-effects but it is not available in the USA.

Clozapine is sort of safe, but it also has anti-cholinergic effects. Still less side-effects than the majority of anti-psychotics, though. Less dopamine antagonism as well.

[YoungSchizo]

 

I've been on ZMA (zinc 30mg, magnesium and B6) for years. Can't really say that it negatively or positively effects my symptoms, don't feel much difference on or off it at all. 

 

As for typical antipsychotic, is it worth looking into it? I mean, aren't those much more evil than atypicals when it comes down to dopamine affinity and/or serious side-effects? 

Abilify is like the only anti-psychotic with negligible / minimal side-effects , including neuro-endocrine but it can still cause anxiety for some people...amisulpride is relatively low on side-effects but it is not available in the USA.

Clozapine is sort of safe, but it also has anti-cholinergic effects. Still less side-effects than the majority of anti-psychotics, though. Less dopamine antagonism as well.

 

 

Abilify I've tried in the past but it was to sedating/zombifing. Amulsipride is available here, I've tried to get that but they rejected my wish because the pdoc was not "familiar" with it's MAO. Clozapine I never thought about because of it's possible negative effect on the liver and I don't want to let my blood checked-up every couple weeks/months.

 

What do you think of this one Lurasidone, it's fairly new. The thing that's important for me while picking a "new" (even though they're all crap) anti-psychotic is that I can still be creative and maintain/gain muscle-mass. I'll probably go with Lurasidone, if that doesn't relieve some symptoms I will force them to give my Amulsipride. 

[Area-1255]

 

 

I've been on ZMA (zinc 30mg, magnesium and B6) for years. Can't really say that it negatively or positively effects my symptoms, don't feel much difference on or off it at all. 

 

As for typical antipsychotic, is it worth looking into it? I mean, aren't those much more evil than atypicals when it comes down to dopamine affinity and/or serious side-effects? 

Abilify is like the only anti-psychotic with negligible / minimal side-effects , including neuro-endocrine but it can still cause anxiety for some people...amisulpride is relatively low on side-effects but it is not available in the USA.

Clozapine is sort of safe, but it also has anti-cholinergic effects. Still less side-effects than the majority of anti-psychotics, though. Less dopamine antagonism as well.

 

 

Abilify I've tried in the past but it was to sedating/zombifing. Amulsipride is available here, I've tried to get that but they rejected my wish because the pdoc was not "familiar" with it's MAO. Clozapine I never thought about because of it's possible negative effect on the liver and I don't want to let my blood checked-up every couple weeks/months.

 

What do you think of this one Lurasidone, it's fairly new. The thing that's important for me while picking a "new" (even though they're all crap) anti-psychotic is that I can still be creative and maintain/gain muscle-mass. I'll probably go with Lurasidone, if that doesn't relieve some symptoms I will force them to give my Amulsipride. 

 

I think that Latuda (Lurasidone) has terribly corny commercials, lol. 

As far as it's mechanism of action , it has an even greater affinity for 5-HT7 than risperidone, but also has zero / negligible histamine affinity which means it should produce far less sedation or be void of sedation...it doesn't seem too bad...and the 5-HT7/2A antagonist properties could be very beneficial for bodybuilding as it would result in cortisol reduction.

[OneScrewLoose]

I feel that Latuda is one of the most well-developed anti-psychotics in a while.

[Area-1255]

I feel that Latuda is one of the most well-developed anti-psychotics in a while.

Seems to be not harmful and the lack of histamine affinity is a beautiful thing for those who have grown weary of the sedative effects of the majority of drugs in that class.

[YoungSchizo]

 

 

 

I've been on ZMA (zinc 30mg, magnesium and B6) for years. Can't really say that it negatively or positively effects my symptoms, don't feel much difference on or off it at all. 

 

As for typical antipsychotic, is it worth looking into it? I mean, aren't those much more evil than atypicals when it comes down to dopamine affinity and/or serious side-effects? 

Abilify is like the only anti-psychotic with negligible / minimal side-effects , including neuro-endocrine but it can still cause anxiety for some people...amisulpride is relatively low on side-effects but it is not available in the USA.

Clozapine is sort of safe, but it also has anti-cholinergic effects. Still less side-effects than the majority of anti-psychotics, though. Less dopamine antagonism as well.

 

 

Abilify I've tried in the past but it was to sedating/zombifing. Amulsipride is available here, I've tried to get that but they rejected my wish because the pdoc was not "familiar" with it's MAO. Clozapine I never thought about because of it's possible negative effect on the liver and I don't want to let my blood checked-up every couple weeks/months.

 

What do you think of this one Lurasidone, it's fairly new. The thing that's important for me while picking a "new" (even though they're all crap) anti-psychotic is that I can still be creative and maintain/gain muscle-mass. I'll probably go with Lurasidone, if that doesn't relieve some symptoms I will force them to give my Amulsipride. 

 

I think that Latuda (Lurasidone) has terribly corny commercials, lol. 

As far as it's mechanism of action , it has an even greater affinity for 5-HT7 than risperidone, but also has zero / negligible histamine affinity which means it should produce far less sedation or be void of sedation...it doesn't seem too bad...and the 5-HT7/2A antagonist properties could be very beneficial for bodybuilding as it would result in cortisol reduction.

 

 

I've read about the commercials thing, here they are not allowed to commercialize pharma medicine.

 

Anyway, wow, that's great to know, ty!

[OneScrewLoose]

How much CBD do you take daily?

[YoungSchizo]

How much CBD do you take daily?

 

I've quit CBD for now because I went off Zyprexa and some symptoms returned, my inner thoughts are hard to control and are somewhat "distorted/scrambled" (don't know how to explain) which CBD does not help against. So, monitoring my faulty thought-process and correcting it is too hard of a job right now.

 

But before that I smoked 1/2 joints, sometimes daily, other times with some days between them (recreationally :D and/or to counter symptoms). CBD made me quite insightful of what happens inside my head/thoughts and what's wrong with it, I don't know for sure but because now that I know what's wrong it, it is probably also why my brainwaves in the PFC-region still works fine and I still have almost full control over thought-intrusions. Which is a "miracle" because I'm in the middle of a serious stress-situation where usually I/my brain (undeliberately) force my brainwaves to go wacky.

 

More info on my CBD adventure here and here.

 

I'll be back on CBD once I start with Lurasidone.

 

edit: Maybe I could still have benefited from the effects of CBD if I had the oil-form (so I could adjust my intake to make it beneficial) but for the time being I don't trust the cheap shit what the market has to offer.

Edited by YoungSchizo, 06 May 2015 - 02:02 PM.