Glutamate in schizophrenia: Neurodevelopmental perspectives and drug development


That’s very interesting. Wish they could develop the right drugs then.

Thanks, my psychiatrist wants to investigate if i can go in ketamine treatment. I dont understand all the technical stuff (tired today) but ketamine is an nmda antagonist, so i might benefit from the treatment according to this article?

I will keep you updated if i undergo ketamine treatment.

Well some say ketamine is not an possibility for schizophrenics because it triggers psychosis, others, mostly case reports, have found good effect:

What is the targets that the current drugs targeting ?
Are they targeting the cause (psychosis factor),the effect,the symptoms be delt by the schizophrened person or the behavioral responses outputs ?

The current treatment ,despite their differences,they are purely Experimental treatment based on the hypothesis that ; there is an imbalance in the level of secretion of one /more of the chemicals that are secreted in the brain and they are related to the higher knowledge processes,emotions and behavioral responses outputs

According to the hypothesis,the defect in the chemical level is the cause responsible for the symptoms of sz,emotional changes and irrational behavioral responses outputs

The questions;
1- Do the results of the treatment prove the credibility of this hypothesis ?
Do the symptoms end forever and the person’s complaint is silent about the barking ?
Does the tragedy of the sz really end with the current treatment ?
Despite the many improvements that the current treatment introduces,the medication still not enough to remove the tragedy of sz from the basic nature of the schizophrened person ?

Did your psychiatrist say that? From what I read, ketamine acts like PCP and causes hypofunctioning of the NMDAR? System, which causes the positive, negative and cognitive symptoms. Seroquel, Clozapine and Zyprexa are most effective for attenuating the effects of antagonism of glutamate receptors.

Yes, she said. Im having a more or less chronic depression and very few positive symptoms, mostly negative symptoms due to my schizotypic disorder

But this drug is far to complicated for me to understand and it’s pharmacology in regard to schizophrenia (low dose administration) is even more complicated.

I am in a position right now where i have nothing left to loose, so if she gives me permission, i will receive the treatment.

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Oh. I see because it’s for depression. It may exacerbate schizophrenia, if you have it.

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supposedly sulforaphane (brocolli sprout extract ) can help increase glutamate to glutathione production or something I dont know the science. There are some articles and a few small studies on it for schizophrenia.

sarcosine is also suppose to improve the glutamate area as well.

Thats about all thats out there right now that I know of that works on those areas

rtms (repetitive transcranial magnetic stimulation) is also known to modulate the glutamate receptors , and other areas where the prefrontal cortex is

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Blocking dopamine can cause negative symptoms sometimes. My psychiatrist said negative symptoms are caused by an imbalance of dopamine even without meds in the brain, some parts of the brain have high dopamine while others have low dopamine. He said there is no meds that target specific brain parts, antipsychotics block dopamine in all the brain. Partial dopamine regulators like Abilify, Rexulti and Vraylar sadly also work on ALL the brain but they can be better sometimes because they boost dopamine when its low and block dopamine when its low. Though we don’t know if it does that to every part of the brain and what’s the normal balanced dopamine levels. There is no universal dopamine levels in humans as far as I know.

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Dopamine is responsible for motivation, learning, pleasure, emotions, etc Antipsychotics reduce the function of these by blocking dopamine.

Couple of interesting take-aways:

An important distinction, therefore, is that while NMDARs may be hypofunctional in schizophrenia, glutamate release and signaling through non-NMDAR subtypes appears excessive. Thus, opportunities for the development of drugs targeting the glutamatergic system include both compounds that increase NMDAR activation as well as compounds that decrease glutamate release.

Elevations in striatal dopamine release in schizophrenia may be driven by glutamatergic abnormalities in the frontal cortex and hippocampus

Healthy cortical function relies on the balance in coordinated activity of excitatory glutamatergic pyramidal neurons and inhibitory GABAergic interneurons. These are tight and complex inter-relationships and it is unknown which abnormalities in glutamatergic or GABAergic processes may be primary, secondary, or compensatory

For example, in a rat developmental model, administration of a glutamate modulating compound (a metabotropic glutamate-5 receptor [mGluR5] positive allosteric modulator [PAM]) reversed adult-onset deficits when administered during adolescence and prevented the emergence of cognitive impairment (Clifton et al., 2013). A more recent study also showed that juvenile administration of an mGluR2/3 agonist prevented the learning and memory deficits and restored the dendritic spine loss that are observed in MAM-treated rats in adulthood (Xing et al., 2018).

I haven’t been able to finish the article yet.


The systematic repetition of the materialistic content of the notion which insist on the existence of physical causes (genetic,chemical and environmental )that produce the symptoms of a health condition be called schizophrenia.

While in the absolute nature,the psychotic factor (H) who is materializing the sz condition and causing its symptoms is not a part from the human genetic material,chemicals of brain,the psychological self and all external environmental conditions

in other words,the cause of sz (condition /symptoms) is known as an actual perceptions without external / internal stimulus ,it represented itself in the human nature as a Perceptual Reactions be occurred automatically without action of internal influence (self-origin) or external environmental effects !!

How you can make a real casual relationship between the psychotic factor and any phenomenon,change,disorder,event or process that occur in the brain of people with sz ?

Oh Abat I missed you :heart_eyes::heart_eyes::heart_eyes:

Thank you for your interesting ,whatever the user name i still the same person

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As I said;
Any form of chemical change (in the front / reversal mental processes )that can be found in the basic nature of people with sz,must occur After the onset of psychosis and be ended or be completely eliminated during the period of sleep

Then the change will return and it appears again to start from the zero point after the waking in the next day
Where, the amount of changes accumulates gradually over time throughout the waking time of the day,causing an increasing in the attention level and lose an amount of the chemical energy

These changes are the reaction of the psychotic factor functional activities on the motor pathway of the electrochemical singles ( that move between cells of the different brain regions which they are concerned with executive the higher mental processes,emotions and carry with them the cognitive commands that direct the personal behavioral responses outputs

The psychotic factor has linking with the signals outputs which coming from the receptors cells,translate its decoded cognitive content by vocal mechanism (reading the thought content phonetically ) …etc

It means practically, it is impossible to present a permanent chemical change in the chemical background Before the onset of psychosis (the emission of the hallucinations entities in the time-place of the conscious state of the human host),and there is no any type of chemical change occurs during the sleep time

Therefore,the correct rational understanding that matches the realities of the internal event scenarios:
-The absence of a permanent chemical change during 24 hours (sleep /waking)
-The absence of an abnormal chemical change related defective gene,
-The absence of an abnormal change that precedes the onset of psychosis or causes
-The chemical change (whatever it was) occurs Gradually during the passage of waking time ,it is a result of the psychotic factor effect on the course of the higher knowledge processes
-The effect stops and no chemical change occurring the period of sleep (whatever the causes of the sleep )

All chemicals be secreted by brain during the sleep stage occur within the framework of its natural level