The Neurochemistry of Schizophrenia

Author(s): Fatima Rafie

Mentor(s): Ashley Blinstrub, Honors College


Schizophrenia is a mental disorder that has no currently known cure or cause. Though researchers believe that there are many genetic and environmental contributors to the condition, there is still much that is yet to be discovered regarding the etiology of schizophrenia. For the purposes of this research, the neurochemical aspect of schizophrenia was explored, in order to provide a comprehensive analysis of current neurochemical models. This research also emphasizes the importance of neurochemical studies by demonstrating how neurochemical studies help to advance the field of treatment. Multiple different scholarly articles concerning both neurochemical models and anti-psychotic drug treatment were analyzed and compared throughout the research process. The neurochemical models described in the research are as follows: the dopamine/D2 model, the GABA model, the NMDAR model, and the serotonin (5-HT) model. Though the dopamine and GABA models were the most prominent neurochemical models, the NMDAR and serotonin (5-HT) models provided insight into the non-striatal mechanisms involved in schizophrenia and presented information that is crucial to the development of antipsychotic drugs. These models are of extreme importance, since all current antipsychotic drugs, or APDs, only use D2 dopamine-receptor-blocking mechanisms in order to diminish schizophrenic symptoms. Not only does this mechanism not account for the other neurochemical models, but D2 dopamine-receptor-blocking APDs can cause extrapyramidal side effects. Therefore, research on the neurochemical aspects of schizophrenia is necessary and critical to the further development of antipsychotic drugs.

Video Transcript

Schizophrenia, defined by the American Psychiatric Association as , “… a chronic brain disorder that affects less than one percent of the U.S. population”, is a mysterious and baffling condition. There is no cure or a currently known cause. Though genetics, environmental conditions, and neurochemical imbalances are speculated to contribute to the characteristic symptoms we see in schizophrenics, there is still much that we don’t currently know about the condition. My name is Fatima Rafie and today I will be examining the neurochemistry of schizophrenia in depth, in order to obtain a better understanding of the many facets of this perplexing condition. 

To start with the most popular neurochemical model, the dopamine model has been the most prominent model I read about while doing my research on this topic. The dopamine model of schizophrenia states that schizophrenic psychosis is a result of elevated levels of striatal dopamine. This excess of dopamine enhances and amplifies environmental stimuli and leads to many of the typical symptoms characteristic of schizophrenia, such as delusions or hallucinations.

In addition to the dopamine model, the GABA model was also very common. This model states that schizophrenic symptoms, specifically working memory deficits, are associated with the decreased synthesis and reuptake of GABA

Although the two aforementioned models were the most prominent, there were a few other, lesser-known neurochemical models that emerged during my research. These models were the NMDAR and Serotonin models. For NMDAR, research has found that the hypofunction of the NMDA receptor may be a possible contributor to schizophrenic psychosis. NMDAR antagonist, brain imaging, and postmortem studies have provided significant evidence that NMDAR hypofunction has a correlation with schizophrenic symptoms

Studies have also found that Serotonin (5-HT) receptors are involved in the non-striatal mechanisms of schizophrenia. 

So, at this point, you may be asking why all this matters and why it is important. This is because all current antipsychotic drugs, or APDs, use D2 dopamine receptor blocking mechanisms in order to diminish schizophrenic symptoms. However, this model is significantly lacking, since it fails to target all the schizophrenic symptoms and can cause extrapyramidal side effects, which are drug-induced symptoms. It also fails to account for the other neurochemical contributors, making APDs not very effective. These reasons are why many schizophrenics are not able to live independently and why it is the seventh most costly mental illness.

In order to solve this issue and to continue to develop more effective APDs, research such as the NMDAR and serotonin studies are absolutely crucial, since they expand upon what we currently know about what is happening at the molecular level.

With my research and with this video, I hope to educate people about the importance of neurochemical studies when it comes to the treatment of  schizophrenia. I also hope to advocate for more research in this field, so that we can work towards developing more effective antipsychotics that will help elevate the standard of care for schizophrenic patients, allowing them to live fuller and more independent lives.

Thank you so much for watching this video and I hope you learned something new about the neurochemistry of schizophrenia.

3 replies on “The Neurochemistry of Schizophrenia”

Great work, Fatima. The video was very informative and well-crafted. Is there’s any research on how scientists could use the NMDAR and/or Serotonin models to develop a more effective treatment?

Yes, there have been some studies regarding both those models and what are called “atypical” APDs. For example, high one of the studies I looked at included APDs with a high serotonin 5-HT receptor affinity that was combined with a low D2 affinity and it showed to be effective.

Hi Fatima! I really like the way you presented this information and how well you constructed the video and its transitions, it looks professionally edited! Concerning the content of the video, being a Neuroscience major and Psychology, everything you talked about and the whole project altogether to be very interesting, particularly when you got into speaking about the impact these medications have, or lack thereof. I know you mentioned that focusing future research on NMDAR and serotonin, but could you elaborate on that more? Based on what you learned while researching information about this issue, what do you believe should be looked at in terms of NMDAR and serotonin? How could that help diminish the remaining symptoms?

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