Schizophrenia and Neurotransmitters | health.am (2022)

When scientists study how the brains of people with mental illness are different, they are commonly interested in two issues: brain structure and function. Researchers can study structure by comparing the brain anatomy in people with schizophrenia to brain anatomy in people without schizophrenia. Ventricle size is a good example of a structural anatomical difference seen in schizophrenia, whereas frontal lobe activity is a good example of a functional anatomical difference seen in schizophrenia.

Another area of interest to researchers is communication within the brain. Studying communication in the brain, a process carried out by substances called neurotransmitters, can help reveal even more about how the brains of people with schizophrenia differ from the brains of people without it. Studying neurotransmitters can reveal both structural and functional differences in the schizophrenic brain. Next, we will discuss how neurotransmitters work and how they appear to be implicated in schizophrenia symptoms.

Neurotransmitters. Neurotransmitters are effectively the “messengers” of the brain, carrying information from one brain cell to another.

Brain cells, called neurons, are responsive to different kinds of neurotransmitters and have receptors built specifically for them. Neurons that are sensitive to specific neurotransmitters tend to cluster together, creating circuits in the brain for processing specific kinds of information.

(Video) Schizophrenia: Neurotransmitter Tracts & Other Causes – Psychiatry | Lecturio

Neurotransmitters are released from a neuron when it signals another brain cell. The neurotransmitters are released into the small space between the two neurons, called the synapse. In the synapse, the neurotransmitters attach, or bind, to the receptors at the ends of another neuron, thus affecting the activity of the new neuron. The new neuron takes in as much of the neurotransmitter as it can and then releases the excess back into the synapse. The excess is reabsorbed by the first neuron, a process known as reuptake. Drugs that treat mood disorders like depression (e.g. Prozac, zoloft) regulate the amount of certain neurotransmitters available in the brain and the process of neurotransmitter reuptake, and affect communication between brain cells.

Figure 4.4 This computer graphic of a synapse shows the release of neurotransmitters (pink spheres at lower center) by vesicles inside the synaptic knob (upper center). The neurotransmitters will cross the gap and bond to the receptors of the adjacent cell, which is how information is transmitted along the nervous system. © Alfred Pasieka/Photo Researchers, Inc.

There are many different neurotransmitters in the brain. Two that have been found to be involved in schizophrenia symptoms are dopamine and glutamate. Dopamine is primarily involved in movement and thoughts. Dopamine has also been associated with novelty seeking, or interest in new experiences and reward. Some illegal drugs, such as cocaine and methamphetamine, work by affecting dopamine function in the brain. Thus, dopamine is associated with feelings of pleasure and well-being.

Dopamine pathways in the brain are highly specialized and may influence different kinds of thinking or behavior. People with high levels of dopamine in certain parts of the brain may also experience psychotic symptoms or paranoid thinking, symptoms of schizophrenia.

(Video) 2-Minute Neuroscience: Schizophrenia

Due to several lines of converging evidence, many scientists believe that dopamine is the cause of many schizophrenic symptoms. The “dopamine hypothesis” dates from the 1960s and emerged from three important observations. In 1952, a drug called clorpromazine was first used to treat schizophrenia.

It worked by blocking dopamine receptors and was successful in treating many schizophrenia patients. A second observation involved the effects of amphetamines. Amphetamines work by making the brain think that there is too much dopamine in the system. People who abuse amphetamines often experience schizophrenia-like symptoms, primarily paranoia and auditory hallucinations. Parkinson’s disease is a disease in which patients experience physical movement problems.

Patients with Parkinson’s are treated with a drug that effectively increases the level of dopamine in the brain. This drug, called L-DOPA, has been associated with complications or side effects that look a lot like schizophrenic symptoms. Patients treated with L-DOPA sometimes experience psychotic symptoms, which provide researchers with more evidence that high levels of dopamine in some parts of the brain are implicated in schizophrenia.

When the brain perceives that there is an excess of dopamine, schizophrenic-like symptoms appear. We still don’t know what causes this excess of dopamine. Do some people produce too much dopamine? Is the breakdown of dopamine somehow inhibited in some people? Or do some people have dopamine receptors that are especially sensitive so their brain thinks that there is extra dopamine even when there isn’t? These are questions that have yet to be answered definitively.

(Video) Schizophrenia: Neurotransmitter Tracts, Causes, Treatment & Assessment – Psychiatry | Lecturio

One problem in studying dopamine in schizophrenia is that we can only directly study the presence of dopamine in autopsies. Presently, we can study the metabolite of dopamine, the substance that remains in the body after dopamine is used.

The metabolite of dopamine, HVA, can be found and measured in our cerebrospinal fluid, which is the fluid we have in our spinal column and in the ventricles of our brain.

In order to measure this fluid, patients must endure a spinal tap, which requires the insertion of a long needle into the spine to access the fluid. This is a painful procedure, and there are risks of infection and complications. Because of these risks, few people are willing to undergo this procedure to be part of an experimental study.

As yet, there is little evidence that people with schizophrenia are producing more dopamine than are people without schizophrenia. Instead, there is some evidence that people with schizophrenia are extremely sensitive to dopamine. Through postmortem studies, researchers have discovered that relative to people without schizophrenia, schizophrenic patients have more receptors for dopamine. Although this evidence is promising, it is unclear whether schizophrenia is caused by an excess of dopamine receptors, or whether the excess of receptors is caused by the illness or treatment.

(Video) Psychopharmacology - Antipsychotics & The Dopamine Hypothesis Schizophrenia

Another neurotransmitter that may play an important role in schizophrenia is glutamate. Glutamate is believed to have an important role in learning and the formation and encoding of memory. Some hallucinogenic drugs, such as PCP, are known to block glutamate receptors. Like amphetamines, PCP can cause paranoia that mimics schizophrenic symptoms.

When people with schizophrenia take PCP, it often makes their symptoms worse. In autopsy studies, lower levels of glutamate have been found in the brains of schizophrenic patients. Dr. Daniel Weinberger, an influential researcher of schizophrenia at the National Institute of Mental Health, has suggested that an interaction between dopamine and glutamate is at the core of schizophrenia. Dopamine receptors also reduce the action of glutamate. If there are too many dopamine receptors, glutamate’s effects will be blocked.

Studying how neurotransmitters work is especially challenging. However, these investigations can provide crucial information about what causes schizophrenia and how best to treat it.

Heather Barnett Veague, Ph.D.
Heather Barnett Veague attended the University of California, Los Angeles, and received her Ph.D. in psychology from Harvard University in 2004. She is the author of several journal articles investigating information processing and the self in borderline personality disorder. Currently, she is the Director of Clinical Research for the Laboratory of Adolescent Sciences at Vassar College. Dr. Veague lives in Stockbridge, Massachusetts, with her husband and children.

References

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  2. American Experience, "People and Events: Recovery from Schizophrenia." Available online. URL: http://www.pbs.org/wgbh/amex/nash/ peopleevents/e_recovery.html. Accessed February 22, 2007.
  3. John F. Nash Jr., "Autobiography." Availalable online. URL: http://nobelprize.org/economics/ laureates/1994/nash-autobio.html. Accessed May 10, 2007.
  4. Sylvia Nasar, A Beautiful Mind. New York: Simon and Schuster, 1998, 335.
  5. American Experience,"Transcript." Available online. URL: http://www.pbs.org/wgbh/amex/nash/filmmore/pt.html. Accessed February 22, 2007.
  6. See note 2.
  7. Robert L. Spitzer et al., eds., DSM-IV-TR Casebook: A Learning Companion to the Diagnostic and Statistical Manual of Mental Disorders. 4th ed., Text Revision. (Washington, DC: American Psychiatric Publishing, 2004), 189 - 90.
  8. H. Hafner et al., "The Influence of Age and Sex on the Onset and Early Course of Schizophrenia." British Journal of Psychiatry 162 (1993): 80 - 86.
  9. E. Fuller Torrey, Surviving Schizophrenia: A Manual for Families, Consumers and Providers, 3rd ed. New York: Harper Perennial, 1995, p. 79.
  10. G.A. Fava and R. Kellner, "Prodromal Symptoms in Affective Disorders." American Journal of Psychiatry 148 (1991): 828 - 830.
  11. British Columbia Schizophrenia Society, "Basic Facts about Schizophrenia," Available online. URL: http://www.mentalhealth.com/book/ p40-sc02.html#Head_4. Downloaded on November 13, 2006.
  12. Quoted in J.N. Butcher, S. Mineka, and J.M. Hooley, Abnormal Psychology. Pearson: Boston, 2004.
  13. Harrison et al., "Recovery from Psychotic Illness: A 15- and 25-year International Follow-up Study." British Journal of Psychiatry 178 (2001): 506 - 517.
  14. N.C. Andreasen, "The Role of the Thalamus in Schizophrenia." Canadian Journal of Psychiatry 42 (1997): 27 - 33.
  15. J. Hooley and S. Candela, "Interpersonal Functioning in Schizophrenia." In Oxford Textbook of Psychopathology, edited by T. Million, P.H. Blaney, and R.D. Davis. New York: Oxford University Press, 1999.
  16. J.D. Hegarty et al., "One Hundred Years of Schizophrenia: A Meta Analysis of the Outcome Literature." American Journal of Psychiatry 151, no. 10 (1994): 1409 - 1416.
  17. E.Q. Wu et al., "The Economic Burden of Schizophrenia in the United States in 2002." Journal of Clinical Psychiatry 66, no. 9 (2005): 1122 - 1129.
  18. C. Wallace, P.E. Mullen, and P. Burgess, "Criminal Offending in Schizophrenia over a 25-year Period Marked by Deinstitutionalization and Increasing Prevalence of Comorbid Substance Use Disorders." American Journal of Psychiatry, 161 (2004): 716 - 727.
  19. Suicide and Mental Health Association International, "NARSAD Publishes Top 10 Myths About Mental Illness Based on Nationwide Survey." Available online. URL: http://suicideandmentalhealth associationinternational.org/factsmythsment.html. Accessed February 22, 2007.

(Video) Biological basis of schizophrenia | Behavior | MCAT | Khan Academy

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FAQs

What do neurotransmitters have to do with schizophrenia? ›

Research suggests schizophrenia may be caused by a change in the level of 2 neurotransmitters: dopamine and serotonin. Some studies indicate an imbalance between the 2 may be the basis of the problem. Others have found a change in the body's sensitivity to the neurotransmitters is part of the cause of schizophrenia.

Which neurotransmitters are involved in schizophrenia? ›

Scientists believe that people with schizophrenia have an imbalance of the neurotransmitters (brain chemicals) serotonin, dopamine, and glutamate . These neurotransmitters allow nerve cells in the brain to send messages to each other.

What neurotransmitter do schizophrenics have too much of? ›

The most common theory about the cause of schizophrenia is that there are too many dopamine receptors in certain parts of the brain, specifically the mesolimbic pathway. 1 This causes an increase in mesolimbic activity which results in delusions, hallucinations, and other psychotic symptoms.

Is schizophrenia not enough dopamine? ›

The authors hypothesize that schizophrenia is characterized by abnormally low prefrontal dopamine activity (causing deficit symptoms) leading to excessive dopamine activity in mesolimbic dopamine neurons (causing positive symptoms).

Why Does too much dopamine cause schizophrenia? ›

High levels of dopamine don't cause schizophrenia symptoms. The role dopamine plays in schizophrenia is more complex than that and involves specific dopamine activity. Over time, researchers have discovered evidence that isn't in line with the original dopamine hypothesis of schizophrenia.

What part of the brain is damaged in schizophrenia? ›

Schizophrenia is associated with changes in the structure and functioning of a number of key brain systems, including prefrontal and medial temporal lobe regions involved in working memory and declarative memory, respectively.

Is serotonin high or low in schizophrenia? ›

Compared with healthy subjects, schizophrenic patients may also have increased levels of serotonin and decreased levels of norepinephrine in the brain.

What happens to the brain in schizophrenia? ›

In schizophrenia, dopamine is tied to hallucinations and delusions. That's because brain areas that "run" on dopamine may become overactive. Antipsychotic drugs stop this. Glutamate is a chemical involved in the part of the brain that forms memories and helps us learn new things.

Which neurotransmitter has been linked to the positive symptoms of schizophrenia? ›

Dopamine Receptor Imaging in Schizophrenia

The dopamine hypothesis of schizophrenia suggests that a dysregulated dopamine system contributes to positive, negative, and cognitive symptoms of the disease.

What neurotransmitter is reduced in schizophrenia? ›

Dopamine is an inhibitory neurotransmitter involved in the pathology of schizophrenia. The revised dopamine hypothesis states that dopamine abnormalities in the mesolimbic and prefrontal brain regions exist in schizophrenia.

What happens if your brain has too much dopamine? ›

Having too much dopamine — or too much dopamine concentrated in some parts of the brain and not enough in other parts — is linked to being more competitive, aggressive and having poor impulse control. It can lead to conditions that include ADHD, binge eating, addiction and gambling.

Is psychosis caused by too much dopamine? ›

This research provided the first direct evidence that psychotic symptoms are promoted by excessive dopamine D2-receptor stimulation, a finding that is suggestive of an increased phasic activity of dopaminergic neurons in the subcortex.

Can low dopamine cause psychosis? ›

Dopamine modulates many brain functions, with dopamine pathways regulating motor control, motivation, interest, reward and activities such as walking and talking. Impairment of such brain functions may underlie the symptoms of psychosis.

Do antipsychotics block dopamine? ›

Most antipsychotic drugs are known to block some of the dopamine receptors in the brain. This reduces the flow of these messages, which can help to reduce your psychotic symptoms.

Is glutamate high or low in schizophrenia? ›

A study using a heat pain stress found a reduced anterior cingulate cortex glutamate response in individuals with schizophrenia compared to healthy controls168, although interpretation is complicated by the fact that baseline glutamate levels were higher in patients.

How do you calm a schizophrenic? ›

Connecting face-to-face with others is the most effective way to calm your nervous system and relieve stress. Since stress can trigger psychosis and make the symptoms of schizophrenia worse, keeping it under control is extremely important.

How Can schizophrenia be cured permanently? ›

While there is no known cure, it is possible to live a meaningful and happy life with schizophrenia. There are many effective treatments, best provided by a team. These include medication, psychotherapy, behavioral therapy, and social services, as well as tools to help you stay in school or keep working.

How do you combat schizophrenia? ›

These may include:
  1. Individual therapy. Psychotherapy may help to normalize thought patterns. ...
  2. Social skills training. This focuses on improving communication and social interactions and improving the ability to participate in daily activities.
  3. Family therapy. ...
  4. Vocational rehabilitation and supported employment.
7 Jan 2020

Can you see schizophrenia on a brain scan? ›

Can a brain scan show schizophrenia? It is not currently possible to determine that a person has schizophrenia simply by looking at a brain scan, but certain changes in the brain that can be observed on a brain scan have been associated with schizophrenia.

Can you see schizophrenia in an MRI? ›

The research literature shows that schizophrenia has neuroanatomical correlates that can be seen at group level by studying MR images. Structural MRI cannot currently be used to identify schizophrenia at the level of the individual.

How are schizophrenics brains different? ›

It covers the surface of the brain and helps to control muscles, hearing, sensory perception, and more. Brain imaging shows that people with schizophrenia have less gray matter volume, especially in the temporal and frontal lobes. These areas of the brain are important for thinking and judgment.

Is GABA good for schizophrenia? ›

A model has been developed suggesting GABA's role (including GABA-dopamine interactions) in schizophrenia. In several clinical studies, the use of adjunctive GABA agonists was associated with greater improvement in core schizophrenia symptoms.

How is GABA affected in schizophrenia? ›

In particular, GABA dysfunction is thought to lead to the disinhibition of glutamatergic pyramidal neurons and a loss of synchronous cortical activity. Postmortem studies also suggest that schizophrenia is associated with dysfunctional GABA signalling at the postsynaptic receptor level.

What role does serotonin play in schizophrenia? ›

Serotonin has been implicated in a variety of behaviors and somatic functions that are disturbed in schizophrenia: cognition, including memory; perception and attention; sensory gating; mood; aggression; sexual drive; appetite; energy level; pain sensitivity; endocrine function; and sleep.

Can schizophrenia go away naturally? ›

If left untreated, schizophrenia rarely gets better on its own. Symptoms of schizophrenia more frequently increase in intensity without treatment and may even lead to the onset of additional mental issues, including: Depression.

Can schizophrenia be caused by trauma? ›

Epidemiological studies show that exposure to early stress in the form of abuse and neglect in childhood increases the risk to later develop schizophrenia (Bonoldi et al., 2013).

Do people with schizophrenia have more dopamine receptors? ›

In fact, when Abi-Dargham et al. examined the number of D2 receptors after partially removing the obscuring effect of endogenous dopamine, the D2 receptors were significantly elevated in schizophrenia patients as compared with control subjects.

What mental disorder has high GABA? ›

GABAergic system is involved in most psychiatric disorders including major depressive disorder (131), schizophrenia (132), bipolar disorder (133) and autism (134).

How do you know if you have enough dopamine? ›

Symptoms of dopamine deficiency (low dopamine levels) may include: You lack motivation, “the drive.” You're tired. You can't concentrate.

What drug increases dopamine? ›

Research has shown that the drugs most commonly abused by humans (including opiates, alcohol, nicotine, amphetamines, and cocaine) create a neurochemical reaction that significantly increases the amount of dopamine that is released by neurons in the brain's reward center.

How do you fix dopamine imbalance? ›

Getting enough sleep, exercising, listening to music, meditating, and spending time in the sun can all boost dopamine levels. Overall, a balanced diet and lifestyle can go a long way in increasing your body's natural production of dopamine and helping your brain function at its best.

What drugs can cause permanent psychosis? ›

The representative drugs that can cause psychosis are amphetamine, scopolamine, ketamine, phencyclidine (PCP), and lysergic acid diethylamide (LSD) [7].

Do high dopamine levels cause schizophrenia? ›

More specifically, research from 2014 notes that hyperactivity of the dopamine D2 receptor in the subcortical and limbic regions of the brain contributes to some symptoms of schizophrenia, including hallucinations and delusions.

What is the fastest way to increase dopamine? ›

How to Increase Dopamine Naturally
  1. Avoid overindulging in alcohol or recreational drug use. ...
  2. Maintaining a healthy diet can increase dopamine levels. ...
  3. Avoid junk food. ...
  4. Exercise regularly to increase dopamine. ...
  5. Spend time outside. ...
  6. Practice healthy sleep habits. ...
  7. Engage in healthy, pleasurable activities. ...
  8. Meditate or practice yoga.

Can dopamine receptors repair themselves? ›

Users may need to take drugs simply to feel a normal amount of well-being. Some recent research indicates, however, that when addicts stop doing drugs, the disabled dopamine receptors in their brains can repair themselves.

How do you get out of psychosis? ›

For example, it can help to:
  1. Try to get enough sleep. Sleep can help give you the energy to cope with difficult feelings and experiences. ...
  2. Think about your diet. ...
  3. Try to do some physical activity. ...
  4. Spend time outside. ...
  5. Avoid drugs and alcohol.

How long does it take for dopamine to come back? ›

Normal, healthy dopamine production depends on a wide variety of factors, but many medical professionals believe that your brain's dopamine production will return to pre-substance misuse levels over a period of 90 days.

What is the main drug used to treat schizophrenia? ›

Haloperidol, fluphenazine, and chlorpromazine are known as conventional, or typical, antipsychotics and have been used to treat schizophrenia for years. However, they sometimes have movement-related side effects, such as tremors and dystonia, a condition that causes involuntary muscle contractions.

Does your brain go back to normal after antipsychotics? ›

For neurological, neuropsychological, neurophysiological, and metabolic abnormalities of cerebral function, in fact, there is evidence suggesting that antipsychotic medications decrease the abnormalities and return the brain to more normal function.

Which antipsychotics increase dopamine? ›

Another property of second-generation antipsychotics is that some of them are 5HT1A agonists. This includes drugs such as ziprasidone, quetiapine and clozapine. What is the importance of this? 5HT1A agonism would increase dopamine release in the prefrontal cortex and also reduce glutamate release.

Which neurotransmitters are involved in schizophrenia? ›

Scientists believe that people with schizophrenia have an imbalance of the neurotransmitters (brain chemicals) serotonin, dopamine, and glutamate . These neurotransmitters allow nerve cells in the brain to send messages to each other.

What does glutamine do in schizophrenia? ›

Results indicate that circulating glutamate and glutamine levels exhibit a dual behavior in schizophrenia, with an increase of glutamine/glutamate ratio at the onset of schizophrenia followed by a decrease with progression of the disorder.

What does glutamate do for schizophrenia? ›

The “glutamate hypothesis of schizophrenia” proposes that schizophrenia symptoms and cognitive impairment are due to hypofunction of NMDARs and excessive glutamate release, especially in brain areas including prefrontal cortex and hippocampus (1).

How does serotonin contribute to schizophrenia? ›

Serotonin has been implicated in a variety of behaviors and somatic functions that are disturbed in schizophrenia: cognition, including memory; perception and attention; sensory gating; mood; aggression; sexual drive; appetite; energy level; pain sensitivity; endocrine function; and sleep.

What neurotransmitter is associated with schizophrenia and Parkinson's disease? ›

The neurotransmitter dopamine (DA) and the dopaminergic neurones play an important role in schizophrenia and Parkinson's disease (PD). A decrease in DA in the substantia nigra of the brain has been implicated as the cause of PD.

Is serotonin high or low in schizophrenia? ›

Compared with healthy subjects, schizophrenic patients may also have increased levels of serotonin and decreased levels of norepinephrine in the brain.

What happens to the brain in a patient with schizophrenia? ›

Studies show that certain brain chemicals that control thinking, behavior, and emotions are either too active or not active enough in people with schizophrenia. Doctors also believe the brain loses tissue over time.

What neurotransmitter is reduced in schizophrenia? ›

Dopamine is an inhibitory neurotransmitter involved in the pathology of schizophrenia. The revised dopamine hypothesis states that dopamine abnormalities in the mesolimbic and prefrontal brain regions exist in schizophrenia.

Does GABA help schizophrenia? ›

A model has been developed suggesting GABA's role (including GABA-dopamine interactions) in schizophrenia. In several clinical studies, the use of adjunctive GABA agonists was associated with greater improvement in core schizophrenia symptoms.

Why do antipsychotics block serotonin? ›

A second generation of antipsychotics, commonly referred to as the atypical antipsychotics, block D2 receptors as well as a specific subtype of serotonin receptor, the 5HT2A receptor. It is believed that this combined action at D2 and 5HT2A receptors treats both the positive and the negative symptoms.

What causes lack of dopamine in the brain? ›

This could be a mental illness, stress, not getting enough sleep, drug abuse, being obese, or eating too much sugar and saturated fat. Low dopamine can also be caused by a problem with the adrenal glands.

Which dopamine receptors are involved in schizophrenia? ›

NMDA-receptors are involved in releasing dopamine into the striatum and frontal cortex in schizophrenia patients [Ref.

What disease is caused by lack of dopamine? ›

Low levels of dopamine have been linked to Parkinson's disease, restless legs syndrome and depression. Low levels of dopamine can make you feel tired, moody, unmotivated and many other symptoms. Treatments are available for many of the medical conditions linked to low dopamine levels.

Is glutamate high or low in schizophrenia? ›

A study using a heat pain stress found a reduced anterior cingulate cortex glutamate response in individuals with schizophrenia compared to healthy controls168, although interpretation is complicated by the fact that baseline glutamate levels were higher in patients.

Is cortisol associated with schizophrenia? ›

For example, research has shown elevated cortisol in first episode and recent onset psychotic patients (3–4), and increased activity of systemic cortisol metabolism in schizophrenia patients (5). Among mood disorders patients, those with psychotic symptoms manifest greater elevations in cortisol (6).

Is norepinephrine increased in schizophrenia? ›

Schizophrenic patients had significantly higher resting and standing plasma norepinephrine levels and significantly greater change. Resting and standing 1ev- els were significantly related to positive and negative symptoms.

Can you see schizophrenia on a brain scan? ›

Can a brain scan show schizophrenia? It is not currently possible to determine that a person has schizophrenia simply by looking at a brain scan, but certain changes in the brain that can be observed on a brain scan have been associated with schizophrenia.

Can you see schizophrenia in an MRI? ›

The research literature shows that schizophrenia has neuroanatomical correlates that can be seen at group level by studying MR images. Structural MRI cannot currently be used to identify schizophrenia at the level of the individual.

How is a schizophrenic brain different? ›

Brain imaging shows that people with schizophrenia have less gray matter volume, especially in the temporal and frontal lobes. These areas of the brain are important for thinking and judgment. What's more, gray matter loss continues over time.

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