Running Head: Schizophrenia Critical Review

Running Head Schizophrenia1schizophrenia2critical Review Schizop

Running Head Schizophrenia1schizophrenia2critical Review Schizop

1 SCHIZOPHRENIA 2 Critical Review: Schizophrenia Schizophrenia is a psychiatric disorder that affects almost all elements of a patient's life. The disease is characterized by hallucination, cognitive impairment, social withdrawal, delusions. All these characteristics are usually seen in Schizophrenia patients. In most cases, a patient is unable to think straight, distinguish fantasy from reality and also can be over-reactive when they interact with others. All the above symptoms can be explained based on the neurological mechanisms of a patient's mental illness.

Over the recent past, there have been various researches linking psychology and neuroscience in search of information on the causes of schizophrenia in patients. “There has been evidence that the disorder is as a result of impaired activation on three brain networks between frontotemporal, frontoparietal and front striatal that serve in cognitive functioning and coordinating cognition and emotion” (Tritsch et al., 2016). A neurotransmitter is a chemical element that is secreted by the neurons, and its function is the transmission of messages from one neuron to the other. The most common types of neurotransmitters in the brain include serotonin, norepinephrine, dopamine, acetylcholine, glutamate, and GABA.

Neurotransmitters play critical roles in brain functioning. Serotonin, for example, regulates mood, appetite, and sleep. Norepinephrine is vital for attentiveness, dreaming, learning, and emotional regulation. Acetylcholine influences memory and hearing, dopamine controls voluntary movements and emotional behavior, glutamate is involved in brain development, memory, and learning, and GABA prevents neurons from firing nerve impulses. These neurotransmitters’ functions are fundamentally linked to behavioral and cognitive processes that are disrupted in schizophrenia.

Research indicates that schizophrenia involves abnormalities in several key neurotransmitter systems, especially dopamine and serotonin. The classic dopamine hypothesis suggests that excessive dopamine activity in certain brain regions contributes to positive symptoms such as hallucinations and delusions. This hypothesis is supported by evidence that antipsychotic medications, which block dopamine receptors, alleviate these symptoms effectively (Kapur & Seeman, 2001).

Neurochemical studies have shown that individuals with schizophrenia exhibit increased dopamine synthesis, release, and receptor density in pathways associated with reward and perception, such as the mesolimbic pathway. This hyperdopaminergic state may lead to the perceptual disturbances characteristic of hallucinations and delusions. Additionally, the dopamine hypothesis has been extended to include deficits in dopamine regulation in the prefrontal cortex, contributing to negative symptoms and cognitive impairments (Howes & Kapur, 2009).

Serotonin’s role in schizophrenia has gained increasing attention. Evidence suggests that serotonergic dysregulation contributes to some symptoms of schizophrenia, especially where atypical antipsychotics, which block serotonin receptors (particularly 5-HT2A), are effective (Meltzer, 2012). Serotonin receptors modulate dopamine activity in various brain regions, and their dysregulation may influence the severity and manifestation of symptoms. For example, abnormalities in serotonin signaling have been linked to mood disturbances, agitation, and cognitive deficits in schizophrenia patients.

Importantly, anatomical studies demonstrate structural brain abnormalities associated with neurotransmitter irregularities in schizophrenia. Imaging studies reveal reduced grey matter volume in the hippocampus and prefrontal cortex, along with ventricular enlargement. For instance, reduced hippocampal volume correlates with impaired memory and emotional regulation, likely influenced by disrupted serotonergic and dopaminergic neurotransmission (Ellison-Wright & Bullmore, 2009). The cerebellum, involved in cognitive functions, also shows volume reduction in schizophrenia, which may relate to neurotransmitter imbalances affecting neural circuitry.

These neuroanatomical and neurochemical changes underlie the core symptoms of schizophrenia. Hallucinations and delusions result from abnormal neurotransmitter activity affecting perception and cognition. Social withdrawal and apathy are associated with prefrontal cortex dysfunction and altered dopamine signaling. Emotional disturbances involve the limbic system, where serotonergic and dopaminergic interactions influence affect regulation (Uhlhaas & Singer, 2015).

Furthermore, the neurochemical alterations impact brain connectivity patterns. Disrupted neural oscillations, particularly in gamma and theta frequency bands, have been observed in schizophrenia, reflecting impaired synchronization of neural activity—an essential component of cognitive processes (Uhlhaas & Singer, 2016). This dysconnectivity manifests behaviorally as difficulties in attention, working memory, and executive functioning, which are characteristic of the disorder.

In conclusion, dopamine and serotonin are critically involved in the neurochemical dysregulation observed in schizophrenia. Elevated dopamine activity in certain pathways is implicated in positive symptoms, while serotonergic abnormalities contribute to mood and cognitive impairments. Understanding these neurotransmitter systems has not only elucidated the pathophysiology of schizophrenia but also guided the development of pharmacotherapies, including antipsychotics targeting multiple neurotransmitter receptors. Ongoing research seeks to further clarify these mechanisms and develop more effective treatments with fewer side effects.

References

  • Ellison-Wright, I., & Bullmore, E. (2009). The anatomy of first-episode and chronic schizophrenia: An anatomical likelihood estimation meta-analysis. American Journal of Psychiatry, 166(8), 912–922.
  • Howes, O. D., & Kapur, S. (2009). The dopamine hypothesis of schizophrenia: Version III—the final common pathway. Schizophrenia Bulletin, 35(3), 549–562.
  • Kapur, S., & Seeman, P. (2001). Dopamine hypothesis of schizophrenia: Where are we now? Schizophrenia Bulletin, 27(3), 599–606.
  • Meltzer, H. Y. (2012). The role of serotonin receptors in the action of atypical antipsychotic drugs. Journal of Clinical Psychiatry, 73(Suppl 1), 3–7.
  • Uhlhaas, P. J., & Singer, W. (2015). Oscillations and neuronal dynamics in schizophrenia: The search for basic symptoms and translational opportunities. Biological Psychiatry, 77(12), 1001–1009.
  • Uhlhaas, P. J., & Singer, W. (2016). Neural oscillations and synchrony in schizophrenia. Nature Reviews Neuroscience, 17(2), 93–105.
  • Singer, J., et al. (2015). Neurochemical mechanisms underlying schizophrenia. Neuroscience & Biobehavioral Reviews, 55, 1–17.
  • Tritsch, N. X., Granger, A. J., & Sabatini, B. L. (2016). Mechanisms and functions of GABA co-release. Nature Reviews Neuroscience, 17(3), 139–147.

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