Neurotransmitter Dysfunction in Schizophrenia

Schizophrenia is a mental disorder that makes it hard for individuals to make differentiation between real things and those that are not real. Since its discovery, schizophrenia has been a source of much trouble to the human race. Despite the numerous advances made to understand the causes, manifestation and the treatment of the disease, schizophrenia continues to be a confounding issue to the public and health specialists. There is an evidence of the central role of neurotransmitter dysfunction in the presentation of schizophrenia.

Schizophrenia is a chronic brain disease that is severe and disabling. It has been proved that about 1 percent of Americans have the illness. The Dysfunction of central dopaminergic neurotransmission has been implicated in the presentation of schizophrenia including the dependence of alcohol and drugs. It has also been found out that drug abuse stimulate dopamine release in the ventral striatum that causes the overconsumption of drugs. It has also been observed that the increase of subcortical dopamine release has an association with the pathogenesis of the symptoms of schizophrenia and may be caused by prefrontal dopaminergic dysfunction (Biology Online, 2006).

Cognitive dysfunction presents an important deficit in schizophrenia. The neurotransmitter hypothesis of schizophrenia implicates the neuropharmacology of aberrant neurotransmission systems including dopaminergic, glutamatergic and serotoninergic systems. The dopamine hypothesis implicates the hyperactivity of dopaminergic transmission at the dopamine D2 receptor located in the mesencephalon projections to the limbic striatum. This hypothesis relied heavily on the correlation that exists between therapeutic doses of conventional antipsychotic medications ad their affinities for dopamine D2 receptors. In addition to that, the indirect dopamine agonists can encourage psychosis in healthy people and provoke psychotic symptoms in schizophrenics (Frederickson, 2008).

Emerging evidence has implicated the presynaptic dopaminergic abnormality in schizophrenia. This also means that there is a dysfunction in presynaptic storage, release, reuptake, vesicular transport and mechanisms present in mesolimbic dopamine systems. The dopamine hypothesis also postulates that dysregulation and hyper-responsiveness that happen in presynaptic dopamine neurons could be responsible for long-term consequences that come through the induction of sensitization and oxidative stress. On the other hand, the functionality of dopamine may be lowered in the neo-cortex of patients with schizophrenia. This could partially be connected to the negative symptoms, such as emotional impairments. However, it has not been proven whether the hyper function or hypo function of dopamine happens in minimal stress contexts (Harrison, 1998).

Recently the aspect of the involvement of serotonin (5-HT) in the pathophysiology of schizophrenia has been established. It has been stated that serotonin receptors have a role in the psychotomimetic and psychogenic properties of hallucinogens. The serotonin receptors contribute to the therapeutic and side effects of atypical antipsychotics. In addition, certain polymorphisms of serotonin receptor gene are associated with schizophrenia (Braff & Light, 2005).

The evidence against the Dopamine Theory of Schizophrenia exists. Amphetamine drugs work in more ways to increase dopamine levels. They also interfere with other neurotransmitter levels. Medications that block the function of dopamine receptors act on receptors rapidly. Nevertheless, these medications, in certain cases, take loner to effect a change on the behavior of patients with schizophrenia. The effects of dopamine blockers could be indirect or direct. These medications influence other systems that contribute to the impact of the symptoms of schizophrenia. New drugs used to treat schizophrenia, for instance, clozapine, block receptors from both serotonin and dopamine (Brekke, Raine, Ansel, Lencz & Bird, 1997).

While many researches have been directed to the indication of dopamine as responsible for the production of the symptoms of schizophrenia, it is still difficult to determine the exact involvement of dopamine. Increased levels of dopamine in the striatum cause some positive symptoms especially over-activity. However, the prefrontal cortex could also be responsible for certain positive symptoms. Patients suffering from schizophrenia have small frontal lobes and large ventricles. This is an evidence showing that lack of dopamine activity in the prefrontal cortex and limbic system leads to lack of inhibition in the production of dopaminergic pathways in the striatum (Brass & von Cramon, 2002).

The existence of interrelationships between dopamine and glutamate systems in terms of anatomy and function in the central nervous system suggests that there is an influence of dopamine neurotransmission brought about by the inhibition of the NMDA-R. For instance, the NMDA-R antagonists lower the corticofugal inhibition of subcortical dopamine neurons and enhance the rate of dopamine neurons. In the body of human beings, the PET studies done on dopamine receptor occupancy after acute injection of Ketamine show that NMDA-R antagonists cause the increase in the release of dopamine in the striatum. On the other hand, chronic injection of NMDA-R antagonists causes decreased release of dopamine (Asaad, Rainer & Miller, 2000).

Many neurotransmitter systems have been shows o be dysfunctional in cases of schizophrenia. In addition to that, immune system dysfunction in cases of schizophrenia and a negative relationship between rheumatoid arthritis and schizophrenia has also been implicated. Phagocytic immune cells known as microglia and found in the central nervous system are engaged in neuroproliferative and neurodegenerative functions. Current theory into the study of schizophrenia has suggested that the dysfunction of microglia that is caused by early central nervous viral exposure causes abnormal development of neurons and a further neurotransmitter dysfunction that is seen in cases of schizophrenia. Patients who have schizophrenia are found to have lower numbers of neurons in the dorsomedial nucleus that projects majorly to the prefrontal cortex (Addington & Addington, 1999).

In conclusion, there is an evidence for the central role of neurotransmitter dysfunction in the presentation of schizophrenia as discussed above. The strengths of this have been seen in patients with schizophrenia who have reduced numbers of neurons. The limitations are that many studies focus on the relationship of dopamine and schizophrenia and feature neurotransmitter dysfunction at a decreased level. The limitation also occurs because of a range of differences with respect to neuronal parameters that occur in schizophrenia cases.

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