There is immense study on the role of glutamate in Schizophrenia. Even so to date the current antipsychotics do not control major glutamatergic action albeit a study at the NMDA receptor location such as the glycine transport inhibitors may give new novel evidence for the discovery of future antipsychotics (Olney et al., 1999)
The Dopamine hypothesis of Schizophrenia
The dopamine (DA) theory of schizophrenia has subjugated the effort to justify the behaviours Schizophrenia is a psychiatric bedlam relating to the messing up of routine thinking, sentiment and every day activities. Egan & Weinberger (1979) described schizophrenia as when a subject or an individual is unable to differentiate what is genuine and unreal. The clinical characteristics of the various disarray of schizophrenia commonly come into view in the late adolescence or the early adulthood. Schizophrenia can exhibit either positive or negative or both signs. Whereas the positive sign is characterised by paranoia, false principles or hallucination, the negative aspect is marked by depression, withdrawal from communal connections. But pleasing of social responses shortfall in attention and memory are ascribed to cognitive effect. Generally, schizophrenia is considered to be neurodevelopment unrest rather than neurogenerative disorder (Harrison et al., 2003). There are several divisions in the brain that can be affected by schizophrenia. The atypical function of the basal ganglia is considered to play a role in paranoia and hallucination. The frontal lobe of the brain plays a role in problem solving and reasoning. Conversely a schizophrenic will have a deficiency in the lobe and as result, having difficulty in forecast and coordinating. Adjustments in neurotransmitter organisation probably replicate defects in early neurodevelopment and as such a factor in the pathogenesis of Schizophrenia. Recent study is purposeful on the two main neurotransmitters; Dopamine (DA) and the glutamate which may be distorted in Schizophrenia. The dopamine hypothesis is ascribed to hyperdopaminergic role as probable root of Schizophrenia but the glutamate hypothesis suggests a hypo function of the coordination. (Kotter, 1994). Amphetamines and phencyclidine (PCP), which is dopamine agonist and glutamate antagonist respectively could generate schizophrenic-like signs in normal subjects (Jarvit & Zukin 1991). The DA agonist generated merely the positive symptoms of Schizophrenia but the glutamate antagonist to observed in schizophrenic subjects. It is centred a bit on the study that amphetamine produces behaviours like the positive symptoms in schizophrenia, as it elevates dopamine levels in the brain (Goldstein & Deutch., 1992). The DA theory has fairly better descriptive control in terms of the positive symptoms, but in any case in its standard form, does not present a reason for the negative symptoms. But the glutamate theory appears to present an account for both positive...