ABSTRACT
Schizophrenia is detected as psychological disturbances linked to several abnormalities through vast provinces of information dispensation in several parts of the brain and cognition. Current treatment of this disease is mostly related to dopamine receptor (mainly D2 and D4) blockage. There are certain limitations to these medications, which has diverted the focus of scientists to the involvement of alternative neurochemical targets. Specific psychoactive agents induce positive and cognitive symptoms that resemble those seen in schizophrenia. These agents act by antagonizing N-methyl-d-aspartate (NMDA) receptors. Therefore, this chapter focuses on the role of the glutaminergic system in the pathophysiology of schizophrenia. Glutamate, being the most abundant neurotransmitter, acts as a crossroad for almost all other neurotransmitter systems in one or other way. Dopaminergic deficits are also considered secondary to underlying glutamatergic dysfunction. It has further been postulated that improper functioning of NMDA receptors enhances neurotransmission in the synaptic cleft, leading to excitotoxicity. A further possibility for the enhanced level of glutamate is a defect in the transporter system. Chromosomal and mutational changes may also be studied for glutamate defects, as no systemic study has yet been done in this area. By studying these theories of glutamate neurotransmitter abnormality, in this chapter the authors frame newfangled concepts and treatment methodologies for schizophrenia based on glutaminergic system abnormalities, which may be important in the future for new drug development in schizophrenia.
