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A number of lines of enquiry suggest that Glutamate may be implicated in schizophrenia.

Postmortem studiesEdit

Interest has also focused on the neurotransmitter glutamate and the reduced function of the NMDA glutamate receptor in schizophrenia. This has largely been suggested by abnormally low levels of glutamate receptors found in postmortem brains of people previously diagnosed with schizophrenia^[1].

Evidence from drug studies of glutamate blocking drugsEdit

The discovery that the glutamate blocking drugs such as phencyclidine and ketamine can mimic the symptoms and cognitive problems associated with the condition.^[2] suggests apossible link

The fact that reduced glutamate function is linked to poor performance on tests requiring frontal lobe and hippocampal function and that glutamate can affect dopamine function, all of which have been implicated in schizophrenia, have suggested an important mediating (and possibly causal) role of glutamate pathways in schizophrenia.^[3] provides further support for this theory and preliminary trials suggesting the efficacy of coagonists at the NMDA receptor complex in reducing some of the positive symptoms of schizophrenia.^[4] are also indicative

See alsoEdit

References & BibliographyEdit

1. ↑ Konradi C, Heckers S. (2003) Molecular aspects of glutamate dysregulation: implications for schizophrenia and its treatment. Pharmacology and Therapeutics, 97(2), 153-79.
   
2. ↑ Lahti AC, Weiler MA, Tamara Michaelidis BA, Parwani A, Tamminga CA. (2001) Effects of ketamine in normal and schizophrenic volunteers. Neuropsychopharmacology, 25(4), 455-67.
   
3. ↑ Coyle JT, Tsai G, Goff D. (2003)

   Physiological studiesEdit

   Converging evidence of NMDA receptor hypofunction in the pathophysiology of schizophrenia. Annals of the New York Academy of Sciences, 1003, 318-27.
   

4. ↑ Tuominen HJ, Tiihonen J, Wahlbeck K. (2005) Glutamatergic drugs for schizophrenia: a systematic review and meta-analysis. Schizophr Res, 72:225-34.
   

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