Pathogenesis for Schizophrenia and Major Depression

Keywords Schizophrenia Major depression Thl/Th2 balance Pro-inflammatory cytokines NMDA hypothesis Glutamate Serotonin Tryptophan Kynurenine Kynurenic acid HPA axis 

Gintamatergic Nenrotransmission and NMDA-Receptor Function in Schizophrenia and Major Depression 

A disturbance in the dopaminergic nenrotransmission plays a key-role in the pathogenesis of schizophrenia (Carlsson, 1988). Most drugs ameliorating psychotic symptoms act as dopamine receptor blockers, in particular D2 receptor blockers. In light 

Treatment with NMDA receptor antagonists leads to a marked, dose-dependent increase of amphetamine-induced dopamine release (Miller and Abercrombie, 1996). In schizophrenics, this amphetamine-induced dopamine release is much higher compared to healthy controls (LarueUe et al., 1996). This observation is in accordance with the view that activation of the nigrostriatal dopamine system can take place by opposing activation of inhibitory striatonigral GABAergic projection neurons (Carlsson et al., 2001). 

Phencyclidine (PCP), Ketamin, and MK-801 all block the N-methyl-D-aspartate (NMDA) receptor complex and are associated with schizophrenia-like symptoms through hypofunction of the gintamatergic nenrotransmission (Krystal et al., 1994 Olney and Farber, 1995). Other NMDA antagonists have psychotogenic properties, too (CPP, CPP-ene, CGS 19755). NMDA receptor hypofunction can explain schizophrenic positive and negative symptoms, cognitive deterioration and structural brain changes (Olney and Farber, 1995). 

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