While growing evidence suggests glutamate dysfunction in schizophrenia, it is important to note that glutamate and da systems in the brain interact at a number of different levels, making it difficult to attribute the effects of NMDA receptor antagonists to purely glutamatergenic abnormalities. Thus, the most complete explanation for schizophrenia may come from a combination or integration of NMDA hypofunctional and pre-nnaptic dysfunction da models (Howes et al., 2015). Some suggest that DA dysfunction in schizophrenia is secondary to disturbed gutamater activity (McGuire, Howes, Stone, ` Fusar-Poli, 2008), because DA neurons are partially regulated by glutamaterge projections. Indeed, it has been shown that NMDA receptor antagonists increase the release of DA in humans, although this can only happen if the DA system is already questioned or sensitized (for example. B after amphetamines) (Howes et al., 2015). Zuckerman L, Weiner I. Post-pubertal appearance of latent inhibition disturbed after prenatal immune activation. Psychopharmacology (Berl) 2003; 169 : 308-313. Martinez, D.
et al. Human dopamine dopamine imaging with positrons emission tomography. Part II: Release of dopamine induced by amphetamine in functional subdivisions of the striatum. J. Cereb. Blood flow. Mr. Metab. 23, 285–300 (2003). After the autopsy, the left hemisphere was treated in a standardized manner by each donor. Tissues can be frozen at 80oC within 30 minutes of autopsy.19 CNS pH58 was measured for each individual as an indicator of the quality of tissue preservation.59 New antipsychotics such as asenepine increase dopamine and glutamate levels in different subcortical and cortical areas (197).
New antipsychotic drugs with new mechanisms induce changes in dopamine and glutamate [Criticism of Paz et al. (198); Seeman et al. (99); Stein (199); Leroy et al. (200); Coyle et al. (201)] For example, metabotrope and NMDA receptors are future targets for new drugs (202, 203). A series of dopamine/serotonin, Glutamate/serotonin and acetylcholine/serotonin-interaction activate signal receptors and molecules in response to antipsychotic drugs and have been observed in different regions of the brain, including prefrontal cortexes and limbic regions, of schizophrenia (20, 98, 176, 182, 194, 204-211). Future drug development should involve signal molecules in dopamine, glutamate, and neurotransmission serotonin such as act and glycogen-synthase kinase-3 (98, 212, 213) and control the synthesis and release of dopamine (114). Stress in schizophrenic patients leads to an increase in dopamine release in the prefrontal cortex, which cannot be counteracted by reduced GABAA receptor activity, as well as a loss of dendritic spine in the prefrontal cortex (214, 215). In schizophrenic patients, cannabis induces hyper-dopaminergic and hypoglutammate activities with positive and negative symptoms (216). In particular, cannabis increases the transmission of dopamine in the nucleus accumbens, which could cause or aggravate psychosis (217). A high-activity polymorphic value in COMT interacts with cannabis abuse in adolescents, which increases the risk of schizophrenia (218).
In addition, genes such as Disrupted-in-Schizophrenia-1 (DISC1) play a role in the stress pathways and dopamine metabolism in schizophrenia [Hains and Arnsten review (219); Lipina et al. (220)] Lack of DVDs and MIA have also been implicated as risk factors for other psychiatric disorders such as autism.