Abstract
Schizophrenia is a multifactorial psychiatric disorder, which affects about 1% of the world's population. Several studies have demonstrated the involvement of the endocannabinoid system in the pathophysiology of schizophrenia. Studies have shown that endocannabinoids can also affect the function of oligodendrocytes. In order to better understand the mechanisms involved, and to help developing less harmful treatments, we will investigate the effects of endocannabinoids and synthetic cannabinoid agonists on a human oligodendrocyte cell line (MO3.13). In addition, we will verify if these treatments may reverse the effects of the NMDAr antagonist MK801 - an in vitro model to study schizophrenia. For this, we will use the two-dimensional liquid nanocromatography coupled to high resolution mass spectrometry. Data will be processed and analysed using in silico system biology tools. Taken together, our approach aims to contribute to the elucidation of the role of activation of cannabinoid receptorsin oligodendrocytes and the possible implications for undertanding the pathophysiology of schizophrenia.
Highlights
Schizophrenia is a severe disorder caused by the interaction of genetic and environmental factors during neurodevelopment[1]
This work aims to analyze the effect of endocannabinoids and synthetic cannabinoids in the proteome of human oligodendrocytes in culture, in order to identify proteins differentially expressed by these different treatments as well as their interaction networks and altered biochemical pathways, besides possible reversions of effects in a model of glutamatergic hypofunction
Aiming to delineate the role of endocannabinoids at a better understanding of schizophrenia, we present our preliminary results
Summary
Schizophrenia is a severe disorder caused by the interaction of genetic and environmental factors during neurodevelopment[1]. Defective in neurotransmission have been implicated in the symptoms of schizophrenia. Endocannabinoids play a role in the regulation of glial cells, important components in the pathophysiology of the disease, especially in relation to neuronal differentiation and survival. This is relevant, considering the reduction of the density of oligodendrocytes and white matter in schizophrenia patients, since these cells are responsible for myelination, which is critical to neurodevelopment.[3]. Alterations that may occur during the proliferation and maturation of oligodendrocytes progenitors may damage neural function related to neurotransmission in schizophrenia.[4]
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