Relationship between behavioral parameters and the expression of glucose transporters, L-type Calcium-channels and plasma membrane Calcium-ATPase in a model of schizophrenia.
Schizophrenia is a chronic and highly disabling psychiatric disorder. The etiology of this disease is complex and still unknown; in this sense, disorders in glutamatergic neurotransmission due to hypofunction of the NMDA receptor (N-methyl-D-aspartate) have been proposed as one of the causes of the pathophysiology of the disease. The administration of ketamine, an NMDA receptor antagonist, emerges as an animal model of schizophrenia. Nevertheless, bioenergetic abnormalities and alterations in cellular calcium homeostasis have also been reported in the brain of schizophrenic patients. From this perspective, a direct link between signs and symptoms and total levels of voltage-activated Ca2+ channels, plasma membrane Ca2+-ATPase and glucose transporters in pathology has not yet been described. Aiming to investigate this relationship, this project will focus on developing a pharmacological paradigm of schizophrenia as a predictive model for the study of the hippocampal expression of GLUT1, GLUT3, Cav1.2, Ca2+-ATPase and its relationship with the negative, positive and cognitive symptoms characteristic of schizophrenia.