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Role of ventro medial prefrontal cortex NMDA-NO pathway in the modulation of behavioural consequences elicited by forced swim stress: intracellular mechanisms

Grant number: 11/13899-6
Support type:Scholarships in Brazil - Doctorate
Effective date (Start): October 01, 2011
Effective date (End): April 30, 2015
Field of knowledge:Biological Sciences - Pharmacology - Neuropsychopharmacology
Principal researcher:Sâmia Regiane Lourenço Joca
Grantee:Vitor Silva Pereira
Home Institution: Faculdade de Ciências Farmacêuticas de Ribeirão Preto (FCFRP). Universidade de São Paulo (USP). Ribeirão Preto , SP, Brazil
Associated scholarship(s):13/00916-5 - Involvement of BDNF-TrkB-mTOR pathway in the antidepressant-like effect induced by nos inhibitors, BE.EP.DR

Abstract

Glutamate, through activation of NMDA receptors, is capable of enhancing the nitric oxide (NO) synthesis. Over the last years, the involvement of the NMDA-NO pathway in the neurobiology of depression has been described. The use of NMDA antagonists, like ketamine, or NO synthesis inhibitors, such as 7-NI, produce antidepressant-like effects in animals, reinforcing the potential of glutamatergic and nitrergic systems as therapeutic targets for the treatment of depression. Recent studies show the participation of intracellular pathways involved in the control of neural plasticity, with emphasis to BDNF-TrkB-mTOR pathway in the antidepressant effects produced by NMDA antagonists. It was already demonstrated that the antidepressant-like effects of ketamina are associated to an increase in BDNF synthesis and that the administration of an mTOR inhibitor into the ventro medial prefrontal cortex (vmPFC) blocks the antidepressant-like effect of ketamine. Likewise, the pharmacological blockade of vmPFC or the infusion of a NMDA antagonist into this area induces antidepressant-like effects. However, it is not known if the antidepressant effects mediated by vmPFC depend on the interaction between the NMDA-NO pathway and the BDNF-TrkB-mTOR pathway. Thus, this project aims to evaluate the role of the glutamatergic neurotransmission, and the intracellular pathways activated by it, such as the production of NO, as well as the participation of the BDNF-TrkB-mTOR pathway, into vmPFC, in the modulation of the behavioral responses of animals submitted to the forced swim test. (AU)

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