RESUMO
Previously, we have shown that the endogenous neuropeptide cycloprolylglycine (CPG) is the positive modulator of AMPA receptors and revealed the dependence of its anxiolytic and antihypoxic action on BDNF/Trk signaling. In the present work, we for the first time conducted in vitro experiments using the AMPA receptor blockers DNQX and GYKI 52466 and the Trk receptor blocker K252a. It is shown that the neuroprotective effect of CPG depends on the activation of both AMPA and Trk receptors.
Assuntos
Neuropeptídeos , Fármacos Neuroprotetores , Fármacos Neuroprotetores/farmacologia , Ácido alfa-Amino-3-hidroxi-5-metil-4-isoxazol Propiônico , Receptor trkB/metabolismo , Receptores de AMPA , Fator Neurotrófico Derivado do Encéfalo/metabolismoRESUMO
Previously we have shown that the neuropeptide cycloprolylglycine is an endogenous positive modulator of AMPA receptors and assumed that the pharmacological effects of CPG are associated with the brain neurotrophic factor. In this paper, we have first demonstrated that DNQX, an inhibitor of AMPA receptors, and K252A, an ihibitor of Trk receptors, prevented the anxiolytic effect of CPG, which confirms the formulated hypothesis.
