Differential cortical and striatal astrocytes glutamate transporters expression and TNF-alpha release

JULIETA SABA; FEDERICO LÓPEZ COUSELO; JUAN TURATI; DELIA RAMÍREZ; LILA CARNIGLIA; ANDREA DE LAURENTIIS; DANIELA DURAND; MERCEDES LASAGA; CARLA CARUSO

Mar del Plata

Congreso; LXIII Reunión Anual de la Sociedad Argentina de Investigación Clínica (SAIC); 2018

Sociedad Argentina de Investigación Clínica (SAIC)

Astrocytes provide metabolic and structural support to the brain and are essential partners in neurotransmission and behavior. GLT1 and GLAST glutamate transporters in astrocytes do most of the work by clearing extracellular glutamate. Their expression and activity are influenced by cytokines, growth factors and reactive oxygen species (ROS). We have previously shown that brain-derived neurotrophic factor (BDNF) reduces ROS accumulation in astrocytes and neurons induced by 3-nitropropionic acid (3-NP), a toxin that causes mitochondrial dysfunction and oxidative stress as it occurs in Huntington?s disease (HD). Being the striatum more susceptible to 3-NP, here we investigated BDNF effect on glutamate transporters expression in primary cortical and striatal astrocytes. Astrocytes were incubated for 24 h with 3-NP ± BDNF. BDNF increased GLT1 expression in cortical and striatal astrocytes per se and in the presence of 3-NP (p