Abstract
Transforming growth factor-beta 1 (TGF-β1) is an inflammation-related cytokine. Its expression in the brain increases under conditions of neurodegenerative diseases and injuries. Previous studies have shown that genomic alterations of TGF-β1 expression in the brain cause neurodegenerative changes in aged mice. The present study revealed that increased production of TGF-β1 in transgenic mice resulted in gliosis at young ages. In addition, the increased TGF-β1 augmented the expression of some key subunits of α-amino-3-hydroxy-5-methyl-4-isoxazoleproprionic acid (AMPA) and N-methyl-D-aspartate (NMDA) receptors in the hippocampus. Treatment of cultured hippocampal neurons with TGF-β1 facilitated neurite outgrowth and enhanced glutamate-evoked currents. Together, these data suggest that increased TGF-β1 alters ionotropic glutamate receptor expression and function in the hippocampus.
