By producing brain-derived neurotrophic factor (BDNF), astrocytes play a role in disease resistance. This study was undertaken to investigate whether primary astrocytes derived from LEW/N and F344/N rats differentially express BDNF. LEW/N astrocytes expressed more BDNF mRNA and protein than F344/N astrocytes in basal and valproic acid (VPA)-stimulated conditions. VPA suppresses HDAC enzyme activity without affecting HDAC gene and protein expression in astrocytes of both strains. Blockade of TrkB receptors resulted in similar fold decreases in basal BDNF mRNA levels between two strains. The results suggest that inhibition of HDAC activity and BDNF-TrkB autocrine loop are involved in regulation of astrocytic BDNF transcription, whereas the mechanisms for elevated constitutive gene BDNF expression of LEW/N astrocytes remain to be investigated.
Date:
2010-03
Relation:
Journal of Neuroimmunology. 2010 Mar;220(1-2):90-98.
