Alberto Martire, Rita Pepponi, Maria Rosaria Domenici, Antonella Ferrante, Valentina Chiodi and Patrizia Popoli
BDNF prevents NMDA-induced toxicity in models of Huntington's disease: the effects are genotype specific and adenosine A2A receptor is involved
We observed that BDNF, similar to adenosine A2A receptors' (A2ARs) stimulation, reduces NMDA-induced toxicity in Huntington's disease (HD) models, whereas increases it in wild-type preparations. In both genotypes, BDNF actions are prevented by A2AR blockade, confirming that A2ARs, directly and by activating TrkBRs, profoundly affect NMDAR functioning. These findings may have very important implications for the neuroprotective potential of both BDNF and A2AR ligands in HD.