Abstract
The application of graphene-family nanomaterials (GFNs) in neuromedicine has recently gained increased attention, but the associated exposure risk for synaptic function and the underlying mechanism remains obscure. The results of this study utilizing nanosized graphene oxide (nGO) suggest that they exert depressive effects on neurotransmission, mainly due to energy deficiency at synaptic contacts. Mitophagy is activated but fails to renew mitochondria and maintain mitochondrial-mediated energy metabolism because of blockage of autophagosome transport through the microtubule system from the axonal terminal to the soma. Further investigation of the underlying mechanism indicates that nGO increases the level of microtubule detyrosination, which restrains loading of the dynactin-dynein motor complex onto microtubules and subsequently inhibits the efficacy of the retrograde transport route. Thus, our study reveals the underlying mechanism by which nGO depresses neurotransmission, and contributes to our understanding of the neurobiological effects of GFNs.