I had never before heard of such a thing as “exchange of mitochondria between different cell types in the central nervous system (CNS).” However, Davis et al. (2o14) had published a report indicating that neurons can release DAMAGED mitochondria and transfer them to astrocytes for disposal and recycling. It was proposed that this ability to exchange mitochondria “might represent a potential mode of cell-to-cell signalling in the CNS”.
The attached paper shows that astrocytes in mice can also release FUNCTIONAL mitochondria that enter neurons. Astrocytic release of extracellular mitochondrial particles was mediated by a calcium-dependent mechanism involving CD38 and cyclic ADP ribose signalling. Transient focal cerebral ischaemia in mice induced entry of astrocytic mitochondria into adjacent neurons, and this entry amplified cell-survival signals. Suppression of CD38 signalling by short interfering RNA (siRNA) decreased extracellular mitochondria transfer and worsened neurological outcomes. These findings suggest a new mitochondrial mechanism of neuroglial cross-talk that may contribute to endogenous neuroprotective and neurorecovery mechanisms after stroke..!!
Nature 28 July 2o16; 535: 551–555