Astrocytes can release functional mitochondria into neurons after stroke, which may contribute to neuroprotection and recovery. The study shows that astrocytes release extracellular mitochondria particles through a calcium-dependent mechanism involving CD38 and cyclic ADP-ribose (cADPR) signaling. These mitochondria enter neurons and enhance survival signals, improving neuronal viability. CD38 inhibition reduced mitochondrial transfer and worsened neurological outcomes. Astrocytic mitochondria support neuronal survival and plasticity, as demonstrated by increased survival signals and dendrite regrowth. In vivo experiments confirmed that astrocytic mitochondria enter neurons after stroke, promoting survival and neuroplasticity. CD38 signaling is crucial for this process, and its suppression led to reduced mitochondrial transfer and impaired recovery. The study also highlights the potential of CD38-mediated mitochondrial transfer as a novel mechanism for neuroglial communication. However, further research is needed to fully understand the dynamics and generalizability of this process. The findings suggest that astrocytic mitochondrial transfer may be a key factor in endogenous neuroprotection and recovery after stroke.Astrocytes can release functional mitochondria into neurons after stroke, which may contribute to neuroprotection and recovery. The study shows that astrocytes release extracellular mitochondria particles through a calcium-dependent mechanism involving CD38 and cyclic ADP-ribose (cADPR) signaling. These mitochondria enter neurons and enhance survival signals, improving neuronal viability. CD38 inhibition reduced mitochondrial transfer and worsened neurological outcomes. Astrocytic mitochondria support neuronal survival and plasticity, as demonstrated by increased survival signals and dendrite regrowth. In vivo experiments confirmed that astrocytic mitochondria enter neurons after stroke, promoting survival and neuroplasticity. CD38 signaling is crucial for this process, and its suppression led to reduced mitochondrial transfer and impaired recovery. The study also highlights the potential of CD38-mediated mitochondrial transfer as a novel mechanism for neuroglial communication. However, further research is needed to fully understand the dynamics and generalizability of this process. The findings suggest that astrocytic mitochondrial transfer may be a key factor in endogenous neuroprotection and recovery after stroke.