These previous studies have provided comprehensive evidence indicating that strategies for neuronal replacement through adult endogenous neurogenesis may be of potential therapeutic value for stroke. However, simple proliferation of NSCs does not guarantee successful recovery from functional impairments. In order to become a therapeutic strategy for stroke, neurogenesis for capacity of self-repair has to be optimized for improvement of the poor survival of newborn neurons. Positive effects of acupuncture are well known as a treatment for achievement of functional recovery after stroke. Thus, acupuncture signals that ascend mainly through the spinal ventrolateral funiculus to the brain may improve adult neurogenesis as a potent form of sensory stimulation. EA treatment enhances stroke-induced striatal neurogenesis and promotes neurological functional recovery via modulation of a key regulator of neurogenesis, retinoic acid. The combination treatments of EA and NGF have a synergistic effect on cell proliferation and survival of NSCs, which is attributed to enhanced functional recovery. Transient forebrain ischemia increases the number of NSCs and results in a peak level of proliferation at around 1–2 weeks after ischemic injury. Thus, we administered EA stimulation from five days to 14 days after MCAO on time showing a peak level of proliferated NSCs. We found that EA treatment after ischemic stroke resulted in improved neuronal function and induced proliferation and differentiation of NSCs. We detected newborn cells when newborn neuroblasts expressed both specific marker, Dcx and NeuN. EA treatment resulted in up-regulation of adult neurogenesis after stroke, however, in SAR131675 accordance with previous studies, very limited survival of newborn neuronal precursors was observed against the total number of BrdU positive proliferated cells. However, the increase in total numbers of BrdU/Dcx or NeuN double-positive cells indicates that EA stimulation may play beneficial roles in enhancement of proliferation and maturation of NSCs. Thus, we compared proliferation and differentiation of NSCs in specific sites, including hippocampus, SVZ, and cortex at early and late phase after MCAO. The number of BrdU positive cells showed a significant increase in the SVZ of MCAO mice, compared with other sites, and EA treatment resulted in an increase in the number of these cells at early phase after MCAO. Neuroblast marker Dcx was observed in proliferated NSCs at early phase after MCAO, however, neuron and astrocyte markers, NeuN and GFAP, were detected at late phase. Fewer BrdU/NeuN and GFAP double-positive cells were detected in the SVZ and cortex at late phase after MCAO, compared with Brdu/Dcx positive cells at early phase, indicating loss or migration of NSCs during maturation. However, a larger number of differentiated cells was detected in the hippocampus, which may have caused migration of NSCs from a ventricular area caudal to the SVZ into the hippocampus in response to ischemia, namely the subcallosal zone and caudal extension of the SVZ.