| Objective To observe the first hole cluster-needling combined environmental stimuli on hypoxic-ischemic brain injury in neonatal rats with hippocampal microtubule-associated protein -2 and synaptophysin expression and synaptic ultrastructure of the impact of the first points of the integration of environmental stimulation on the cluster-needling hypoxic-ischemic brain injury affect the material basis of neural plasticity and its mechanism. Methods Of production of HIBD newborn animals were randomly divided into five groups. Using Morris water maze test of learning and memory capacity of each group was detected by immunohistochemistry in hippocampal CA1 area MAP-2 and synaptophysin expression, transmission electron microscopy observation of neuronal synapses and synaptic ultrastructure number. Results (1) the first hole cluster-needling the integration of environmental stimulation can contribute to hypoxic-ischemic brain injury in rats with learning and memory capabilities; (2) the first hole cluster-needling the integration of environmental stimulation of hippocampal CA1 area increased expression of MAP-2; (3) the first hole cluster-needling combined environmental stimuli can increase hippocampal synaptophysin expression in CA1 area; (4) the first hole cluster-needling combined environmental stimuli can reduce HI-induced synaptic ultrastructure injury, to improve the synaptic structure neural transmission of information to promote the hypoxic-ischemic brain tissue ultrastructure recovery; (5) the first hole cluster-needling combined environmental stimuli can promote an increase in the number of synapses. Conclusion Of scalp cluster-needling combined environmental stimulation can contribute to hypoxic-ischemic brain injury in rats with learning and memory capabilities; hippocampal CA1 area MAP-2 and synaptophysin expression increased in hypoxic-ischemic brain ultrastructure to resume and the increase in the number of synapses may be involved in the first cluster-needling acupoint stimulation on HIBD and environmental impact of neural plasticity mechanisms. |