| Objective:1.To explore the mechanism of acupoint catgut-embedding in inhibit excitatory amino acid cytotoxicity and promote synaptic plasticity for improving learning and memory,and to provide experimental evidence and theoretical support for clinical application of acupoint catgut embedding therapy for ischemic-cognitive impairment.2.To clarify the regulation of acupoint catgut embedding on protein kinase C interacting protein1(PICK1),glutamate receptor 2(GluR2),Ca2+ level and morphology and ultrastructure of CA1 in hippocampus of rats with chronic ischemic cognitive impairment.Methods:A total of 56 SPF class male SD rats were randomly divided into sham operation model,catgut embedding and medication groups(n= 14 in each group).The chronic ischemic cognitive impairment model was established by permanent ligation of bilateral common carotid artery,The embedding was applied to "Baihui"(GV20),"Dazhui"(GV14),"Shenshu"(BL23)and "Xuanzhong"(GB39),1 times a week,a total of 4 weeks.Rats of the medication group were injected by GM-1(0.33mg/kg),once daily for 4 weeks.The rats,learning-memory ability was detected by Morris water maze,the Nissl,s body pathological changes in rats and area of rat hippocampus Nissl staining,hippocampus were tested by Niss1 staining test.To observe the changes of ultrastructure in hippocampal CA1 region of rats by transmission electron microscope.The expression levels of PICK1 and GluR2 in the hippocampus were detected by western bolt(WB),the concentration of Ca2+ in hippocampus of rats was measured by BCA protein concentration method.Results:Compared with the sham operation group,rats of the model group showed a prolonged escape latency times in position navigation experiment and a reduced the frequency times in the space exploration test through the platform quadrant,and the hippocampus Nissl staining showed only a small amount of Nissl bodies,arranged dispersedly,somatic cell volume plummeted,and large loss structure unclear,and the nuclei were hyperchromatic pyknotic,the rat hippocampus Nissl staining showed Niss1 bodies decreased,CA1 of rat hippocampus synaptic count decreased,synaptic mitochondria stiff,part of the Golgi fuzzy,ribosome reduced number of presynaptic vesicles,and the membrane boundary is not clear,postsynaptic density is sparse,synaptic active zone length,and in expression levels of rat hippocampus,PICK1 protein was increased and the relative expression of GluR2 protein decreased,and the concentration of calcium ion increased obviously(P<0.01).Compared with the model group,After acupoint catgut embedding treatment,the behavioral assessment numerical significantly improved(P<0.05,P<0.01),the morphology of hippocampus,Nissl showed rich Nissl body,only a few cells with hyperchromatic nuclei pyknosis,and loss of small,Niss1 body area increased,mitochondrial outer membrane and mitochondria in rat hippocampal C A1 area crest clearly visible,plump shape,and the expression levels of PICK1 protein in rat,hippocampus decresed(P<0.01)and the GluR2 protein increased(P<0.05)lCa2+ concentration decreased significantly(P<0.01),The effects of acupoint catgut embedding treatment was not obviously difference from those of medication in the grade of learning and memory,morphological changes of hippocampus Nissl bodies,and there was no morphological changes in the ultrastructure of the Nissl’s corpuscle,dyed area and the synapse of CA1 region.And the expression levels of hippocampus PICK1,GluR2 protein,and con-centration of calciumion(P>0.05).Conclusion:Catgut implantation at acupoint can effectively improve the ability of learning and memory in rats with chronic ischemic cognitive impairment and to inhibit the interaction between PICK1 protein and A-amino-3-hydroxy 1-5-methy1-4-pro pionate(AMPA)receptor in rat hip-pocampus,so as to increase the expression of AMPA receptor subunit GluR2 content,decreased the Ca2+ permeability,then to decrease the Ca2+ flow,reduce the toxicity of excitatory amino acids,improve synaptic plasticity,which may contribute to its effect in improving learning-memory dysfunction. |
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