Résumé
[Abstract] Objective To explore the role of purinergic ligand-gated ion chennel 7 receptor(P2X7R) in cognitive dysfunction in Parkinson’s disease rats. Methods Ninty rats was divided into 5 groups with 6 rats in each group with 3 repeats. The rat model of PD was established by 6-hydroxydopamine (6-OHDA). PD rats were injected with P2X7R agonists 2,3-adenosine 5-triethylammonium triphosphate (BzATP) and antagonists Comassie brilliant blue G (CBBG). The learning and memory ability and pain response of rats in the water maze were measured, and the expression of P2X7 in hippocampus was detected by Real-time PCR and Western blotting. Results Compared with the normal rats, PD rats had slow learning speed and weak memory ability. CBBG improved the learning and memory ability of PD rats, while BzATP decreased the learning and memory ability of PD rats. The result of Real-time PCR showed that compared with the control group, the expression of P2X7R mRNA was the highest in hippocampal tissue, the expression of P2X7R in CBBG group was down-regulated, and that of P2X7R in BzATP group was up-regulated. Compared with the PD group, Western blotting of P2X7R showed that the expression of P2X7 protein increased significantly in BzATP group, while the expression of P2X7 protein was lower in CBBG group. Conclusion Cognitive impairment exists in PD rats. CBBG can improve the learning and memory function of PD rats, and BzATP can inhibit the learning and memory function of PD rats.
Résumé
Schizophrenia is one of the common mental diseases. Because the mechanism of the schizophrenia is significantly complicated, the cause is still unknown. N-methyl-D-aspartate receptor antagonist can simulate the positive and negative symptoms, as well as the cognitive disorder of schizophrenia. Thus it has been widely used to establish the animal models of schizophrenia. The relationship of the three blocking agents of ion channels (phencyclidine, MK-801, ketamine) and the establishment of schizophrenia animal models is reviewed in this article.