The research on the property of GluR1 subunit in rat models of motor complication of Parkinson' s disease after CaMKⅡ inhibitor KN-93 treatment
10.3760/cma.j.issn.1674-6554.2010.10.009
- VernacularTitle:钙调激酶Ⅱ抑制剂对帕金森病运动并发症大鼠谷氨酸受体GluR1亚基特性的影响
- Author:
Maowen BA
;
Min KONG
;
Guoping YU
;
Xuwen SUN
;
Zhuli LIU
- Publication Type:Journal Article
- Keywords:
Parkinson' s disease;
Motor complication;
Glutamate receptor (GluR);
Phosphorylation;
Ca2 +/calmodulin-dependent protein kinase Ⅱ (CaMKⅡ)
- From:
Chinese Journal of Behavioral Medicine and Brain Science
2010;19(10):888-890
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the alteration of phosphorylated GluR1Ser831 and behavioural effects in a rat model of levodopa-induced motor complications after Ca2 +/calmodulin-dependent protein kinase Ⅱ (CaMKⅡ) inhibitor KN-93 treatment. Methods The hemi-parkinsonian rat model was produced by injecting stereotaxically 6-OHDA to right medial forebrain bundle. Then, rats were intraperitoneally treated with levodopa ( 50 mg/kg with benserazide 12.5 mg/kg,twice daily) for 22 days. On day 23 ,rats received KN-93 before levodopa administration. Rotational duration was estimated. After sacrificed, subcellualr distribution of GluR1 and phosphorylated GluR1Ser831 were observed by western blot. Results The study showed that CaMKⅡ inhibitor KN-93 prolonged rotational duration. Moreover, KN-93 could regulate subcellular distribution of GluR1 and reduce hyperphosphorylation of GluR1 Ser831, which was closely associated with levodopa-induced motor complications. The expression of membrane GluR1 and phosphorylated GluR1Ser831 was (83.4 ±4.2)% and (47.2 ±5.2)% ,respectively. Conclusions These results indicated that activation of CaMKⅡ contributed to development of motor complications, through a mechanism that involved an increase in phosphorylated GluR1 Ser831. Pharmaceuticals which act to inhibit CaMKⅡ may be useful in the treatment of the motor complications in parkinsonian patients.
