脑有对卒中型自发性高血压大鼠脑卒中的治疗作用

为探讨脑复清对脑卒中型自发性高血压大鼠（ＳＨＲｓｐ）脑卒中的治疗作用，给ＳＨＲｓｐ饮１％ＮａＣｌ盐水，大鼠脑卒中发生后分别用脑复清０．５ｇ／ｋｇ．ｄ、１．０ｇ／ｋｇ．ｄ、２．０ｇ／ｋｇ．ｄ、２．０ｇ／ｋｇ．ｄ治疗，并与维脑路通１．０ｇ／ｋｇ．ｄ、２．０ｇ／ｋｇ．ｄ及溶媒剂作比较，治疗１４天。脑复清３组及维脑路通２组大鼠脑中卒临床症状评分（１．３－１．６分）均显著好于溶媒对照组（３．３，均Ｐ〈０．０     

葛根素（普乐林）对SHRsp脑卒中预防和治疗作用的研究

目的：研究普乐林注射液对卒中型自发性高血压大鼠（ＳＨＲｓｐ）脑卒中的预防和治疗作用。材料和方法：将８０只周龄（雌雄各半）ＳＨＲｓｐ随机分为普乐林２００ｍｇ／ｋｇ，１００ｍｇ／ｋｇ及对照组，饮１．０％～１．５％，ＮａＣｌ盐水。实验一，在高盐负荷开始即灌胃治疗，８周后断头处死，取颈动脉及脑组织做电镜检查。取脑组织光镜下检查脑卒中发生率。实验二；脑卒中发生后开始灌胃治疗，连续１０天，记录大鼠脑卒中临床表     

老年人踝部血压与心血管事件的关系

踝臂收缩压比值低下提示高死亡率及心血管事件，比值高并动脉钙化时增加死亡风险。该研究探讨老年人踝臂指数（ABI）异常及动脉硬化与死亡率、心血管事件（包括脑卒中）的关联度。方法：共有2886名70-79岁的老年人人选该研究，平均随访致死事件及心血管事件（包括冠心病、脑卒中及充血性心力衰竭）6．7年。结果：80％ABI处于0．9～1．3的正常范围，     

血胆固醇与脑胆固醇关系的研究

目的 研究血胆固醇（TC）对脑TC及脑β-淀粉样蛋白（A13）生成的影响。方法 给高TC血症的Wistar大鼠饲喂考来烯胺和邻苯二甲酸二异辛酯（diethylhexyl phthalate，DEHP）促进胆汁酸的合成，降低其血TC后，测定其脑1℃及AB的含量；以测定脑羟甲基戊二酰辅酶A还原酶HMG-COAR）和脑TC24S-羟化酶（CYP46）的mRNA表达水平，反映脑TC的合成水平和转出水平。结果 高TC血症大鼠脑AB含量明显增高（P〈0．05），脑TC以及脑HMG-COAR和CYP46的mRNA表达水平未变；考来烯胺饮食组大鼠血TC水平明显降低（P〈0．01），脑中AB含量和对照组一样保持在低水平，脑TC的含量有增高趋势，HMG-COAR mRNA表达增加（P〈0．05），CYP46mRNA表达无变化；DEHP饮食组血TC及脑中的AB无显著变化，脑1℃的含量明显增高（P〈0．05），脑HMG-COAR mRNA表达增加（P〈0.05），CYP46 mRNA表达降低（P〈0．01）。结论 脑TC的含量不受血TC的直接影响，而与其自身代谢有关；整体动物脑Aβ生成量增加与脑TC浓度无关。     

急性脑卒中202例心电图分析及与预后的关系

目的 探讨急性脑卒中心电图改变特点及对预后的影响。方法 对202例急性脑卒中合并有心电图异常的118例患者的临床资料进行回顾性分析。结果 急性脑卒中心电图异常占58．4％，其发生率与年龄呈正相关（P〈0．01）。出血性脑卒中心电图异常发生率明显高于缺血性脑卒中（P〈0．01）。出血性脑卒中患者中，心电图异常以心肌缺血或类心肌梗死及窦性心动过速为主，缺血性脑卒中患者中，心电图改变无明显特异性。合并有心电图异常的急性脑卒中死亡率明显增高。结论 急性脑卒中患者中，≥50岁患者心电图异常发生率高，出血性脑卒中合并心电异常发生率高，且死亡率明显增加。     

L-精氨酸对糖尿病大鼠NO-cGMP信号通路的影响

目的探讨L-精氨酸（Arg）对糖尿病（DM）大鼠一氧化氮（NO）-环磷酸鸟苷（cGMP）信号通路的调控作用。方法给大鼠腹腔注射链脲佐菌素制备DM模型，随机分为DM组、L—Arg治疗组及正常对照组；用药12W末处死大鼠，测定3组大鼠血糖、胰岛素含量以及血浆、心肌、肾脏、睾丸组织中NO、cGMP含量和NOS活性。结果DM组大鼠血糖含量较正常对照组显著升高（P〈0．01），而胰岛素水平（P〈0．01）及血浆、心肌、肾脏、睾丸组织NO水平（分别P〈0．01，P〈0．05，P〈0．05，P〈0．01）和血浆、心肌、睾丸组织cGMP含量（分别P〈0．01，P〈0．01，P〈0．05）及血浆、肾脏、睾丸组织一氧化氮合酶（NOS）活性（分别P〈0．01，P〈0．01，P〈0．05）均较正常对照组明显降低；L—Arg可明显降低DM大鼠血糖水平（P〈0．01），增加胰岛素含量（P〈0.01），同时显著增加血浆、心肌、肾脏、睾丸组织NO水平和血浆、心肌、睾丸组织cGMP含量及血浆、睾丸组织NOS活性（均P〈0．01）。结论DM大鼠NO-cGMP信号通路存在缺陷，L—Arg对DM大鼠NO—cGMP信号通路具有调控作用。     

全国2万例急性缺血性脑卒中早期抗血小板治疗临床对照研究结果(CAST临床试验)

目的：探讨急性缺血性脑卒中早期抗血小板治疗，对降低病人病死率、改善机体残疾率的临床疗效。本试验简称CAST临床试验。方法：采取多中心、随机、双盲治疗。对发病48小时内的急性缺血性脑卒中，经头颅计算机断层摄影术（CT）或临床检查基本排除出血性脑卒中即可入选。每日口服阿司匹林160mg或安慰剂4周。结果：自1993年11月至1997年4月全国413家医院共入选21106例病人。治疗期间阿司匹林组死亡343例，较对照组（死亡398例）下降14.0％（P=0．04）。再发缺血性脑卒中阿司匹林组显著低于对照组（1．6％比2．1％，P=0．01）。出血性脑卒中的发生，阿司匹林组较对照组略有增加，但差别不显著（1．1％比0．9％，P＞0．1）。结论：本项研究显示，对急性缺血性脑卒中病人进行早期抗血小板治疗，可显著降低住院期间死亡率及再发脑卒中发生率，并在一定程度上促进病人的功能康复。     

自发性高血压大鼠心肌胶原增生与心肌局部血管紧张素Ⅱ及醛固酮

为探讨高血压大鼠（ＳＨＲ）心肌胶原增生与心肌局部血管紧张素Ⅱ（ＡｎｇⅡ）、醛固酮（Ａｌｄ）的关系。方法应用羟脯氨酸法测定大鼠心肌胶原含量，用放免法测定心肌局部ＡｎｇⅡ、Ａｌｄ含量，将两者进行线性相关分析。结果自发性高血压大鼠（ＳＨＲｎ＝７）与对照组（ＷＫＹｎ＝７）相比，心肌胶原含量增加（Ｐ＜０．０１）。相关分析表明，心肌胶原含量与心肌局部ＡｎｇⅡ含量呈正相关（ｒ＝０．７２，Ｐ＜０．０５），与心肌局部Ａｌｄ含量呈显著正相关（ｒ＝０．８８５，Ｐ＜０．００１），而与血压（ＳＢＰ）无明显相关（ｒ＝０．３９８，Ｐ＞０．０５）。结论ＳＨＲ心肌胶原含量较正常大鼠增加，并且与心肌局部ＡｎｇⅡ、Ａｌｄ含量增加有关。     

苯丙氨酸阻止幼年自发性高血压大鼠血压升高机理的初步探讨

３％苯丙氨酸喂饲幼年（５～６周）自发性高血压大鼠能阻止血压随年龄的升高。喂饲６周后对照及处理大鼠血压分别为２５．８±４．４ｋＰａ（１９４／３３ｍｍＨｇ）及２２．９±３．０ｋＰａ（１７２／２２ｍｍＨｇ），差异有显著性。大鼠喂饲苯丙氨酸后血清谷丙转氨酶（ＡＳＴ），谷草转氨酶（ＡＬＴ）及尿素氮（ＢＵＮ）等指标值下降。提示长期应用苯丙氨酸对肝、肾无不良反应。喂饲苯丙氨酸的大鼠尾核酪氨酸羟化酶活性显著增高，而中枢儿茶酚胺含量不增加，。提示尾核儿茶酚胺更新加快，这种作用可能是苯丙氨酸抑制自发性高血压鼠血压升高的机理之一。     

脑卒中后继发癫痫的临床分析

目的调查分析脑卒中与癫痫的关系。方法对2003年1-12月在本院住院的脑卒中（初发或复发）患者50例，分析脑卒中后癫痫的发病率及危险因素。结果脑卒中后癫痫的发病率为6％。脑卒中后癫痫的发病率与患者的年龄、脑卒中部位、类型（出血性或缺血性）无关（χ^2分别为2．286、3．435、0．955，P〉0．05），与患者性别及脑卒中次数有关（分别χ^2=5．673，P〈0．05；χ^2=6．996，P〈0．01）。结论复发性脑卒中使脑卒中后癫痫的发病率提高，危险性增大，更易在合并感染等某种因素下诱发，加重病情。应积极预防脑卒中复发，控制感染等诱发因素，降低癫痫发病率，提高生活质量。     

Age-dependent glycolysis and gluconeogenesis enzyme activities in starved-refed rats

Food intake, plasma glucose, insulin (I) and glucagon (G), hepatic glycogen and fructose 2,6-bisphosphate (F-2, 6-P2) and liver glucokinase, glucose 6-phosphatase (G6-Pase), 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase (6-PF-2 kinase/F-2, 6-P2ase), pyruvate kinase (PK-L) and phosphoenolpyruvate carboxykinase (PEPCK) activities were measured in 2 and 22-month-old rats before 3 d starvation and after 2, 4, 6, 24 and 48 h refeeding a high carbohydrate (HC, 74% w/w) diet. Expressed per 100 g of body weight, the food intake of old rats was 55% lower than that of young rats and the amount of carbohydrate absorbed hourly during the first 6 h of refeeding was 2.4-fold higher in young than in old rats. During the first 6 h of refeeding plasma glucose increased 2-fold and returned to normal values after 24 h in young rats, while plasma glucose did not change during refeeding in old rats. In young rats [I] fell by 85% after starvation and returned to normal values 2 h after refeeding. [I] was higher in old than in young rats; it decreased by 40% after starvation and returned to the basal value 4 h after refeeding. No marked changes were observed in plasma [G] in both groups. No difference was observed in hepatic glycogen in the two groups, while F-2, 6-P2 was higher in old than in young rats. In young rats, the opposite changes in liver glucokinase and G6-Pase activities occurring after starvation and during refeeding were     

Long-term melatonin administration reduces hyperinsulinemia and improves the altered fatty-acid compositions in type 2 diabetic rats via the restoration of Delta-5 desaturase activity

The objective of this study was to investigate the effect of long-term melatonin administration on plasma levels of triglycerides, insulin and leptin, and on the fatty-acid metabolism of plasma and hepatic lipids in type 2 diabetic rats. Otsuka Long-Evans Tokushima Fatty (OLETF) rats, an animal model of type 2 diabetes mellitus, were divided into two groups: one untreated (n=6), and one implanted with time-releasing melatonin pellets (1.1 mg/day for 30 wk) under the abdominal skin (n=6). Age-matched Long-Evans Tokushima Otsuka (LETO) rats (n=6) were used as healthy controls. The untreated diabetic rats had the increased plasma levels of triglycerides, cholesterol, insulin and leptin at 35 wk, as compared with the healthy control rats (n=6). The diabetic rats also had augmented ratios of 20:3n-6/20:4n-6 fatty acids, owing to diminished activity of Delta-5 desaturase, an insulin-permissive enzyme, in the liver. Melatonin administration to OLETF rats reduced the hypertriglyceridemia (-39%, P < 0.05), hyperinsulinemia (-33%, P < 0.01) and hyperleptinemia (-43%, P < 0.01), and restored hepatic Delta-5 desaturase activity (148%, P < 0.005). This resulted in a return to normal ratios of 20:3n-6/20:4n-6 fatty acids in plasma and hepatic lipids. There was a significant correlation (r=0.64, P < 0.005) between plasma levels of insulin and the ratios of 20:3n-6/20:4n-6 in plasma phospholipids of all rats in the three groups. Thus, subcutaneous implantation of a melatonin-releasing pellet thus resulted in improved lipid metabolism in diabetic rats, probably through restored insulin resistance.     

Intermittent protein-calorie malnutrition in the young rat causes long-term impairment of the insulin secretory response to glucose in vitro

The effect of a limited period of protein-calorie malnutrition in young rats on insulin secretion in the adult has been studied. Three-week-old rats were weaned onto diets containing 5% protein (low protein; LP) or 15% protein (control; C) and maintained for 3 weeks on their respective diets. A third experimental group was weaned onto standard rat chow (18% protein; normal diet; N). From 6 weeks of age onwards all rats were fed the standard rat chow. Pancreatic islets were isolated from rats aged 3, 6 and 12 weeks and their insulin secretory response to glucose or arginine was tested. At 12 weeks the effects of the secretagogues were also tested using perfusion of isolated pancreatic glands. In islets from 6-week-old LP rats the glucose-stimulated insulin release was only 25% of that of C and N rats of the same age. Islets from C and N rats responded to arginine in the presence of a low glucose concentration with a small increase in insulin secretion, whereas no such response could be demonstrated in islets from 6-week-old LP rats. Islets from 6- and 12-week-old N rats responded to glucose and arginine. Islets from 12-week-old C rats had a similar response to glucose but did not respond to arginine in the presence of a low glucose concentration. In islets from 12-week-old LP rats the secretory response to glucose remained only 40% that of C and N rats and there was no response to arginine in the presence of a low glucose concentration.(ABSTRACT TRUNCATED AT 250 WORDS)     

Predominance of hemodynamic rather than metabolic factors in the pathogenesis of diabetic glomerulopathy.

Six groups of Munich-Wistar rats underwent micropuncture study 2-10 weeks and morphologic studies 11-13 months after induction of streptozotocin diabetes or after sham treatment. Diabetic rats received diets containing 6% (group D6), 12% (D12), or 50% protein (D50) and were maintained under similar conditions of moderate hyperglycemia by daily injections of ultralente insulin. Age- and weight-matched normal control rats were also given 6% (Group N6), 12% (N12), or 50% protein (N50). Kidney weight, whole-kidney and single-nephron glomerular filtration rate, glomerular plasma flow, and mean glomerular transcapillary hydraulic pressure difference were higher in D50 rats than in all other groups and predisposed this group to marked and progressive albuminuria. Likewise, histological examination of the kidneys disclosed areas of sclerosis in 19.6% of glomeruli in D50 rats; the frequency of such lesions was less than 2.5% in all other groups. These findings indicate that the metabolic disorder seen in stable, moderately hyperglycemic diabetic rats does not lead to glomerulopathy as long as elevations in glomerular pressures and flows are prevented.     

Overexpression of neuropeptide Y in the central nucleus of the amygdala decreases ethanol self-administration in "anxious" rats

BACKGROUND: Neuropeptide Y (NPY) has been implicated in a variety of behaviors including those associated with anxiety and ethanol administration. The current experiment investigated the predictive role of anxiety-like behaviors in ethanol self-administration and the relationship of NPY in the central nucleus of the amygdala (CeA) with anxiety and ethanol self-administration. METHODS: Rats were divided into anxious and nonanxious groups based on behavior in the elevated plus maze. Following elevated plus maze testing, rats were allowed to consume increasing concentrations of ethanol (2, 4, and 6%) in a 2-bottle choice procedure over a period of 31 days. anxious rats showed an increased preference for 4% ethanol and 6% ethanol compared with non-anxious rats. Following 20-day access to 6% ethanol, rats underwent gene transfer surgery with replication-defective recombinant herpes simplex 1 vectors encoding prepro-NPY, an antisense NPY RNA, or LacZ (control) into the CeA. RESULTS: In anxious rats, bilateral injections into the CeA with the NPY-antisense vector increased 6% ethanol preference, while the vector encoding NPY decreased 6% ethanol preference. Herpes simplex viral-mediated alterations in CeA NPY expression did not alter ethanol preference in nonanxious rats. CONCLUSIONS: These results suggest that virally mediated alterations in NPY levels in the CeA differentially affect ethanol consumption in rats with low and high basal levels of anxiety.     

Changes in cardiac energy metabolism during early development of female SHR

We investigated effects of hypertension and early development on myocardial energy metabolism as reflected by maximal enzyme activities, glucose transporter content, and endogenous substrates in female Wistar-Kyoto (WKY) rats and spontaneously hypertensive rats (SHR). Left ventricular hypertrophy and systolic hypertension were evident in SHR at 6 weeks of age and these differences increased at 14 and 22 weeks of age. 3-Hydroxyacyl-CoA dehydrogenase (HOAD) activity in the left ventricle was 18% lower in 6-week-old rats than both 14- and 22-week-old rats, but not different between WKY rats and SHR. Hexokinase activity was 15% lower in 6-week-old SHR than WKY rats and decreased progressively with age in both strains. Glucose transporter (GLUT) 1 content was nearly twofold greater in 6-week-old rats than both 14- and 22-week-old rats. We found no difference in citrate synthase activity or GLUT4 content among groups. Glycogen concentration was 44% lower in SHR than WKY rats, whereas triglyceride was slightly (16%) higher in SHR than WKY rats. Older animals had higher levels both glycogen and triglyceride than younger animals. We conclude that the left ventricle of both SHR and WKY rats may change from predominantly glucose to fatty acid oxidation for energy production during early development.     

Ontogeny and nutritional regulation of the serum growth hormone-binding protein in the rat

The ontogeny and the nutritional regulation of the serum growth hormone-binding protein in Wistar rats was studied in vitro using Ultrogel AcA34 filtration of serum incubated with 125I-bovine growth hormone. The level of the specific binding of GH to serum GH-binding protein was low in 1-week-old rats (female rats 2.3 +/- 0.9%; N = 6, and male rats 2.1 +/- 8%; N = 6) and increased with puberty, to reach 10-fold higher levels in 12-week-old adult female (26.1 +/- 2.3%; N = 6) and 5-fold higher levels in adult male rats (11.2 +/- 0.9%; N = 6). From 6 weeks of age and onwards, the level of serum GH-binding protein was significantly higher in female than in male rats, reflecting sexual dimorphism. The nutritional dependence of GH-binding protein was supported by the 46% decline of serum GH-binding protein levels in 6-week-old female rats fasted for 3 days (11.6 +/- 0.9 and 6.3 +/- 1.1% in control and fasted rats, respectively; N = 8/group; p less than 0.001). After 4 days of refeeding, no difference was found between control and experimental animals. During development and after nutritional manipulation, Scatchard analysis revealed that the changes in GH-binding protein were due to changes in binding capacity and not affinity. The levels of serum GH-binding protein were positively correlated with the levels of hepatic GH binding sites, suggesting that the regulation of both proteins is closely related during development and in states of nutritional sufficiency and deprivation.     

Age-dependent hepatic lipogenic enzyme activities in starved-refed rats

Food intake, plasma glucose, insulin (I) and triiodothyronine (T3) and liver glucose 6-phosphate dehydrogenase (G6P-DH), malic enzyme (ME). ATP-citrate lyase, acetyl-CoA carboxylase (AcCoACx) and fatty acid synthase (FAS) activities were measured in 2 and 22 months old rats before, after 3 d starvation and 2,4,6. 24 and 48 h refeeding a high carbohydrate (74% w/w) diet. Expressed per 100 g of body weight, the carbohydrate intake of old rats was 55% lower than that of young rats. Plasma insulin was higher in old than in young rats and decreased (-40%) after starvation and returned to control values 4 h after refeeding. In young rats plasma insulin fell after starvation (-85%) and returned to normal values 2 h after refeeding. No significant differences were observed in plasma [T3] between the two groups. During the first 6 h of refeeding, plasma glucose increased 2-fold and returned to control values after 24 h in young rats. In old rats, plasma glucose returned to its control value after 2 h. Compared to the starved level, 48 h after refeeding, G6P-DH, ME, ATP-citrate lyase, AcCoACx and FAS activities increased 5- to 6-fold in young rats, while in old rats the increase was much smaller and represented 35% of that observed in young rats. These results suggest, that the age-related reduction in inducibility of hepatic lipogenic enzymes of rats refed a high carbohydrate diet after starvation may be due to a spontaneous decrease in the carbohydrate intake and to a decrease effectiveness of insulin (insulin resistance).     

Effect of age on potassium- and tyramine-induced release of norepinephrine from cardiac synaptosomes in male F344 rats.

Potassium (K+)-induced norepinephrine (NE) release was examined in preparations of cardiac synaptosomes and sliced atria from 6-, 24-, and 26-mo-old male F344 rats. Cardiac synaptosomes were prepared from rat hearts by collagenase digestion followed by homogenization in 0.32 M sucrose and centrifugation. The synaptosome preparations and the sliced atria were labeled with 3H-NE and then placed in a superfusion system. K(+)-induced net fractional release of NE from synaptosomes prepared from 24- and 26-mo-old rats (4.3% and 3.0%, respectively) was significantly reduced when compared to NE release from synaptosomes from 6-mo-old rats (5.2%). K(+)-induced NE release from sliced atria from 24-mo-old rats (4.7%) was also significantly reduced when compared to NE release from atria from 6-mo-old rats (6.3%). Perfusion of cardiac synaptosomes with buffer prepared without calcium (CA++free, < 5 microM) reduced K(+)-induced release by 50% in all age groups studied. Perfusion with tyramine induced identical rates of NE release from cardiac synaptosomes prepared from 6- and 24-mo-old rats. These results confirm that depolarization-induced NE release from cardiac sympathetic nerves is reduced in the old male F344 rat.     

帕金森病运动并发症发生机制中G蛋白偶联受体激酶6与N-甲基-D-天冬氨酸受体关系的研究

目的 研究G蛋白偶联受体激酶6(GRK6)在帕金森病(PD)运动并发症发生机制中与N-甲基-D-天冬氨酸(NMDA)受体的关系.方法 建立PD运动并发症大鼠模型,25只大鼠分为3组.异动症(LID)组10只,腹腔注射左旋多巴甲酯23 d;MK-801处理组10只,第23天左旋多巴甲酯注射前腹腔注射MK-801;PD组5只,腹腔注射0.2%维生素C液.另设假手术组5只为对照组.观察MK-801处理左旋多巴诱导的运动并发症模型大鼠的行为变化,并用免疫组织化学方法和Western印迹方法检测大鼠纹状体区GRK6蛋白的表达情况.结果 PD组大鼠长期使用左旋多巴后出现明显的异常不自主运动,与人类LID具有相似特征.免疫组化结果显示.PD组损伤侧纹状体区GRK6阳性细胞指数减少至(4.81±1.31)×103(P＜0.05),LID组损伤侧GRK6阳性细胞指数进一步减少至(3.23±0.41)×103(P＜0.01).MK-801组LID大鼠异常不自主运动评分减少,药效期延长,同时损伤侧纹状体区GRK6阳性细胞指数增多至(4.64±1.39)×103(P＜0.05).Western印迹法检测结果同免疫组化基本相符,PD组损毁侧/未损毁侧纹状体区GRK6含量比值为(83.7±2.1)%,LID组GRK6值降低为(76.8±2.2)%,而MK-801组GRK6值升高至(91.1±2.7)%(P＜0.01).结论 NMDA受体拮抗剂能逆转大鼠运动并发症的发生,其机制可能与GRK6增多,抑制了谷氨酸受体的过度活化有关.

Abstract：

Objective To investigate the relationship between G protein-coupled receptor kinase 6 (GRK6) and N-methyl-D-aspartate (NMDA) receptor in the mechanism study underlying motor complications in Parkinson's disease (PD).Methods The rat models (n= 25) of Parkinsonism related motor complications were established and were randomly divided into levodopa-induced dyskinesia (LID) group (n= 10,intraperitoneal injection of levodopa for 23 d),MK-801 treatment group (n= 10,intraperitoneal injection of MK-801 at day23 after intraperitoneal injection with levodopa for 22 days) and PD group (n= 5,intraperitoneal injection of vitamin C).Another 5 rats were served as controls (sham-operation group).The behavior changes of rats in MK-801 treatment group were observed,and the expression of GRK6 in the striate of rats was detected by immunohistochemistry and Western blot.Results After the chronic treatment with levodopa methyl ester,PD rats displayed abnormal involuntary movements,which was similar to levodopainduced dyskinesia in PD patients.Immunohistochemistry showed that GRK6-positive cells of lesion side were decreased in LID rats as compared with PD rats [(3.23±0.41 ) × 103 vs.(4.81 ± 1.31 ) ×103,P＜0.01].Rats in MK-801 treatment group displayed the decreased AIM scores and increased peak rotation,and the increased GRK6-positive cells of lesion side as compared with LID rats (P＜0.05).Western blot showed that the levels of GRK6 was 83.7% ±2.1% in PD group (presented as lesion side/unlesion side),76.8% ± 2.2% in LID group and 91.1% ± 2.7% in MK-801 treatment group (intergroups comparison:all P＜0.05).These results were in accordance with the results of immunohistochemistry.Conclusions Antagonist of NMDA receptor can be used to reduce the motor complications in rats.It may be due to increased GRK6 which inhibits the overactivation of glutamic acid receptors.