实验性帕金森病纹状体、大脑皮质、海马组织Glu含量的变化

目的:探索帕金森病(PD)的发病机制。方法:应用大鼠选择性偏侧(右侧)PD动物模型,观测正常对照组,PD组(造模后2周)左右侧纹状体(ST)、大脑皮质(CC)、海马(HP)组织谷氨酸(Glu)含量的变化。结果:PD组右侧ST、CC、HP组织Glu含量显著低于左侧和正常对照组左右侧(P<0.01);PD组左侧ST、CC、HP组织Glu含量与正常对照组比较无显著差异性(P>0.05);正常对照组左右侧ST、CC、HP组织Glu含量无显著差异性(P>0.05)。结论:神经递质Glu参于PD累及部位ST、CC、HP损伤的发病机制     

Neuroactive amino acids influence gonadotrophin output by a suprapituitary mechanism in either rodents or primates

Systemic administration of excitatory amino acids (Glu or NMA) rapidly enhances LH release (rodents or primates) and GABA blocks this action (rodents). In the present study rodent and primate pituitaries were incubated with NMA, Glu and/or GABA, with or without added LH-RH. Only LH-RH affected LH release. Therefore the probable site of NMA, Glu or GABA action on LH release in both rodents and primates is suprapituitary.     

Synthesis of N-acetyl-l-aspartyl-l-glutamic acid; [3H]NAAG

[³H]NAAG, N-acetyl-l -aspartyl-l -glutamic acid, has been widely used as a substrate in glutamate carboxypeptidase II (GCPII) reactions, either to determine the inhibitory constants at 50% inhibition (IC₅₀) of novel compounds or to measure GCPII activities in different tissues harvested from various disease models. The importance of [³H]NAAG, combined with its current commercial unavailability, prompted the development of a reliable eight-step synthetic procedure towards [³H₂]NAAG starting from commercially available pyroglutamate. Pure [³H]NAAG of high molar activity (49.8 Ci/mmol) and desired stereochemistry was isolated in high radiochemical yield (67 mCi) and radiochemical purity (>99%). The identity was confirmed by mass spectrometry and co-injection with unlabeled reference.     

雌二醇对去卵巢大鼠学习记忆能力及脑内氨基酸水平的影响

目的：研究雌二醇对去卵巢大鼠学习记忆能力及脑内氨基酸水平的影响。方法：采用双侧卵巢切除术（ovariectomy,OVX）建立大鼠雌激素缺乏模型,雌二醇组于OVX后第7周每日皮下注射（sc）雌二醇75,300μg ·kg^-1至第16周,假手术组与模型组每EtSC0．5mL·kg^-1溶剂。第15周通过Morris水迷宫检测大鼠的学习记忆能力,第16周处死大鼠,用高效液相色谱法测定大鼠前皮层和海马的4种氨基酸的含量。结果：与假手术组相比,模型组大鼠学习记忆能力明显下降,前皮层和海马谷氨酸（glutamicacid,Glu）含量及谷氨酸/γ-氨基丁酸（glutamicacid／γ-aminobutyricacid,Glu／GABA）明显下降;与模型组相比,雌二醇75μg ·kg^-1治疗组,学习记忆能力明显改善,其前皮层和海马Glu含量及GIu／GABA明显升高;而雌二醇300μg ·kg^-1治疗组大鼠学习记忆能力无明显改善,其前皮层Glu／GABA明显增加,但海马Glu／GABA无明显变化。结论：雌二醇75μg ·kg^-1改善去卵巢大鼠的学习记忆能力的作用,可能与其增加脑内海马Glu／GABA比值有关。     

A method for determining nonelectrolyte uptake by adult Schistosoma mansoni using compartmental analysis of hexose fluxes

A steady-state compartmental analysis of galactose, glucose and 3-O-methylglucose fluxes was conducted on male and female Schistosoma mansoni. The method has several advantages over previously used initial rate studies. A nonlinear log-linear plot of glucose exchange is discussed in terms of differentiating between metabolized and nonmetabolized substrates in transport studies. K_t values and marker distribution volumes are estimated from the compartmental analysis and it is concluded that 3-O-methylglucose is not suited as a substrate for hexose transport studies in S. mansoni.     

大鼠急性脑缺血再灌注损伤中康络素对谷氨酸抑制作用的实验研究

目的 :探讨康络素对脑缺血再灌注损伤的保护作用。方法 :采用 Pulsinelli的四血管闭塞法制备大鼠急性脑缺血再灌注模型 ,利用高压液相色谱法观察脑缺血再灌注期间谷氨酸、γ-氨基丁酸含量变化 ,通过图象分析仪测定神经元的面数密度及康络素对以上指标的影响。结果 :谷氨酸、γ-氨基丁酸含量于缺血后明显升高 ,再灌注后降低 ,康络素可降低谷氨酸含量 ,与盐水对照组相比差异显著 (P<0 .0 1) ,同时增加神经元面数密度。结论 :康络素通过抑制谷氨酸释放可减轻脑缺血再灌注期间脑组织损伤。     

中风膏对脑缺血再灌注损伤大鼠脑组织中Glu、NMDA-R1及海马神经元内钙离子浓度的影响

目的：在系统回顾缺血性脑卒中相关文献的基础上,通过大鼠短暂性全脑缺血再灌注模型实验,探讨了中风膏对缺血性脑卒中引起再灌注脑损伤的治疗及作用机理。分析了中医益气活血法在缺血性脑卒中发病急性期用药的可行性、有效性、及安全性。方法：参照双侧颈总动脉夹闭法（2VO）及气虚血瘀的中医证型复制了缺血性脑卒中大鼠再灌注模型,造模成功后,予以中风膏灌胃治疗,阳性对照药选用益气活血,化瘀通络之步长脑心通。根据卒中评分标准,观察大鼠神经行为体征改变,分别测定相关指标。结果：本实验证明大脑神经元对缺血有不同的敏感性,其中海马区最为敏感,具有全脑缺血变化的全部特征。实验研究发现中风膏治疗组大鼠的神经行为体征较治疗前明显改善,中风膏组与阳性对照组疗效相当,均对缺血性脑卒中有很好的疗效。结论：本实验从细胞、分子水平探索认为中风膏治疗大鼠急性期缺血性脑卒中的机理可能是阻断脑缺血缺氧后的损伤级联反应,抑制兴奋氨基酸中Glu的释放,减少NMDA-R1的过度激活,减轻脑组织中Ca^2＋超载及脑缺血后引发的神经细胞毒性作用,从而保护脑组织,减轻脑组织的再灌注损伤,起到神经保护剂的作用。     

Safety assessment of transgenic Bacillus thuringiensis with VIP insecticidal protein gene by feeding studies.

The aim of this study was to evaluate the toxicology safety of a genetically modified (GM) Bacillus thuringiensis with vegetative insecticidal protein (VIP) gene. Acute and subacute toxicity studies by using its powder preparation were conducted in Wistar rats. The result of the acute study showed the no-observable-adverse-effect level (NOAEL) of this GM B. thuringiensis powder preparation was greater than 5000 mg/kg body weight (BW). In the subacute study, the data analysis of body weight gain, food and water consumptions, clinical observations, haematology, serum biochemistry, organ weight ratios and histopathological findings did not show significant differences between control and treated groups. These results proved the NOAEL of this GM B. thuringiensis powder preparation in subacute test was greater than 5000 mg/kg BW. Since both the acute and subacute oral toxicity were not detected at the highest dose recommended by OECD guidelines, this GM B. thuringiensis could be generally regarded as safe for use in bio-pesticide industry.     

Suppressing action of cholinergic agents on synaptic transmissions in the corpus striatum of rats.

The action of acetylcholine (Ach) and of carbamylcholine (Cch) on activities of the corpus striatum were studied in vitro in thin striatal sections of rats and in vivo in rats anesthetized with α-chloralose. Cch and Ach suppressed field potentials (N₂-wave) and single-cell discharges elicited in slices by electric stimulation. They caused weak and inconsistent changes in firing evoked by glutamate (Glu). When the cholinergic agents were administered at concentrations more than 10 times that needed to suppress the N₂-wave, background firing was initiated or was modified in pattern by Cch. Atropine or tubocurarine was without effect on the N₂-wave. The suppressing action of Ach and Cch on the N₂-wave was blocked by atropine. Cch suppressed similarly negative field potentials elicited in vivo by local stimulation in the striatum of anesthetized rats. Whereas Cch suppressed single-cell discharges evoked by local electric stimulation, it was without effect on firing induced by Glu. Likewise, Cch suppressed firing elicited by motor cortex stimulation, but did not block activation of striatal neurons by nigral stimulation. These observations suggest that the cholinergic agents block synaptic transmission in the striatum without causing excitation or inhibition in postsynaptic neurons, and that the action of these agents is input-specific.