参叶益智胶囊改善记忆功能的作用机理研究

目的：从胆碱能神经递质方面探讨参叶益智胶囊改善记忆功能的作用机理。方法：对3月龄和12月龄小鼠分别给予参叶益智胶囊及对照药物后，测定小鼠大脑皮质和海马胆碱己酰转移酶(ChAT)、胆碱酯酶(AchE)活性及己酰胆碱(Ach)含量。结果：参叶益智胶囊对12月龄小鼠大脑皮质和海马ChAT、AchE活性及Ach含量的影响是双向调节作用。即升高ChAT活性，降低AchE活性，从而使Ach含量提高或维持在一相对恒定的水平上。结论：参叶益智胶囊可以调节老龄小鼠正常的胆碱能神经生理功能。     

水煎山楂液对小肠平滑肌影响机制的研究

目的：探讨水煎山楂液对小肠平滑肌的影响机制方法：通过使用一定浓度水煎山楂液分别与Ach、阿托品和维拉帕米、CaCl2的联合作用下,观察小肠平滑肌的收缩情况结果：水煎山楂液使M受体抑制和兴奋状态下的平滑肌收缩幅度增加,不能使钙离子通道抑制状态的平滑肌收缩幅度增加。结论：水煎山楂液对小肠平滑肌影响机制主要与激动M受体有关。     

Regulation of hemodynamics in major salivary glands by parasympathetic vasodilation

Background

Since salivary fluid is created from blood plasma, hemodynamics in the salivary glands play an important role in the production of saliva. Trigeminal sensory input induces both salivary secretion and reflex parasympathetic vasodilation in salivary glands. This glandular vasodilation is thought to be important for the regulation of glandular hemodynamics due to the rapidity with which blood flow is increased. This review article summarizes recent research on the involvement of parasympathetic vasodilation in regulating hemodynamics in the salivary gland.

Leukotriene receptor antagonist attenuated airway inflammation and hyperresponsiveness in a double-stranded RNA-induced asthma exacerbation model

Background

Viral infections are the most common triggers of asthma exacerbation, but the key molecules involved in this process have not been fully identified. Although cysteinyl leukotrienes (cysLTs) have been postulated as the key mediators, their precise roles remain largely unclear. To investigate the roles of cysLTs in virus-induced asthma exacerbation, we developed a murine model using a viral double-stranded RNA analog, polyinosinic–polycytidylic acid (poly I:C), and analyzed the effect of leukotriene receptor antagonist (LTRA) administration.

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.     

Effect of gastrin-releasing peptide (GRP) on guinea pig gallbladder contrction in vitro

Few studies have reported the effects of gastrin-releasing peptide (GRP)/bombesin on the guineas pig gallbladder, and the results are contradictory. Because such contradictory results may, in part, be due to technical factors, we investigated the effect of GRP on guinea pig gallbaladder smooth muscle, using a improved horizontal organ bath. The guinea pigs were killed and the gallbladder was removed. Four longitudinal uscle strips (2×12mm) were suspended in Krebs-Ringer solution at 37°C and aerated with 95% O₂ and 5% CO₂. The mechanical activity of the strips was recorded isotonically by displacement-voltage transducers. via L-arms, to which a piezoelectric element with a frequency of 100Hz and movement of 50μm was applied. GRP contracted gallbladder muscle strips dose dependently, but the calculated maximal response was 22.4% and 20.1% of the acetylcholine-and cholecystokinin octapeptide (CCK8)-induced responses, respectively. The GRP-induced contraction was unaffected by the muscarinic blocker, atropine, or by the CCK receptor antagonist, loxiglumide. It is concluded that GRP weakly, but apparently directly, stimulates guinea pig gallbladder contraction.     

复智散对阿尔茨海默病模型小鼠认知功能及脑内胆碱能系统的影响

目的观察复智散（FZS）对阿尔茨海默病（AD）模型小鼠认知功能及脑内胆碱能系统的影响。方法采用β-淀粉样肽（Aβ25-35）小鼠侧脑室注射制作AD小鼠模型，应用水迷宫和小鼠穿梭程序自动控制仪检测小鼠的认知功能，采用比色法测定小鼠脑内胆碱乙酰基转移酶（ChAT）和乙酰胆碱脂酶（AchE）活性，采用碱性羟胺法测定乙酰胆碱（Ach）含量。结果FZS能明显改善AD小鼠的认知功能，且对脑内胆碱能系统有明显的调节作用，不仅能够降低AchE活性，而且能够增强ChAT活性，增加脑内Ach的含量。结论FZS可通过对脑内胆碱能系统的调节来改善其认知功能，从而达到治疗AD的效果。     

Eosinophil peroxidase induces expression of cholinergic genes via cell surface neural interactions

Eosinophils localize to and release their granule proteins in close association with nerves in patients with asthma and rhinitis. These conditions are associated with increased neural function. In this study the effect of the individual granule proteins on cholinergic neurotransmitter expression was investigated. Eosinophil peroxidase (EPO) upregulated choline acetyltransferase (ChAT) and vesicular acetylcholine transporter (VAChT) gene expression. Fluorescently labeled EPO was seen to bind to the IMR-32 cell surface. Both Poly-l-Glutamate (PLG) and Heparinase-1 reversed the up-regulatory effect of EPO on ChAT and VAChT expression and prevented EPO adhesion to the cell surface. Poly-l-arginine (PLA) had no effect on expression of either gene, suggesting that charge is necessary but insufficient to alter gene expression. EPO induced its effects via the activation of NF-κB. MEK inhibition led to reversal of all up-regulatory effects of EPO. These data indicate a preferential role of EPO signaling via a specific surface receptor that leads to neural plasticity.     

THE FIMBRIA-FORNIX/CINGULAR BUNDLE PATHWAYS: A REVIEW OF NEUROCHEMICAL AND BEHAVIOURAL APPROACHES USING LESIONS AND TRANSPLANTATION TECHNIQUES

Extensive lesions of the fimbria-fornix pathways and the cingular bundle deprive the hippocampus of a substantial part of its cholinergic, noradrenergic and serotonergic afferents and, among several other behavioural alterations, induce lasting impairment of spatial learning and memory capabilities. After a brief presentation of the neuroanatomical organization of the hippocampus and the connections relevant to the topic of this article, studies which have contributed to characterize the neurochemical and behavioural aspects of the fimbria-fornix lesion “syndrome” with lesion techniques differing by the extent, the location or the specificity of the damage produced, are reviewed. Furthermore, several compensatory changes that may occur as a reaction to hippocampal denervation (sprouting, changes in receptor sensitivity and modifications of neurotransmitter turnover in spared fibres) are described and discussed in relation with their capacity (or incapacity) to foster recovery from the lesion-induced deficits. According to this background, experiments using intrahippocampal or “parahippocampal” grafts to substitute for missing cholinergic, noradrenergic or serotonergic afferents are considered according to whether the reported findings concern neurochemical and/or behavioural effects. Taken together, these experiments suggest that appropriately chosen fetal neurons (or other cells such as, for instance, genetically-modified fibroblasts) implanted into or close to the denervated hippocampus may substitute, at least partially, for missing hippocampal afferents with a neurochemical specificity that closely depends on the neurochemical identity of the grafted neurons. Thereby, such grafts are able not only to restore some functions as they can be detected locally, namely within the hippocampus, but also to attenuate some of the behavioural (and other types of) disturbances resulting from the lesions. In some respects, also these graft-induced behavioural effects might be considered as occurring with a neurochemically-defined specificity. Nevertheless, if a graft-induced recovery of neurochemical markers in the hippocampus seems to be a prerequisite for also behavioural recovery to be observed, this neurochemical recovery is neither the one and only condition for behavioural effects to be expressed, nor is it the one and only mechanism to account for the latter effects. © 1997 Elsevier Science Ltd. All Rights Reserved.     

镉对大鼠胚胎损害作用的实验研究

目的 :探讨镉对大鼠胚胎的毒性效应及可能机制。方法 :雌雄性 SD大鼠按 2∶ 1同笼交配获取 38只孕鼠 ,随机分为 4组 (对照组 ,低镉组 ,中镉组 ,高镉组 )。分别在妊第7、1 0、1 3天经腹腔注射生理盐水和不同剂量的氯化镉 ( Cd Cl2 ) ,妊 2 1 d,剖宫取胎鼠 ,活杀取出胎鼠的肝、脑组织称重后测定 Cd、Zn、Ach、AKP、DNA含量。结果 :1高镉组未见存活胎鼠 ;2染镉组胎鼠肝中镉增加 ( P<0 .0 5 ) ,脑中锌有下降趋势 ;3染镉组胎鼠肝组织中的AKP活性 ,脑组织中的 Ach、DNA含量较对照组减低。结论 :1高剂量的镉可使孕鼠胚胎发育异常 ;2母鼠染镉可致胎鼠肝中 AKP酶活性降低及脑组织中 Ach、DNA含量减少 ,抗脂质过氧化能力减弱。