静松灵、乌拉坦对家兔胃和十二指肠肌电活动的影响

采用胃、肠浆膜表面埋植双极引导电极、多道电极同时记录法，测定了静松灵、乌拉坦对家兔胃窦、十二指肠肌电活动的影响。经统计分析表明，静松灵能显著地抑制胃窦、十二指肠肌电活动的锋电峰值和电簇频率（Ｐ〈０．０１），乌拉坦则能够明显地抑制胃窦、十二指肠肌电活动的锋电峰值（Ｐ〈０．０１），但对锋电簇频率没有明显的影响（Ｐ〈０．０５）。静松灵的抑制效应主要是通过Ｍ受体起作用。     

槟榔对动物胃肠运动的影响

从在体、离体水平观察槟榔（Areca catechu L.)对动物胃肠运动的影响，并初步探讨其作用机理。结果表明，槟榔明显增高家兔十二指肠肠管的张力，减小收缩波平均振幅，不影响收缩频率；山莨菪碱、异搏定能减弱槟榔对十二指肠肠管张力的增高作用。槟榔对小鼠胃肠推进运动有显著加强作用。由研究结果得到提示：槟榔兴奋家兔十二指肠，此效应可能由胆碱能M受体介导，且涉及家兔十二指肠平滑肌细胞膜上对异搏定敏感的Ca^2 通道。槟榔煎剂能促进小鼠胃肠推进运动。     

“催乳保健Ⅱ号”对绵羊胃肠、子宫肌电活动作用的研究

采用浆膜表面埋植双极引导电极、多道电极同时记录法,测定“催乳保健Ｉ号”对绵羊皱胃、小肠、大肠、子宫、输卵管肌电活动的影响。结果表明：“催乳保健Ｉ号”对皱胃肌电活动的峰值、峰电频率和电活动时程均有明显的增强作用（Ｐ＜００１）;对空肠、回肠、结肠肌电活动的峰电频率和电活动时程也有明显的增强作用（Ｐ＜００１）,但对峰电峰值无明显影响（Ｐ＞００５）;而对十二指肠肌电活动的峰电峰值、峰电频率和电活动时程均有明显的抑制作用（Ｐ＜００１）;对盲肠肌电活动的峰电频率和电活动时程也有明显的抑制作用（Ｐ＜００１）,但对峰电峰值无明显影响（Ｐ＞００５）;对子宫体肌电活动的峰电峰值、峰电频率有明显抑制作用（Ｐ＜００１）,但对电活动时程有明显的增强作用（Ｐ＜００１）;对子宫角肌电活动的峰电峰值、峰电频率有明显增强作用,对电活动时程有明显抑制作用（Ｐ＜００１）;对输卵管肌电活动的峰电频率、电活动时程（Ｐ＜００１）和峰电峰值（Ｐ＜００５）均有明显增强的作用。“催乳保健Ｉ号”对胃肠肌电活动的兴奋作用与Ｍ受体有关,对子宫、输卵管肌电活动的兴奋作用与Ｍ受体无关。     

几种受体阻断剂对新疆细毛羊回盲结肠综合肌电的调控作用

绵羊回肠后部、盲肠和结肠初袢平滑肌的Ｍ受体，对综合肌电的峰电发生和增强起着调控主导作用。α抑制型受体起着与Ｍ受体相反的效应，Ｈ１受体对这些部位综合肌电的峰电活动也有较明显的增强作用，而β受体在以上部位平滑肌中分布的密度较小。     

五羟色胺、谷氨酸、组氨酸、脑啡肽在家兔离体十二指肠纵肌收缩中的作用

以家兔离体十二指肠纵肌方向的张力为指标，观察了五羟色胺（5－HT），谷氨酸（Glutamate)，组氨酸（Histidine)，脑啡肽（Leu-Enk)，对十二指肠的作用，实验表明，5－HT对十二指肠纵肌有明显的兴奋作用，5－HT可兴奋乙酰胆碱（Ach)能神经元，Ach又可抑制5－HT能神经元的活动；Glumatame对十二指肠纵肌的活动有明显的抑制作用。Histidine对十二指肠纵肌的作用与肠的机能状态有关；Leu-Enk对十二指肠纵肌活动有抑制作用，纳洛酮（Naloxone)可以阻断这种作用。     

枳实、青皮对平滑肌运动的影响

概述了枳实、青皮对平滑肌运动的影响及其作用机理的有关研究，枳实煎剂对胃肠、子宫平滑肌的作用及作用机理及平滑肌所处的机能状态有关；在体时呈兴奋作用，离体时呈抑制作用；枳实对胃肠平滑肌的兴奋作用是通过兴奋胆碱能途径及抑制神经纤维一氧化氮合成酶的活性实现的，其抑制作用是通过一氧化氮及肾上腺素能系统实现的，青皮煎剂影响胃肠、子宫、膀胱平滑肌的收缩活动，但因作用部位不同其作用及作用机理也不同，对胃平滑肌呈抑制作用，主要是由胆碱能M受体介导；对肠平滑肌（除回肠）呈抑制作用，主要是药物直接作用于平滑肌的结果；对子宫平滑肌、回肠纵行肌呈抑制作用，而对膀胱平滑肌却呈兴奋作用，上述效应均是通过肾上腺素能途径实现的。     

组织胺在兔十二指肠纵肌收缩中的作用及递质间的相互关系

以家兔离体十二指肠纵肌方向的张力为指标，观察了乙酰胆碱（Ａｃｈ）、去甲肾上腺素（ＮＥ）、组织胺（Ｈｉｓｔａｍｉｎｅ）对十二指肠的作用，探讨了组织胺对Ａｃｈ，ＮＥ的调制作用．实验表明，在正常情况下兔离体十二指肠收缩活动比较规律，并出现梭形波，纵肌的张力变化呈现周期性．Ａｃｈ对十二指肠的作用依其剂量的不同而不同．ＮＥ通过β抑制性受体对十二指肠产生抑制作用，而β兴奋性受体和α兴奋性受体介导兴奋．组织胺对十二指肠的作用与肠的机能状态有关，Ｈ１型受体介导兴奋．阈下剂量的组织胺可激活ＮＥ的α受体使ＮＥ表现为兴奋作用，对Ａｃｈ具有调制作用     

兔胃电活动的观察

目前,胃肠电活动的研究十分活跃。胃肠道激素的研究进展很快;但是,这些物质对胃肠电活动的影响研究者较少。这是今后消化道运动生理的重要课题。为此,我们用在胃窦部埋植电极的方法,观察记录兔的胃电活动和异博定等药物对胃电活动的影响,为探讨胃肠电活动的规律提供资料。     

兔回肠纵肌肾上腺素能爱体作用分析及递质间的相互作用

实验采用兔离休回肠纵肌标本，观察了经典递质去甲肾上腺素（ＮＥ．）和乙酰胆碱（ＡＣｈ．）对兔回肠纵肌收缩的效应及其相互关系，并对其作用的受体途径进行了分析．实验结果表明；（１）ＡＣｈ能加强回肠纵肌收缩，ＮＥ有抑制作用，但二者的作用可以变化；（２）酚妥拉明使收缩力量增加，心得安使其减弱；（３）ＮＥ能加强Ａｃｈ的兴奋作用，这一加强作用可放心得安阻断．ＡＣｈ对ＮＥ的抑制作用无明显影响．以上结果提示，兔回肠纵肌α肾上腺素能受体介导抑制，β受体介导兴奋，ＮＥ加强Ａｃｈ的兴奋效应与β受体密切相关．     

“催乳保健II号”对绵羊胃肠,子宫肌电活动作用的研究

采用浆膜表面埋植双极引导电极,多道电极同时记录法,测定“催乳保健ＩＩ号”对绵羊皱胃,小肠,大肠,子宫,输卵管肌电活动的影响,结果表明,“催乳保健ＩＩ号”对皱胃肌电活动的峰值,峰电频率和电活动时程均为有明显增强作用（Ｐ〈０．０１）,对空肠,回肠,结肠肌的电活动的峰电群频率和电活动时程也有明显的增强作用（Ｐ〈０．０１）,但对峰电峰值无明显影响（Ｐ〉０．０５）;而对十二指肠肌电活动的峰电峰值,峰电频率的     

Effect of electroacupuncture in Weijing points on gastrointestinal interdigestive migrating motor complex and brain gut peptides release in dogs

Interdigestive gastrointestinal migrating motor complex (MMC) activities were recorded by strain gauge implanted on the serosa in 7 conscious dogs. We studied the effects of electroacupuncture (EAP) Weijing points Zusanli (S36), Tianshu (S25), Liangmen (S21) on MMC and release of motilin and gastrin, and compared them with that of EAP Pangguangjing points. The results indicated that EAP Weijing points could not only strengthen MMC contractions in antrum, duodenum and proximal jejunum, but also increase plasma concentration of motilin and gastrin. Anti-motilin serum, proglumide, atropine, or hexamethonium could markedly block the effect of EAP on reinforcing MMC contraction and release of motilin and gastrin. We could get the conclusions that such enhancing effect of EAP Weijing points on MMC and brain-gut peptides release is mediated by motilin and gastrin, on which both cholinergic nerve and sympathetic nerve play important roles.     

去甲肾上腺素与内源性阿片肽在兔离体十二指肠电活动中的相互作用

实验采用银质双极电极,记录了家兔离体十二指肠综合肌电,并对去甲肾上腺素(NE)与内源性阿片肽在兔离体十二指肠电活动中的相互作用进行了观察.结果表明:NE 和吗啡对兔离体十二指肠综合肌电峰波簇均有抑制作用,NE 对基本节律无明显影响,而吗啡能使基本节律紊乱、峰电位幅度降低,其作用随剂量增加而变化.纳洛酮可减弱吗啡和 NE 的效应.     

Mice lacking the M3 muscarinic acetylcholine receptor are hypophagic and lean

Members of the muscarinic acetylcholine receptor family (M1-M5) have central roles in the regulation of many fundamental physiological functions. Identifying the specific receptor subtype(s) that mediate the diverse muscarinic actions of acetylcholine is of considerable therapeutic interest, but has proved difficult primarily because of a lack of subtype-selective ligands. Here we show that mice deficient in the M3 muscarinic receptor (M3R-/- mice) display a significant decrease in food intake, reduced body weight and peripheral fat deposits, and very low levels of serum leptin and insulin. Paradoxically, hypothalamic messenger RNA levels of melanin-concentrating hormone (MCH), which are normally upregulated in fasted animals leading to an increase in food intake, are significantly reduced in M3R-/- mice. Intra-cerebroventricular injection studies show that an agouti-related peptide analogue lacked orexigenic (appetite-stimulating) activity in M3R-/- mice. However, M3R-/- mice remained responsive to the orexigenic effects of MCH. Our data indicate that there may be a cholinergic pathway that involves M3-receptor-mediated facilitation of food intake at a site downstream of the hypothalamic leptin/melanocortin system and upstream of the MCH system.     

大鼠耳蜗血管纹胆碱能M受体的表达及意义

目的:研究胆碱能M受体在耳蜗血管纹的表达.方法:采用RT-PCR技术检测大鼠耳蜗血管纹上胆碱能M受体的基因表达.结果:扩增出标志M2、M3、M4和M5受体亚型基因表达的PCR产物,未扩增出标志M1受体亚型的产物.结论:胆碱能M2、M3、M4和M5受体亚型在耳蜗血管纹有表达,提示胆碱能M受体可能参与了血管纹功能的调节,为研究胆碱能M受体在血管纹上的功能提供分子生物学基础.     

Activation of specific interneurons improves V1 feature selectivity and visual perception

Inhibitory interneurons are essential components of the neural circuits underlying various brain functions. In the neocortex, a large diversity of GABA (γ-aminobutyric acid) interneurons has been identified on the basis of their morphology, molecular markers, biophysical properties and innervation pattern. However, how the activity of each subtype of interneurons contributes to sensory processing remains unclear. Here we show that optogenetic activation of parvalbumin-positive (PV+) interneurons in the mouse primary visual cortex (V1) sharpens neuronal feature selectivity and improves perceptual discrimination. Using multichannel recording with silicon probes and channelrhodopsin-2 (ChR2)-mediated optical activation, we found that increased spiking of PV+ interneurons markedly sharpened orientation tuning and enhanced direction selectivity of nearby neurons. These effects were caused by the activation of inhibitory neurons rather than a decreased spiking of excitatory neurons, as archaerhodopsin-3 (Arch)-mediated optical silencing of calcium/calmodulin-dependent protein kinase IIα (CAMKIIα)-positive excitatory neurons caused no significant change in V1 stimulus selectivity. Moreover, the improved selectivity specifically required PV+ neuron activation, as activating somatostatin or vasointestinal peptide interneurons had no significant effect. Notably, PV+ neuron activation in awake mice caused a significant improvement in their orientation discrimination, mirroring the sharpened V1 orientation tuning. Together, these results provide the first demonstration that visual coding and perception can be improved by increased spiking of a specific subtype of cortical inhibitory interneurons.     

Acetylcholine induces burst firing in thalamic reticular neurones by activating a potassium conductance

Recent studies have emphasized the role of acetylcholine (ACh) as an excitatory modulator of neuronal activity in mammalian cortex and hippocampus. Much less is known about the mechanism of direct cholinergic inhibition in the central nervous system or its role in regulating neuronal activities. Here we report that application of ACh to thalamic nucleus reticularis (nRt) neurones, which are known to receive a cholinergic input from the ascending reticular system of the brain stem, causes a hyperpolarization due to a relatively small (1-4 nS) increase in membrane conductance to K+. This cholinergic action appears to be mediated by the M2 subclass of muscarinic receptors and acts in conjunction with the intrinsic membrane properties of nucleus reticularis neurones to inhibit single spike activity while promoting the occurrence of burst discharges. Thus, cholinergic inhibitory mechanisms may be important in controlling the firing pattern of this important group of thalamic neurones.     

怀牛膝对未孕大鼠子宫平滑肌峰电活动的影响

在 Wistar未孕大鼠子宫角浆膜面上埋植一对 Ag- Ag Cl双极电极 ,腹腔注射不同剂量怀牛膝水煎剂后观察大鼠在体子宫平滑肌峰电活动的改变 .结果显示 :怀牛膝水煎剂显著增加未孕大鼠子宫肌电爆发波的最大振幅和峰面积 (P <0 .0 5 ) ,可延长爆发波持续时间和增加爆发波动作电位个数 (P <0 .0 5 ) ;怀牛膝水煎剂明显增大未孕大鼠子宫肌电单波的正波最大振幅、负波最大振幅和峰面积 (P <0 .0 5 ) .怀牛膝显著兴奋在体子宫平滑肌峰电活动的效应类似催产素 .     

Rapid BDNF-induced retrograde synaptic modification in a developing retinotectal system

In cultures of hippocampal neurons, induction of long-term synaptic potentiation or depression by repetitive synaptic activity is accompanied by a retrograde spread of potentiation or depression, respectively, from the site of induction at the axonal outputs to the input synapses on the dendrites of the presynaptic neuron. We report here that rapid retrograde synaptic modification also exists in an intact developing retinotectal system. Local application of brain-derived neurotrophic factor (BDNF) to the Xenopus laevis optic tectum, which induced persistent potentiation of retinotectal synapses, led to a rapid modification of synaptic inputs at the dendrites of retinal ganglion cells (RGCs), as shown by a persistent enhancement of light-evoked excitatory synaptic currents and spiking activity of RGCs. This retrograde effect required TrkB receptor activation, phospholipase Cgamma activity and Ca2+ elevation in RGCs, and was accounted for by a selective increase in the number of postsynaptic AMPA-subtype glutamate receptors at RGC dendrites. Such retrograde information flow in the neuron allows rapid regulation of synaptic inputs at the dendrite in accordance to signals received at axon terminals, a process reminiscent of back-propagation algorithm for learning in neural networks.     

Acetylcholine hyperpolarizes central neurones by acting on an M2 muscarinic receptor

Acetylcholine (ACh) is considered to act as a neurotransmitter in the mammalian brain by binding to membrane receptors and bringing about a change in neurone excitability. In the case of muscarinic receptors, cell excitability is usually increased; this effect results from a closure of membrane potassium channels in cortical cells. However, some central neurones are inhibited by ACh, and we hypothesized that these two opposite effects of ACh resulted from interactions with different subtypes of muscarinic receptor. We made intracellular recordings from neurones in the rat nucleus parabrachialis, a group of neurones in the upper pons some of which themselves synthesize ACh. ACh and muscarine caused a membrane hyperpolarization which resulted from an increase in the membrane conductance to potassium ions. The muscarinic receptor subtype was characterized by determining the dissociation equilibrium constant (KD) for pirenzepine during the intracellular recording; the value of approximately 600 nM indicates a receptor in the M2 class. This muscarinic receptor is quite different from that which brings about a decrease in potassium conductance in other neurones, which has a pirenzepine KD of approximately 10 nM (M1 receptors). It is possible that antagonists selective for this kind of M2 receptor would be useful in the management of conditions, such as Alzheimer's disease, which are associated with a reduced effectiveness of cholinergic neurones.