K~+ Channels and Their Effects on Membrane Potential in Rat Bronchial Smooth Muscle Cells

In order to investigate the K~+ channels and their effects on resting membrane potential(Em) and excitability in rat bronchial smooth muscle cells (BSMCs), the components of outward K~+channel currents and the effects of K~+ channels on Em and tension in rat bronchial smooth musclewere observed by using standard whole-cell recording of patch clamp and isometric tension recordingtechniques. The results showed that under resting conditions, total outward K~+ channel currents infreshly isolated BSMCs were unaffected by ATP-sensitive K~+ channel blocker. There were two typesof K~+ currents: voltage-dependent delayed rectifier K~+ channel (Kv) and large conductance calcium-activated K~+ channel (BK_(Ca)) currents. 1 mmol/L 4-aminopyridine (4-AP, an inhibitor of Kv)caused a significant depolarization (from — 8.7±5.9mV to —25.4±3.1mV, n=18, P<0.001).In contrast, 1 mmol/L tetraethylammonium (TEA, an inhibitor of BK_(Ca)) had no significant effect onEm (from —37.6±4.8 mV to —36.8±4.1 mV, n=12, P>0.05). 4     

心房颤动犬心房肌细胞2型理阿诺受体的分布和表达

目的探讨心房颤动(房颤)时心房肌细胞2型理阿诺受体表达和分布的改变。方法杂种犬10只,分为正常对照组和单纯房颤组,每组5只。单纯房颤组用起搏器进行房颤式快速起搏,起搏频率(500±20)次/min,正常对照组不植入起搏器。24周后取出心脏,用逆转录聚合酶链反应、免疫荧光染色技术检测犬心房肌细胞2型理阿诺受体在mRNA水平的表达和蛋白水平的表达和分布。结果与正常对照组比较,单纯房颤组犬2型理阿诺受体在mRNA和蛋白水平的表达明显低于正常对照组(P<0.05);在细胞质、细胞膜2型理阿诺受体分布均显著减少。结论房颤时心房肌细胞2型理阿诺受体表达下调,2型理阿诺受体可能不是心房肌细胞主要的钙信号调控的受体。     

Suppression of alcohol and saccharin preference in rats by a novel Ca2+ channel inhibitor,Goe 5438

The effect of the novel 1,4-dihydronaphthyridine Ca²⁺ channel inhibitor Goe 5438 (CI-951) on voluntary ethanol consumption was examined in selectively bred alcohol-preferring (P) rats in a free choice two bottle preference test versus water. Intraperitoneally injected Goe 5438 dose-dependently (5, 10 or 20 µmol/kg, twice daily) inhibited ethanol and increased water intake over the 24 h period (injection day). The drug decreased ethanol preference, originally above 90%, by 6%, 19% and 45% at respective doses, on the injection day. That inhibitory effect of the highest dose of Goe 5438 on ethanol preference remained significant also on days 2 and 3 after injections (–51% and –18%, respectively). Goe 5438, in the highest dose, also tended to decrease granulated chow consumption during the injection day only. To further test whether the inhibition of ethanol preference is secondary to decrease in reinforcing properties of ethanol and not due to interference with satiety mechanisms, we compared the effect of two higher doses (10 and 20 µmol/kg, intraperitoneally, twice daily) of Goe 5438 on spontaneous preference for a non-caloric 0.04% saccharin solution in Sprague-Dawley rats. We observed a dose-dependent suppression of preference (by 44% and 58%, respectively) during the injection day, but not the subsequent 24 h period. However, Goe 5438 also significantly alleviated food pellet intake on the injection day. In conclusion, Goe 5438 produces potent and long-lasting inhibition of voluntary ethanol consumption, which may be secondary to attenuation of reinforcing properties of ethanol. Additionally, this particular Ca²⁺ channel inhibitor appears to have mild anorectic properties which may be conducive to acute suppression of alcohol intake.     

Sodium channels accumulate at the tips of injured axons

The axolemmal distribution of voltage-gated sodium channels largely determines the regions of axonal electrical excitability. Using a wellcharacterized anti–sodium channel antibody, we examined peripheral nerve fibers focally injured by exposure to the neurotoxic agent, potassium tellurite (K₂TeO₃). Immunocytochemical and radioimmunoassay data showed a focal accumulation of sodium channels within the tips of injured axons. The major increase in sodium channel concentration occurred between 7 and 11 days after toxin exposure; however, immunocytochemically, excess sodium channels persisted in several axonal endings for a much longer time. The accumulation of sodium channels at injured axonal tips may be responsible, in part, for ectopic axonal excitability and the resulting abnormal sensory phenomena (especially pain and paresthesias) which frequently complicate peripheral nerve injury in humans. © 1994 John Wiley & Sons, Inc.     

Impact response of periodontal tissues

A new impact response method using a fracture of a pencil-lead to produce an excitation pulse is proposed. Impact excitations (rectangular pulse, triangular pulse and half-sine pulse) are strictly given in physical and mathematical definitions and complete solutions to the impact excitations are provided for Noyes' model of the human tooth. When a relatively long triangular pulse is applied to Noyes' model, which can express the physical characteristic of periodontal tissues, a sinusoidal damped vibration of a single degree-of-freedom model is approximately obtained. The acceleration response is characterised by the physical parameters (T, δ and A_o) and mechanical elements (m₁, c₁ and k) of which a single degree-of-freedom model is composed. By means of this method, the values of the parameters and elements in the cases of healthy maxillary, healthy mandibular and pathological mandibular incisors are obtained. The single degree-of-freedom model can express the high-frequency spectra of Noyes' model. The pathological tooth is characterised by a longer damped time constant and a larger acceleration maximum. This impact response method can effectively be applied to clinical diagnosis in view of the physical parameters and mechanical elements which have been derived.     

MRI and SPECT findings in amyotrophic lateral sclerosis

Summary MRI was performed in 21 patients and single photon emission computed tomography (SPECT) withN-isopropyl-p-¹²³I iodoamphetamine in 16 patients, to visualize upper motor neurone lesions in amyotrophic lateral sclerosis. T2-weighted MRI revealed high signal along the course of the pyramidal tract in the internal capsule and cerebral peduncle in 4 of 21 patients. SPECT images were normal in 4 patients, but uptake was reduced in the cerebral cortex that includes the motor area in 11.     

钙池操纵的Ca2+通道的激活机制研究进展

钙池操纵的Ca~(2 )通道(store-operated Ca~(2 ) channels,SOC)是非兴奋细胞Ca~(2 )内流的主要通道之一,参与多种病理和生理过程,在钙信号通路的研究中,SOC的激活机制一直是人们关注的焦点之一,迄今为止,钙内流因子模型(Ca~(2 ) innux factor model,CIF model)和构象耦联模型fconformational coupling model)受到广泛关注.部分学者已经从很多不同类型的细胞中提取出CIF,并证实钙非依赖性的磷脂酶A_2(Ca~(2 )-independent phospholipase A_2,iPLA_2)作为CIF的底物,在某些类型细胞的SOC激活过程中发挥重要作用,并进一步提出了ER- CIF-iPLA_2-CaM-LysoPLs-SOC通路模型.瞬时受体电位(transient receptor potential,TRP)通道蛋白与1.4,5-磷酸肌醇受体(inositol 1,4,5 trisphosphate receptor,IP_3R)的结构连接作为构象耦联模型的基础已被广泛证实,随着对IP_3R,Ryanodine受体、肌动蛋白等在钙信号通路中所发挥作用的深入研究,构象耦联模型将得到不断补充和完善.SOC激活机制的破解,将对进一步完善非兴奋细胞的钙通道特性及其调节机制理论带来重大突破.     

钾离子通道的活性状态对蛛网膜下腔注射腺苷抗伤害性作用的影响

目的探讨ATP敏感型钾离子通道的活性状态对鞘内注射腺苷类似物R-phenylisopropyladenosine(R-PIA)抗伤害性作用的影响.方法雄性SD大鼠在苯巴比妥钠麻醉下,蛛网膜下腔留置PE-10导管,测定注药后鼠尾对光热刺激的反应(抗伤害作用).结果蛛网膜下腔注射R-PIA产生剂量依赖性的甩尾时间曲线上移(P＜0.05).蛛网膜下腔注药后10min起效,镇痛时间长达60min.ATP敏感型通道开放剂nicorandil和阻滞剂glibenclamide单独蛛网膜下腔应用无镇痛作用(P＞0.05),但nicorandil明显增强R-PIA的抗伤害性作用,相反glibenclamide明显减弱R-PIA的抗伤害性作用(P＜0.05).结论蛛网膜下腔注射R-PIA可产生明显的剂量依赖性抗伤害作用,此作用受ATP敏感型钾离子通道活性调节.     

Fatal encephalitis in a patient with refractory celiac disease presenting with myorhythmia and carpal spasm.

We report the case of a woman with refractory celiac disease who developed abnormal spontaneous movements of the extremities and face consistent with myorhythmia. Investigation led to a diagnosis of encephalitis, confirmed by postmortem examination. The movements were likely caused by nonparaneoplastic encephalitis associated with refractory celiac disease. Etiologic and diagnostic considerations and treatment options are discussed.     

小鼠背根神经节中三个不同的钙激活氯离子通道基因家族的表达(英文)

目的在背根神经节(dorsal root ganglion,DRG)中等大小感觉神经元中可以观察到钙激活氯离子流(I_(Cl(Ca)))。在坐骨神经损伤模型中,在大多数大中神经元上诱导出类似的氯离子流。本文旨在探讨引起这个离子流的分子基础。方法使用常规的定量RT-PCR方法检测在DRG中三个基因家族的表达,这三个基因家族都具有诱导I_(Cl(Ca))的特点。结果在成年小鼠的DRG中,分别显示了在正常状态和坐骨神经损伤3天后CLCA,Bestrophin和Tweety基因家族成员的转录产物。结论mBestl和Tweety2可能在损伤诱导的DRG神经元I_(Cl(Ca))中发挥作用。