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81.
Chronic Nicotine Administration Differentially Affects Neurotransmitter Release from Rat Striatal Slices 总被引:6,自引:3,他引:3
Abstract: The objective of these experiments was to determine whether the chronic administration of nicotine, at a dose regimen that increases the density of nicotine binding sites, alters the nicotine-induced release of [3H]dopamine ([3H]DA), [3H]norepinephrine ([3H]NE), [3H]serotonin ([3H]5-HT), or [3H]acetylcholine ([3H]ACh) from rat striatal slices. For these experiments, rats received subcutaneous injections of either saline or nicotine bitartrate [1.76 mg (3.6 µmol)/kg, dissolved in saline] twice daily for 10 days, and neurotransmitter release was measured following preloading of the tissues with [3H]DA, [3H]NE, [3H]5-HT, or [3H]choline. Chronic nicotine administration did not affect the accumulation of tritium by striatal slices, the basal release of radioactivity, or the 25 mM KCl-evoked release of neurotransmitter. Superfusion of striatal slices with 1, 10, and 100 µM nicotine increased [3H]DA release in a concentration-dependent manner, and release from slices from nicotine-injected animals was significantly (p < 0.05) greater than release from saline-injected controls; release from the former increased to 132, 191, and 172% of release from the controls following superfusion with 1, 10, and 100 µM nicotine, respectively. Similarly, [3H]5-HT release increased in a concentration-related manner following superfusion with nicotine, and release from slices from nicotine-injected rats was significantly (p < 0.05) greater than that from controls. [3H]5-HT release from slices from nicotine-injected rats evoked by superfusion with 1 and 10 µM nicotine increased to 453 and 217%, respectively, of release from slices from saline-injected animals. The nicotine-induced release of [3H]NE from striatal slices was also concentration dependent but was unaffected by chronic nicotine administration. [3H]ACh release from striatal slices could not be detected when samples were superfused with nicotine but was measurable when tissues were incubated with nicotine. The release of [3H]ACh from slices from nicotine-injected rats was significantly (p < 0.05) less than release from controls and decreased to 36, 83, and 77% of control values following incubation with 1, 10, or 100 µM nicotine, respectively. This decreased [3H]ACh release could not be attributed to methodological differences because slices from nicotine-injected rats incubated with nicotine exhibited an increased [3H]DA release, similar to results from superfusion studies. In addition, it is unlikely that the decreased release of [3H]ACh from striatal slices from nicotine-injected rats was secondary to increased DA release because [3H]ACh release from slices from hippocampus, which is not tonically inhibited by DA, also decreased significantly (p < 0.05) in response to nicotine; hippocampal slices from nicotine-injected rats incubated with 1 and 10 µM nicotine decreased to 42 and 70%, respectively, of release from slices from saline-injected animals. Results indicate that the chronic administration of nicotine increases the ability of nicotine to induce the release of [3H]DA and [3H]5-HT and decreases the ability of nicotine to evoke the release of [3H]ACh but does not alter the nicotine-induced release of [3H]NE from brain slices. 相似文献
82.
人工饲养的蒙新河猪其动情周期可划分为4个阶段:动情前期、动情期(发情交配期)、动情后期和停滞期(动情间隔期)。动情期间雌雄河狸均表现出活跃好动,浮躁不安,食量减小;发情交配期雌雄河狸均发出低沉嘶哑的叫声,雄性叫声频率比性略高,爬跨交配是动情期发情的高峰,动情周期各阶段的行为特征,在雌性与阴道涂片细胞学及外生殖器形态、色泽、阴道分泌物周期性变化特征相吻合,在雄性则与睾丸及阴茎形态特征吻合,在人工饲养 相似文献
83.
芦苇耐盐变异植株及其细胞学鉴定 总被引:5,自引:0,他引:5
用甲基磺酸乙酯(EMS)处理芦苇(Phragm itescom m unis Trin.)胚性愈伤组织。从处理后的愈伤组织诱导获得芦苇耐盐变异植株R5002-12。变异植株能在含有1% NaCl的MS培养基上生长。细胞学检查变异植株是混倍体,染色体数目变异范围在100至33 之间。分蘖植株具有相似的形态学及染色体变异特性 相似文献
84.
85.
The interfering effects of copper, zinc, and cobalt on the uptake of mugineic acid-ferric complex were studied in barley ( Hordeum vulgare , cv. Minorimugi) grown in nutrient solution. Short-term uptake experiments of 3 h were performed utilizing both ionic and mugineic acid-complex forms of each metal at two different concentrations. Copper was most effective in decreasing iron uptake when added in an ionic form at either concentration. The inhibition order at higher concentrations followed Cu(II) > Zn(II) ≥ Co(II), Co(III), which is consistent with the stability constants of these metal complexes with mugineic acid. The displacement of iron from its mugineic acid complex by these metals is suggested as a probable explanation for the decreased iron uptake. The inhibitory effect of metal complexes with mugineic acid on iron uptake was only found in cases with higher concentrations of Cu(II) and Zn(II) complexes. Deformation of the specific iron transport system in the plasma membrane due to their adsorption may be responsible for this effect. 相似文献
86.
Summary A DNA segment carrying the full-length, intronless firefly luciferase gene was inserted into the high expression secretion vector, pIN-III -ompA. Upon induction of gene expression, luciferase activity was detected in extracts prepared from periplasmic fractions. The results indicated that the OmpA signal peptide was able to direct secretion of firefly luciferase across the cytoplasmic membrane. This has important implications for using this luciferase as a reporter in studying protein export and targeting. 相似文献
87.
88.
Jian Wang C. Bruce Verchere Christopher H. S. McIntosh John C. Brown 《Cell communication & adhesion》1994,1(4):343-353
The intracellular free Ca2+ ion concentration ([Ca2+]i) was measured using fura-2 microspec-trofluorimetry in individual rat pancreatic β-cells prepared by enzymatic digestion and fluorescence-activated cell sorting. The mean basal concentration of [Ca2+]i in β-cells in the presence of 4.4 mM glucose and 1.8 mM Ca2+ was 112±1.6 nM (n=207). The action of acetylcholine (ACh) was concentration-dependent, and raising the concentration resulted in [Ca2+]i spikes of increasing amplitude and duration in some, but not all of the β-cells. In addition, the β-cells demonstrated variable sensitivity to ACh. The increases in [Ca2+]i were rapid, transient and were blocked by atropine at 10-6M. A brief exposure to 50 mM K+ resulted in a transient increase in [Ca2+]i similar to that induced by ACh, but resistant to atropine. A high concentration of ACh (100μL 10-4M or 10-3M) induced [Ca2+]i oscillations in 11 out of 57 β-cells in the presence of 4.4 mM glucose. Using calcium channel blockers and Ca2+ free medium, the source of the increase in [Ca2+]i was deduced to be from extracellular spaces. Changing the temperature from 22 to 37°C did not affect the action of ACh on [Ca2+]i. These data strongly suggest that ACh exerted a direct action on [Ca2+]i in normal rat pancreatic β-cells and support a role for Ca2+ as a second messenger in the action of ACh. 相似文献
89.
Since cytoplasmic Ca2+ levels are reported to regulate neurite elongation, we tested whether calcium-activated kinases might be necessary for growth cone motility and neurite elongation in explant cultures of goldfish retina. Kinase inhibitors and activators were locally applied by micropipette to retinal growth cones and the responses were observed via phase-contrast videomicroscopy. In some cases, growth rates were also quantifed over several hours after general application in the medium. The selective inhibitors of protein kinase C, calphostin C (0.1–1 μM) and chelerythrin (up to 50 μM), caused no obvious changes in growth cones or neurite elongation, and activators of PKC (phorbols, arachidonic acid, and diacylglycerol) also were generally without effects, although phorbols slowed the growth rate. Inhibitors of protein kinase A and tyrosine kinases also produced no obvious effects. The calmodulin antagonists, calmidazolium (0.1 μM), trifluoperazine (100 μM), and CGS9343B (50 μM), however, caused a reversible growth cone arrest with loss of filopodia and lamellipodia. The growth cone became a club-shaped swelling which sometimes moved a short distance back the shaft, leaving evacuated filaments at points of strong filopodial attachments. A similar reversible growth cone arrest occurred with the general kinase inhibitors: H7 at 200 but not at 100 μM, and staurosporine at 100 but not 10 nM, suggesting possible involvement of a calmodulin-dependent kinase (camK) rather than PKC. The selective inhibitor of camKII, KN-62 (tested up to 50 μM), produced no effects but the specific myosin light-chain kinase (MLCK) inhibitors ML-7 (3–5 μM) and ML-9 (5–10 μM) reversibly reproduced the effect, suggesting that MLCK rather than camKII is necessary for growth cone motility. The MLCK inhibitors' effects both on growth cone morphology and on F-actin filaments (rhodamine-phalloidin staining) were similar to those caused by cytochalasin D (5 μM), and are discussed in light of findings that inhibiting MLCK disrupts actin filaments in astrocytes and fibroblasts. 1994 John Wiley & Sons, Inc. 相似文献
90.
RGDS肽对大鼠主动脉球囊内膜剥脱后血管壁增殖的影响 总被引:1,自引:0,他引:1
在大鼠主动脉球囊内膜剥脱术后血管壁细胞过度增殖模型上,用合成的血小板膜纤维蛋白原受体(glycoproteinⅡb/Ⅲacomplex,GPⅡb/Ⅲa)拮抗剂RGDS(Arg-Gly-Asp-Ser,50μmol·kg-1·d-1)治疗可有效地抑制损伤血管壁的细胞计数增加和内膜增厚以及血管平滑肌细胞增殖,显著降低其血管组织3H-TdR和3H-Leu的参入增加程度。实验结果提示RGDS肽作为血管成型术的辅佐剂,对于防治血管再狭窄可能具有潜在的临床应用前景。 相似文献