Mediation of responses to calcium in taste cells by modulation of a potassium conductance

Calcium salts are strong taste stimuli in vertebrate animals. However, the chemosensory transduction mechanisms for calcium are not known. In taste buds of Necturus maculosus (mud puppy), calcium evokes depolarizing receptor potentials by acting extracellularly on the apical ends of taste cells to block a resting potassium conductance. Therefore, divalent cations elicit receptor potentials in taste cells by modulating a potassium conductance rather than by permeating the cell membrane, the mechanism utilized by monovalent cations such as sodium and potassium ions.     

Taste receptor cells that discriminate between bitter stimuli

Recent studies showing that single taste bud cells express multiple bitter taste receptors have reignited a long-standing controversy over whether single gustatory receptor cells respond selectively or broadly to tastants. We examined calcium responses of rat taste receptor cells in situ to a panel of bitter compounds to determine whether individual cells distinguish between bitter stimuli. Most bitter-responsive taste cells were activated by only one out of five compounds tested. In taste cells that responded to multiple stimuli, there were no significant associations between any two stimuli. Bitter sensation does not appear to occur through the activation of a homogeneous population of broadly tuned bitter-sensitive taste cells. Instead, different bitter stimuli may activate different subpopulations of bitter-sensitive taste cells.     

A gustotopic map of taste qualities in the mammalian brain

The taste system is one of our fundamental senses, responsible for detecting and responding to sweet, bitter, umami, salty, and sour stimuli. In the tongue, the five basic tastes are mediated by separate classes of taste receptor cells each finely tuned to a single taste quality. We explored the logic of taste coding in the brain by examining how sweet, bitter, umami, and salty qualities are represented in the primary taste cortex of mice. We used in vivo two-photon calcium imaging to demonstrate topographic segregation in the functional architecture of the gustatory cortex. Each taste quality is represented in its own separate cortical field, revealing the existence of a gustotopic map in the brain. These results expose the basic logic for the central representation of taste.     

Genetic tracing shows segregation of taste neuronal circuitries for bitter and sweet

The recent discovery of mammalian bitter, sweet, and umami taste receptors indicates how the different taste qualities are encoded at the periphery. However, taste representations in the brain remain elusive. We used a genetic approach to visualize the neuronal circuitries of bitter and sweet tastes in mice to gain insight into how taste recognition is accomplished in the brain. By selectively expressing a transsynaptic tracer in either bitter- or sweet and/or umami-responsive taste receptor cells, and by comparing the locations of the tracer-labeled neurons in the brain, our data revealed the potential neuronal bases that underlie discrimination of bitter versus sweet.     

ATP signaling is crucial for communication from taste buds to gustatory nerves

Taste receptor cells detect chemicals in the oral cavity and transmit this information to taste nerves, but the neurotransmitter(s) have not been identified. We report that adenosine 5'-triphosphate (ATP) is the key neurotransmitter in this system. Genetic elimination of ionotropic purinergic receptors (P2X2 and P2X3) eliminates taste responses in the taste nerves, although the nerves remain responsive to touch, temperature, and menthol. Similarly, P2X-knockout mice show greatly reduced behavioral responses to sweeteners, glutamate, and bitter substances. Finally, stimulation of taste buds in vitro evokes release of ATP. Thus, ATP fulfils the criteria for a neurotransmitter linking taste buds to the nervous system.     

Endothelin stimulation of cytosolic calcium and gonadotropin secretion in anterior pituitary cells

The presence of endothelin, a vasoconstrictor peptide, in the hypothalamus and posterior pituitary suggests that it also regulates neural and other nonvascular target cells. In pituitary gonadotrophs, low doses of endothelin evoked oscillations in the intracellular calcium concentration, and high doses induced a biphasic calcium response. Mobilization of intracellular calcium predominated during the spike phase of the calcium response to endothelin, whereas calcium entry through dihydropyridine-sensitive channels contributed to both the spike and plateau phases of the calcium response. Endothelin was a potent as hypothalamic gonadotropin-releasing hormone (GnRH) in stimulation of gonadotropin release in perifused pituitary cells. Endothelin bound specifically to pituitary cells with a dissociation constant of 70 picomolar, and induced rapid formation of inositol trisphosphate and diacyglycerol. Although intracellular calcium concentration and gonadotropin secretory responses to endothelin were independent to the GnRH receptor, endothelin and GnRH appeared to have a common signal transduction mechanism. These observations suggest that endothelin can act as a neuropeptide to regulate anterior pituitary function.     

Sodium current-induced release of calcium from cardiac sarcoplasmic reticulum

The role of sodium-calcium exchange at the sarcolemma in the release of calcium from cardiac sarcoplasmic reticulum was investigated in voltage-clamped, isolated cardiac myocytes. In the absence of calcium entry through voltage-dependent calcium channels, membrane depolarization elicited release of calcium from ryanodine-sensitive internal stores. This process was dependent on sodium entry through tetrodotoxin-sensitive sodium channels. Calcium release under these conditions was also dependent on extracellular calcium concentration, suggesting a calcium-induced trigger release mechanism that involves calcium entry into the cell by sodium-calcium exchange. This sodium current-induced calcium release mechanism may explain, in part, the positive inotropic effects of cardiac glycosides and the negative inotropic effects of a variety of antiarrhythmic drugs that interact with cardiac sodium channels. In response to a transient rise of intracellular sodium, sodium-calcium exchange may promote calcium entry into cardiac cells and trigger sarcoplasmic calcium release during physiologic action potentials.     

Effect of membrane potential changes on the calcium transient in single rat cardiac muscle cells

The mechanism that links membrane potential changes to the release of calcium from internal stores to cause contraction of cardiac cells is unclear. By using the calcium indicator fura-2 under voltage-clamp conditions, changes in intracellular calcium could be monitored in single rat ventricular cells while controlling membrane potential. The voltage dependence of the depolarization-induced increase in intracellular calcium was not the same as that of the calcium current (Isi), which suggests that only a small fraction of Isi is required to trigger calcium release from the sarcoplasmic reticulum. In addition, sarcoplasmic reticulum calcium release may be partly regulated by membrane potential, since repolarization could terminate the rise in intracellular calcium. Thus, changes in the action potential will have immediate effects on the time course of the calcium transient beyond those associated with its effects on Isi.     

紫楠木材的构造特征

以四川紫楠(Phoebe sheareri)活立木为研究对象,通过观察紫楠木材宏观及微观构造,测定管孔、木纤维等结构的参数,分析木射线、轴向薄壁细胞、纹孔、结晶体等的构造特征,对紫楠木材的构造特征进行客观的分析和评价。结果表明:都江堰紫楠宏观上表现为边材呈淡灰色,心材淡褐色,心边材区分明显,味苦;微观上表现为散孔材,导管横切面多为卵圆形,薄壁细胞和射线细胞内含油细胞,射线组织为异形Ⅱ型或异形Ⅲ型,细胞内及细胞间隙含有大量球状树胶类物质,木射线细胞内存在块状含钙物质。     

游离氨基酸改善作物风味品质综述

从游离氨基酸对于植物源食品风味品质的影响着手,将氨基酸对食物味道/气味的贡献、调控氨基酸含量的手段等研究成果进行梳理,重点概述了影响氨基酸味道的因素,包括氨基酸味觉阈值、味觉成分间的协同/抑制作用等研究结果;对游离氨基酸合成气体成分的代谢过程进行了扼要总结;分析了养分调控手段、激素喷施、田间管理措施对植物体内游离氨基酸含量的影响。主要进展如下:施肥、套袋、嫁接等采前措施均可通过调控鲜味、甜味、苦味氨基酸含量及游离氨基酸总量,对作物风味品质产生影响。以上措施所引起的游离氨基酸含量变化的相关生理和分子机制仍需进一步深入研究。     

梅子苦味寡肽及氨基酸之萃取、分离与鉴定(英文)

先将梅子破碎、冷冻干燥后,以溶剂萃取肽,再将之浓缩,将萃取液经凝胶过滤分离肽后,以高效液相层析仪将各组分进一步分离得肽．由凝胶过滤分离出之肽,以官能品评找出具有苦味之部分,结果显示３个梅子品种在第１９～２８试管中具有苦味;经以高效液相层析仪分析,结果其肽含量与苦味之强弱呈正相关．由杏仁苷阈值试验得知梅子中所含有之杏仁苷尚未达到苦味阈值之要求,由此可证明其中具有其他苦味寡肽及游离氨基酸之存在     

Depolarization without calcium can release gamma-aminobutyric acid from a retinal neuron

Calcium influx is often an essential intermediate step for the release of neurotransmitter. However, some retinal neurons appear to release transmitter by a mechanism that does not require calcium influx. It was uncertain whether depolarization released calcium from an intracellular store or released transmitter by a mechanism that does not require calcium. The possibility that voltage, and not calcium, can regulate the release of transmitter was studied with pairs of solitary retinal neurons. Horizontal and bipolar cells were isolated from fish retinas and juxtaposed in culture. Communication between them was studied with electrophysiological methods. A horizontal cell released its neurotransmitter, gamma-aminobutyric acid, when depolarized during conditions that buffered the internal calcium concentration and prohibited calcium entry. The speed and amount of material released were sufficient for a contribution to synaptic transmission.     

Ca(2+)-induced Ca2+ release in sea urchin egg homogenates: modulation by cyclic ADP-ribose

Calcium-induced calcium release (CICR) may function widely in calcium-mediated cell signaling, but has been most thoroughly characterized in muscle cells. In a homogenate of sea urchin eggs, which display transients in the intracellular free calcium concentration ([Ca2+]i) during fertilization and anaphase, addition of Ca2+ triggered CICR. Ca2+ release was also induced by the CICR modulators ryanodine and caffeine. Responses to both Ca2+ and CICR modulators (but not Ca2+ release mediated by inositol 1,4,5-trisphosphate) were inhibited by procaine and ruthenium red, inhibitors of CICR. Intact eggs also displayed transients of [Ca2+]i when microinjected with ryanodine. Cyclic ADP-ribose, a metabolite with potent Ca(2+)-releasing properties, appears to act by way of the CICR mechanism and may thus be an endogenous modulator of CICR. A CICR mechanism is present in these nonmuscle cells as is assumed in various models of intracellular Ca2+ wave propagation.     

苦瓜营养成分分析及利用评价

通过对不同苦瓜品种营养成分的测定,了解到苦瓜中含有大量的维生素Ｃ、粗蛋白和可溶性糖,同时有益人体健康的钙、镁、铁等微量元素的含量远远超过了番茄、茄子、辣椒等蔬菜,研究结果表明,苦瓜是一种营养价值高的保健蔬菜。     

影响Ca2+代谢和钙通道的药物对小麦受叶锈菌侵染后诱发的HR的作用

为进一步探讨小麦抵抗叶锈菌侵染的防卫反应的信号转导机制,利用小麦品种洛夫林10和不同叶锈菌生理小种组成亲和与不亲和组合,研究影响Ca2+代谢和钙通道的药物对小麦受叶锈菌侵染后诱发的HR的作用。结果表明:在接种前给小麦叶片分别预注射Ca2+螯合剂(EGTA)和Ca2+通道抑制剂(LaCl3和Verapamil),均可使寄主叶片发生过敏性反应(HR)的面积明显减少,并且随着注射药物浓度的增高,寄主细胞发生HR的面积逐渐减小;在只注射Ca2+释放剂(A23187)而不接种的试验中,寄主细胞也发生HR,且HR面积随A23187浓度增加而有所增加,但并不成正比。证明胞内Ca2+浓度升高可能是诱发小麦叶片发生HR所必需的,Ca2+在小麦抵抗叶锈菌侵染的信号传导途径中可能发挥重要作用。     

Phosphate release and force generation in skeletal muscle fibers

Rapid laser pulse-induced photolysis of an adenosine triphosphate precursor in muscle fibers abruptly initiated cycling of the cross-bridges. The accompanying changes in tension and stiffness were related to elementary mechanochemical events of the energy-transducing mechanism. When inorganic phosphate was present at millimolar concentrations during liberation of adenosine triphosphate in the absence of calcium, relaxation was accelerated. Steady active tension in the presence of calcium was decreased but the approach to final tension was more rapid. These results suggest that, during energy transduction, formation of the dominant force-generating cross-bridge state is coupled to release of inorganic phosphate in a reaction that is readily reversible.     

Synaptic plasticity in spinal lamina I projection neurons that mediate hyperalgesia

Inflammation, trauma, or nerve injury may cause enduring hyperalgesia, an enhanced sensitivity to painful stimuli. Neurons in lamina I of the spinal dorsal horn that express the neurokinin 1 receptor for substance P mediate this abnormal pain sensitivity by an unknown cellular mechanism. We report that in these, but not in other nociceptive lamina I cells, neurokinin 1 receptor-activated signal transduction pathways and activation of low-threshold (T-type) voltage-gated calcium channels synergistically facilitate activity- and calcium-dependent long-term potentiation at synapses from nociceptive nerve fibers. Thereby, memory traces of painful events are retained.     

Chemotransduction in the carotid body: K+ current modulated by PO2 in type I chemoreceptor cells

The ionic currents of carotid body type I cells and their possible involvement in the detection of oxygen tension (Po2) in arterial blood are unknown. The electrical properties of these cells were studied with the whole-cell patch clamp technique, and the hypothesis that ionic conductances can be altered by changes in PO2 was tested. The results show that type I cells have voltage-dependent sodium, calcium, and potassium channels. Sodium and calcium currents were unaffected by a decrease in PO2 from 150 to 10 millimeters of mercury, whereas, with the same experimental protocol, potassium currents were reversibly reduced by 25 to 50 percent. The effect of hypoxia was independent of internal adenosine triphosphate and calcium. Thus, ionic conductances, and particularly the O2-sensitive potassium current, play a key role in the transduction mechanism of arterial chemoreceptors.     

Regulation of calcium release is gated by calcium current, not gating charge, in cardiac myocytes

In skeletal muscle, intramembrane charge movement initiates the processes that lead to the release of calcium from the sarcoplasmic reticulum. In cardiac muscle, in contrast, the similarity of the voltage dependence of developed tension and intracellular calcium transients to that of calcium current suggests that the calcium current may gate the release of calcium. Nevertheless, a mechanism similar to that of skeletal muscle continues to be postulated for cardiac muscle. By using rapid exchange (20 to 50 milliseconds) of the extracellular solutions in rat ventricular myocytes in which the intracellular calcium transients or cell shortening were measured, it has now been shown that the influx of calcium through the calcium channel is a mandatory link in the processes that couple membrane depolarization to the release of calcium. Thus, intramembrane charge movement does not contribute to the release of calcium in heart muscle.     

Intracellular calcium release mediated by sphingosine derivatives generated in cells

Soluble and hydrophobic lipid breakdown products have a variety of important signaling roles in cells. Here sphingoid bases derived in cells from sphingolipid breakdown are shown to have a potent and direct effect in mediating calcium release from intracellular stores. Sphingosine must be enzymically converted within the cell to a product believed to be sphingosine-1-phosphate, which thereafter effects calcium release from a pool including the inositol 1,4,5-trisphosphate-sensitive calcium pool. The sensitivity, molecular specificity, and reversibility of the effect on calcium movements closely parallel sphingoid base-mediated inhibition of protein kinase C. Generation of sphingoid bases in cells may activate a dual signaling pathway involving regulation of calcium and protein kinase C, comparable perhaps to the phosphatidylinositol and calcium signaling pathway.