China
Africa
Explore chapters and articles related to this topic
Calcium Metabolism in Enzymatically Dissociated Rat Heart Cells and in Intact Perfused Ferret Hearts
Published in Samuel Sideman, Rafael Beyar, Analysis and Simulation of the Cardiac System — Ischemia, 2020
Eduardo Marban, Shawn W. Robinson, W. Gil Wier, Masafumi Kitakaze, Martin M. Pike, David T. Yue, V. P. Chacko
Two technical problems that you have undoubtedly thought about deeply: first, how do you calculate the buffering in view of the multitudinous calcium sites in addition to your BAPTA? The buffering calculation is anything but simple, even in a free buffer. Second, you alluded to the slowness of the release of calcium from the BAPTA. How does that influence your calculations of the buffering capacity and the exchanges that occur during ischemia during each beat?
Cellular and Molecular Imaging of the Diabetic Pancreas
Published in Michel M. J. Modo, Jeff W. M. Bulte, Molecular and Cellular MR Imaging, 2007
One of the most interesting approaches utilizes Ca2+ metabolism by the beta-cell as a tool to deliver MR contrast agent. The influx of Ca2+ into beta-cells precedes insulin secretion. Therefore, surrogate paramagnetic ions can be used as Ca2+ mimics. One such candidate is Mn2+. Mn2+ accumulates in beta-cells in proportion to the glucose concentration presented to the cells, presumably via Ca2+ channels. Images collected of isolated pancreatic islets in the presence of an ultrahigh concentration of MnCl2 (25 mM) at two different glucose concentrations (5 and 20 mM) showed that a clear contrast enhancement is obtained when the stimulatory levels of glucose are higher (Figure 19.1;45 reviewed in Woods et al.41). Another method utilizes conformational changes in the chelates. This method was used to design a Ca2+-sensitive MR agent. This agent uses a heptadentate DO3A substructure to chelate Gd3+, thereby leaving two coordination sites vacant for ligation by water. Two of these units were attached to a 1,2-bis(o-aminophenoxy)ethane-N,N,N’,N’-tetraacetic acid (BAPTA) derivative via propyloxy linkers to allow the carboxylates of the BAPTA to coordinate the vacant sites on Gd3+.41 In the absence of Ca2+, the carboxylates of the central BAPTA unit bind to the water sites on the two appended GdDO3A moieties, thereby excluding water molecules from each Gd3+ center. Upon exposure to Ca2+, these same carboxylates are required to bind Ca2+ into the central BOPTA moiety and are released from each GdDO3A unit, thereby exposing Gd3+ to water and facilitating inner-sphere relaxation (Figure 19.2). Ca2+ binding to GdDOPTA occurs in the micromolar range and gives rise to an increase in relaxivity from 3.26 to 5.76 mM−1sec−1 (500 MHz, 25°C), an enhancement of some 80%.41 This agent has been proposed as a natural sensor of Ca2+ metabolism and, indirectly, insulin secretion and beta-cell mass and function. An analogous strategy was applied for the design of a Zn2+-sensitive T1 agent.41,46 In view of the role that Ca2+ and Zn2+ play in glucose responsiveness and insulin secretion, the development of contrast agents sensitive to the concentration of these ions would provide invaluable information about the metabolic and functional competence of beta-cells.
Advances in Understanding the Mechanisms Underlying Synaptic Plasticity
Published in Avital Schurr, Benjamin M. Rigor, BRAIN SLICES in BASIC and CLINICAL RESEARCH, 2020
Timothy J. Teyler, Idil Cavus, Chris Coussens, Pascal DiScenna, Lawrence Grover, Yi-Ping Lee, Zeb Little
It was originally believed that NMDA receptor activation is essential for LTP induction at synapses formed by Schaffer collaterals and commissural fibers in area CA1 of the hippocampus. It has been known that LTP induction at mossy fiber synapses in area CA3 of the hippocampus is independent of NMDA receptors.16 In 1990, we demonstrated that LTP of Schaffer collateral/commissural synapses in area CA1 of the hippocampus can also be induced through a non-NMDAr mechanism by high-frequency (200 Hz), but not low-frequency (25 Hz) tetanic stimulation.17 Induction of non-NMDA LTP is inhibited by nifedipine, a blocker of L-type voltage-dependent calcium channels (VDCCs). It is now evident that non-NMDA LTP is not limited to CA1 hippocampus, but that LTP induction in other regions of the central nervous system may occur through both NMDAr and non-NMDAr mechanisms.1,18–25 It is not known if Ca2+ entry through VDCCs mediates all of these instances of non-NMDA LTP. An important alternative source of Ca2+ is via activation of metabotropic glutamate receptors (mGLUrs), which in turn enhances the production of inositol triphosphate (IP3) to release Ca2+ from intracellular endoplasmic reticulum stores (as well as stimulate PKC). It has been proposed that mGLUrs are necessary for NMDA LTP in area CA1.26,27 Seen in isolation when the NMDAr is blocked by the specific antagonist APV and the appropriate tetanus conditions are present, non-NMDA LTP is Ca2+ dependent, is expressed more slowly than NMDA LTP, requires higher frequency tetanic stimulation for its expression, and possesses different onset and decay kinetics than NMDA LTP (Figure 2). Its Ca2+ dependency has been demonstrated by the blocking effect of the intracellular injection of 1,2-bis(2-aminophenoxy)ethane-N,N,N’,N’,-tetraacetic acid (BAPTA).17 The mechanisms underlying non-NMDA LTP are presently unknown, but may include some of the same mechanisms suggested to underlie NMDA LTP. Under the appropriate tetanus conditions, both NMDA LTP and non-NMDA LTP can be simultaneously elicited from the same population of cells.28 Both forms of LTP share several common features: Both are Ca2+ -dependent.Both rely upon voltage-dependent processes to mediate postsynaptic Ca2+ influx.Both result in increases in the magnitude of the postsynaptic EPSP and population spike.Both can be elicited by tetanic activation of afferents.Both are input specific.
Trafficking of carbonic anhydrase 12 and bicarbonate transporters by histamine stimulation mediates intracellular acidic scenario in lung cancer cells
Published in Journal of Enzyme Inhibition and Medicinal Chemistry, 2023
Hyeong jae Kim, Jeong Hee Hong
CBE activity is also modulated by the involvement of CA12 through protein interaction and supply of bicarbonate source14,26. Thus, we verified whether histamine-modulated CA12 attenuated CBE activity. Histamine receptor activation enhanced CBE activity in both normal and cancer cell lines (Figure 3(A–D)). The histamine receptor activation-mediated enhanced CBE activities were not mediated by CA12 localisation in both cells. We found that the basal CBE activity of A549 cells was higher than that of Beas-2B cells (Figure 3(E)). It has been known that CBE activity is dependent on an increase in the intracellular calcium concentration27. Thus, A549 cells were treated with BAPTA-AM and BAPTA to chelate free calcium in both the cytosolic and extracellular media. Treatment of BAPTAs reduced histamine receptor activation-mediated CBE activity in A549 cells (Figure 3(F,G)). These results address that histamine treatment enhanced CBE activity with involvement of an increase in intracellular calcium concentration.
Cellular Calcium Signals in Cancer Chemoprevention and Chemotherapy by Phytochemicals
Published in Nutrition and Cancer, 2022
Xue Li, Shuhan Miao, Feng Li, Fen Ye, Guang Yue, Rongzhu Lu, Haijun Shen, Yang Ye
Kalanchoe tubifora is extensively used in the treatment of coughs, fever and abscesses and exhibits anti-inflammatory, anti-microbial and cytotoxic activities. Kalantuboside B (KB) is a natural bufadienolide bioactive obtained from K. tubiflora (120) that has many pharmacological effects, such as cardioactive property and anti-inflammatory and anti-tumor activities. Hseu et al. used BAPTA-AM to investigate the relationship between KB-induced apoptosis and the Ca2+-dependent pathway. The authors found that KB enhanced the cytoplasmic Ca2+ levels and decreased the expression of the downstream p53 tumor suppressor and autophagy-related protein. Furthermore, pretreatment of BAPTA-AM decreased the cell viability (10%) in A2058 cells exposed to KB (121). These results suggested that KB may induce cancer cell death through increasing the levels of cytoplasmic Ca2+.
Loss of mGluR1-LTD following cocaine exposure accumulates Ca2+-permeable AMPA receptors and facilitates synaptic potentiation in the prefrontal cortex
Published in Journal of Neurogenetics, 2021
L5 pyramidal neurons were visually identified with differential interference contrast (DIC) microscopy. Glass electrodes (5–8 MΩ) were pulled with a P-87 micropipette puller (Sutter Instrument). For current clamping, electrodes were filled with (in mM) 130 K-gluconate, 8 NaCl, 10 HEPES, 0.4 EGTA, 2 Mg-ATP, and 0.25 GTP-Tris, pH 7.25. For voltage clamping, electrodes were filled with (in mM) 142 Cs-gluconate, 8 NaCl, 10 HEPES, 0.4 EGTA, 2.5 QX-314, 2 Mg-ATP, and 0.25 GTP-Tris, pH 7.25 with CsOH. The BAPTA intracellular solution contained (in mM) 15 BAPTA, 115 K-gluconate, 8 NaCl, 10 HEPES, 2 Mg-ATP, and 0.25 GTP-Tris, pH 7.25 with KOH. Whole-cell patch-clamping was done using an Axoclamp 2B or Multiclamp 700B amplifier (Molecular Devices). A concentric metal electrode (FHC) was used to evoke EPSCs or EPSPs by stimulating layer 2/3 synapses (0.033 Hz, 200 µs).