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PubMed2002

Rat ENaC expressed in Xenopus laevis oocytes is activated by cAMP and blocked by Ni(2+).

We used oocytes of the South African clawed toad Xenopus laevis to express the three subunits of the epithelial Na(+) channel from rat distal colon (rENaC). We combined conventional dual-microelectrode voltage-clamp with continuous capacitance (C(m)) measurements and noise analysis to evaluate the effects of cAMP and Ni(2+) on rENaC. Control oocytes or rENaC-expressing oocytes exhibited no spontaneous fluctuations in current. However, in rENaC-expressing oocytes amiloride induced a marked plateau-shaped rise of the power density spectra. Recordings using four different concentrations of amiloride revealed that the blocker-channel interactions were of the first order. A cocktail of the membrane permeant cAMP analogue chlorophenylthio-cAMP and IBMX (cAMP cocktail) increased amiloride-sensitive current (I(ami)) and conductance (G(ami)). Furthermore, C(m) was also increased following cAMP application, indicating an increase in plasma membrane surface area. Noise analysis showed that cAMP increased the number of active channels in the oocyte membrane while single-channel current decreased. From these data we conclude that cAMP triggered exocytotic delivery of preformed rENaCs to the plasma membrane. Ni(2+) (2.5 mM) inhibited about 60% of the rENaC current and conductance while C(m) remained unaffected. Noise analysis revealed that this inhibition could be attributed to a decrease in the apparent channel density, while single-channel current did not change significantly. These observations argue for direct effects of Ni(2+) on channel activity rather than induction of endocytotic removal of active channels from the plasma membrane.

Amiloride↗
PubMed2003

Ca(2+) and frequency dependence of exocytosis in isolated somata of magnocellular supraoptic neurones of the rat hypothalamus.

In addition to action potential-evoked exocytotic release at neurohypophysial nerve terminals, the neurohormones arginine vasopressin (aVP) and oxytocin (OT) undergo Ca(2+)-dependent somatodendritic release within the supraoptic and paraventricular hypothalamic nuclei. However, the cellular and molecular mechanisms that underlie this release have not been elucidated. In the present study, the whole-cell patch-clamp technique was utilized in combination with high-time-resolved measurements of membrane capacitance (C(m)) and microfluorometric measurements of cytosolic free Ca(2+) concentration ([Ca(2+)](i)) to examine the Ca(2+) and stimulus dependence of exocytosis in the somata of magnocellular neurosecretory cells (MNCs) isolated from rat supraoptic nucleus (SON). Single depolarizing steps (> or =20 ms) that evoked high-voltage-activated (HVA) Ca(2+) currents (I(Ca)) and elevations in intracellular Ca(2+) concentration were accompanied by an increase in C(m) in a majority (40/47) of SON neurones. The C(m) responses were composed of an initial Ca(2+)-independent, transient component and a subsequent, sustained phase of increased C(m) (termed DeltaC(m)) mediated by an influx of Ca(2+), and increased with corresponding prolongation of depolarizing step durations (20-200 ms). From this relationship we estimated the rate of vesicular release to be 1533 vesicles s(-1). Delivery of neurone-derived action potential waveforms (APWs) as stimulus templates elicited I(Ca) and also induced a DeltaC(m), provided APWs were applied in trains of greater than 13 Hz. A train of APWs modelled after the bursting pattern recorded from an OT-containing neurone during the milk ejection reflex was effective in supporting an exocytotic DeltaC(m) in isolated MNCs, indicating that the somata of SON neurones respond to physiological patterns of neuronal activity with Ca(2+)-dependent exocytotic activity.

Action Potentials↗
PubMed2003

Sustained Ca2+ transfer across mitochondria is Essential for mitochondrial Ca2+ buffering, sore-operated Ca2+ entry, and Ca2+ store refilling.

Mitochondria have been found to sequester and release Ca2+ during cell stimulation with inositol 1,4,5-triphosphate-generating agonists, thereby generating subplasmalemmal microdomains of low Ca2+ that sustain activity of capacitative Ca2+ entry (CCE). Procedures that prevent mitochondrial Ca2+ uptake inhibit local Ca2+ buffering and CCE, but it is not clear whether Ca2+ has to transit through or remains trapped in the mitochondria. Thus, we analyzed the contribution of mitochondrial Ca2+ efflux on the ability of mitochondria to buffer subplasmalemmal Ca2+, to maintain CCE, and to facilitate endoplasmic reticulum (ER) refilling in endothelial cells. Upon the addition of histamine, the initial mitochondrial Ca2+ transient, monitored with ratio-metric-pericam-mitochondria, was largely independent of extracellular Ca2+. However, subsequent removal of extracellular Ca2+ produced a reversible decrease in [Ca2+]mito, indicating that Ca2+ was continuously taken up and released by mitochondria, although [Ca2+]mito had returned to basal levels. Accordingly, inhibition of the mitochondrial Na+/Ca2+ exchanger with CGP 37157 increased [Ca2+]mito and abolished the ability of mitochondria to buffer subplasmalemmal Ca2+, resulting in an increased activity of BKCa channels and a decrease in CCE. Hence, CGP 37157 also reversibly inhibited ER refilling during cell stimulation. These effects of CGP 37157 were mimicked if mitochondrial Ca2+ uptake was prevented with oligomycin/antimycin A. Thus, during cell stimulation a continuous Ca2+ flux through mitochondria underlies the ability of mitochondria to generate subplasmalemmal microdomains of low Ca2+, to facilitate CCE, and to relay Ca2+ from the plasma membrane to the ER.

Biological Transport↗
PubMed2003

TRPC3-like protein is involved in the capacitative cation entry induced by 1alpha,25-dihydroxy-vitamin D3 in ROS 17/2.8 osteoblastic cells.

In ROS 17/2.8 rat osteoblastic-like cells a capacitative Ca(2+) entry (CCE) pathway operates which is activated by either 1alpha,25-dihydroxy-vitamin D3 (1alpha,25(OH)(2)D3 or thapsigargin (Tpg)-induced depletion of Ca(2+) stores. In view of recent evidence favoring a role for transient receptor potential (TRP) proteins in mediating CCE, we investigated if channels involved in the 1alpha,25(OH)(2)D3-sensitive CCE in rat osteoblasts were related to an endogenous TRP-canonical (TRPC) isoform homologue. By reverse transcription (RT)-PCR using mRNA from ROS 17/2.8 cells and primers based on conserved regions within the mammalian TRPC3/6/7 subfamily, two fragments were amplified of 390 and 201 bp with 100 and 94% sequence identity, respectively, with human TRPC3. Northern blot analysis showed the presence of a 3.5 kb transcript and both immunobloting and immunocytochemistry using a specific anti-TRPC3 antibody confirmed endogenous expression of a TRPC3-like protein ( approximately 110 kDa) with membrane localization. In ROS 17/2.8 cells intranuclearly microinjected with anti-TRPC3 antisense oligodeoxynucleotides (ODN), both the initial rate and magnitude of CCE activated by either 1alpha,25(OH)(2)D3 or Tpg were markedly reduced, whereas no changes were detected in control-injected cells. The present findings constitute the first evidence to date suggesting that an endogenous TRPC3-like protein is functionally involved in the CCE route activated by 1alpha,25(OH)(2)D3 in a secosteroid target cell. We anticipate TRPC3 as a candidate for mediating store-operated non-selective cation entry into osteoblasts.

Animals↗
PubMed2005

Arachidonic acid mediates non-capacitative calcium entry evoked by CB1-cannabinoid receptor activation in DDT1 MF-2 smooth muscle cells.

Cannabinoid CB1-receptor stimulation in DDT1 MF-2 smooth muscle cells induces a rise in [Ca2+]i, which is dependent on extracellular Ca2+ and modulated by thapsigargin-sensitive stores, suggesting capacitative Ca2+ entry (CCE), and by MAP kinase. Non-capacitative Ca2+ entry (NCCE) stimulated by arachidonic acid (AA) partly mediates histamine H1-receptor-evoked increases in [Ca2+]i in DDT1 MF-2 cells. In the current study, both Ca2+ entry mechanisms and a possible link between MAP kinase activation and increasing [Ca2+]i were investigated. In the whole-cell patch clamp configuration, the CB-receptor agonist CP 55, 940 evoked a transient, Ca2+-dependent K+ current, which was not blocked by the inhibitors of CCE, 2-APB, and SKF 96365. AA, but not its metabolites, evoked a transient outward current and inhibited the response to CP 55,940 in a concentration-dependent manner. CP 55,940 induced a concentration-dependent release of AA, which was inhibited by the CB1 antagonist SR 141716. The non-selective Ca2+ channel blockers La3+ and Gd3+ inhibited the CP 55,940-induced current at concentrations that had no effect on thapsigargin-evoked CCE. La3+ also inhibited the AA-induced current. CP 55,940-induced AA release was abolished by Gd3+ and by phospholipase A2 inhibition using quinacrine; this compound also inhibited the outward current. The CP 55,940-induced AA release was strongly reduced by the MAP kinase inhibitor PD 98059. The data suggest that in DDT1 MF-2 cells, AA is an integral component of the CB1 receptor signaling pathway, upstream of NCCE and, via PLA2, downstream of MAP kinase.

Arachidonic Acid↗
PubMed2002

Basal lamina of ovarian follicle regulates an inward Cl(-) current in differentiated granulosa cells.

Patch-clamp experiments were conducted to study the effects of basal lamina (basement membrane) of preovulatory chicken ovarian follicle on membrane currents in differentiated chicken granulosa cells in a homologous system. The membrane capacitance (measure of total membrane area) was smaller in cells cultured on intact basal lamina than that of control cells. The granulosa cells expressed outward and two inward currents. A small fraction of the cells (3%) expressed only a transient fast-activating and -inactivating inward current carried by Ca(2+). The majority of the cells, however, expressed a slowly activating and inactivating inward current (carried by Cl(-)) that was superimposed on the transient Ca(2+) current. All cells expressed an outward current characteristic of the delayed-rectifier K(+) current. The removal of extracellular Ca(2+) led to elimination of the slow inward Cl(-) current, indicating that it is a Ca(2+)-dependent Cl(-) current. Both peak amplitude and current density of the inward Cl(-) current were significantly lower in cells cultured on freshly isolated intact basal lamina (or basal lamina stored at 4 degrees C for 12 mo) than those of control cells; however, basal lamina had no significant effect on the density of the outward current. Similar to the observations made for intact basal lamina, solubilized basal lamina suppressed the inward Cl(-) current in differentiated granulosa cells. These data show that homologous basal lamina modulates a Ca(2+)-dependent Cl(-) current in differentiated granulosa cells. These findings provide a partial explanation for the mechanisms that subserve the reported effects of basal lamina (basement membrane) on the metabolic functions of differentiated granulosa cells.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed2003

SUR1 regulates PKA-independent cAMP-induced granule priming in mouse pancreatic B-cells.

Measurements of membrane capacitance were applied to dissect the cellular mechanisms underlying PKA-dependent and -independent stimulation of insulin secretion by cyclic AMP. Whereas the PKA-independent (Rp-cAMPS-insensitive) component correlated with a rapid increase in membrane capacitance of approximately 80 fF that plateaued within approximately 200 ms, the PKA-dependent component became prominent during depolarizations >450 ms. The PKA-dependent and -independent components of cAMP-stimulated exocytosis differed with regard to cAMP concentration dependence; the K(d) values were 6 and 29 micro M for the PKA-dependent and -independent mechanisms, respectively. The ability of cAMP to elicit exocytosis independently of PKA activation was mimicked by the selective cAMP-GEFII agonist 8CPT-2Me-cAMP. Moreover, treatment of B-cells with antisense oligodeoxynucleotides against cAMP-GEFII resulted in partial (50%) suppression of PKA-independent exocytosis. Surprisingly, B-cells in islets isolated from SUR1-deficient mice (SUR1(-/-) mice) lacked the PKA-independent component of exocytosis. Measurements of insulin release in response to GLP-1 stimulation in isolated islets from SUR1(-/-) mice confirmed the complete loss of the PKA-independent component. This was not attributable to a reduced capacity of GLP-1 to elevate intracellular cAMP but instead associated with the inability of cAMP to stimulate influx of Cl(-) into the granules, a step important for granule priming. We conclude that the role of SUR1 in the B cell extends beyond being a subunit of the plasma membrane K(ATP)-channel and that it also plays an unexpected but important role in the cAMP-dependent regulation of Ca(2+)-induced exocytosis.

ATP-Binding Cassette Transporters↗
PubMed2001

Reduction of pacing output coupling capacitance for sensing the evoked response.

Sensing of the intracardiac evoked response (ER) after a pacing stimulus has been used in implantable pacemakers for automatic verification of capture. Reliable detection of ER is hampered by large residual afterpotentials associated with pacing stimuli. This led to the development of various technological solutions, like the use of triphasic pacing pulses and low polarizing electrode systems. This study investigated the effect of reducing the coupling capacitance (CC) in the pacemaker output circuitry on the magnitude of afterpotential, and the ability to automate detection of ventricular evoked response. A CC of 2.2 microF and four different blanking and recharge time settings were clinically tested to evaluate its impact on sensing of the ventricular ER and pacing threshold. Using an automatic step-down threshold algorithm, 54 consecutive patients, aged 70 +/- 10 years with acutely (n = 27) or chronically (n = 27) implanted ventricular pacing leads were enrolled for measurement testing. Routine measurements, using a standard pacing system analyzer (PSA), were (mean +/- SD) impedance 569 +/- 155 omega, R wave amplitude baseline to peak 9.8 +/- 3.7 mV and threshold 0.9 +/- 0.7 V at 0.4-ms pulse width. This new capture verification scheme, based on a CC of 2.2 microF and recharge/blanking timing setting of 10/12 ms, was successful in 52 patients which is equivalent to a success rate of 96%. In a subgroup of 26 patients implanted with bipolar ventricular leads (10 chronic, 16 acute), data were collected in unipolar (UP) and bipolar (BP) pace/sense configurations. Also, ER signals were recorded with two different band-pass filters: a wider band (WB) of 6-250 Hz and a conventional narrow band (NB) of 20-100 Hz. WB sensing from UP lead configuration yielded statistically significant larger signal to artifact ratios (SAR) than the other settings (P < 0.01). A dedicated unipolar ER sensing configuration using a small output capacitor and a wider band-pass filter enables adequate automatic capture verification, without any restrictions on pacing lead models or pacing/sensing configurations.

Aged↗
PubMed2003

Identification of interstitial cells of Cajal in the rabbit portal vein.

Two layers of interstitial cells (ICs) of Cajal were detected by c-kit and methylene blue staining in the media of the rabbit portal vein in subendothelial intramuscular and deeper intramuscular positions, displaced radially from each other by about 40-70 microm. Two morphologically distinct types of ICs were found among enzymatically dispersed cells from this vessel: small multipolar cells with stellate-shaped bodies not exceeding 20 microm, and spindle-shaped cells from 40 to 300 microm in length with numerous branching processes. Relaxed smooth muscle cells (SMCs) had a more constant length (90-150 microm). The cell membrane capacitance was 46.5+/-2.2 pF in SMCs, 39.7+/-2.4 pF in spindle-shaped ICs and 27.8+/-0.7 pF in multipolar ICs. Although darker under phase contrast, after loading with fluo-4 AM, single isolated ICs of both types usually had brighter fluorescence than SMCs and displayed various spontaneous calcium events, including Ca(2+) sparks and Ca(2+) waves. Ca(2+) waves were usually followed by contraction of SMCs but no change in shape of ICs. In some ICs spontaneous [Ca(2+)](i) transients (lasting about 2s) which propagated towards the end of the processes were observed. Physical contacts between the processes of ICs and the body of one or more SMCs survived the isolation procedure. Application of noradrenaline (1-10 microM), caffeine (1-10 mM) or high-K(+) solution (60mM) led to a rise of [Ca(2+)](i) in both SMCs and ICs evoking contraction of SMCs but not ICs. No differences in electrophysiological characteristics between single enzymatically isolated IC and SMC were detected; thus, the resting membrane potential estimated under current-clamp conditions was -46.5+/-2.0 mV in spindle-shaped ICs and -45.6+/-2.7 mV in SMCs. Under voltage-clamp, both ICs and SMCs revealed a well-developed voltage-gated nifedipine-sensitive L-type Ca(2+) current, a set of K(+) currents, including spontaneous transient outward currents (STOCs) but no Na(+) current. This study for the first time directly demonstrated the presence in vascular tissue of ICs. Possible roles for ICs including their involvement in spontaneous activity of the vessel were discussed.

Aniline Compounds↗
PubMed2002

Capacitive micromachined ultrasonic transducers: next-generation arrays for acoustic imaging?

Piezoelectric materials have dominated the ultrasonic transducer technology. Recently, capacitive micromachined ultrasonic transducers (CMUTs) have emerged as an alternative technology offering advantages such as wide bandwidth, ease of fabricating large arrays, and potential for integration with electronics. The aim of this paper is to demonstrate the viability of CMUTs for ultrasound imaging. We present the first pulse-echo phased array B-scan sector images using a 128-element, one-dimensional (1-D) linear CMUT array. We fabricated 64- and 128-element 1-D CMUT arrays with 100% yield and uniform element response across the arrays. These arrays have been operated in immersion with no failure or degradation in performance over the time. For imaging experiments, we built a resolution test phantom roughly mimicking the attenuation properties of soft tissue. We used a PC-based experimental system, including custom-designed electronic circuits to acquire the complete set of 128 x 128 RF A-scans from all transmit-receive element combinations. We obtained the pulse-echo frequency response by analyzing the echo signals from wire targets. These echo signals presented an 80% fractional bandwidth around 3 MHz, including the effect of attenuation in the propagating medium. We reconstructed the B-scan images with a sector angle of 90 degrees and an image depth of 210 mm through offline processing by using RF beamforming and synthetic phased array approaches. The measured 6-dB lateral and axial resolutions at 135 mm depth were 0.0144 radians and 0.3 mm, respectively. The electronic noise floor of the image was more than 50 dB below the maximum mainlobe magnitude. We also performed preliminary investigations on the effects of crosstalk among array elements on the image quality. In the near field, some artifacts were observable extending out from the array to a depth of 2 cm. A tail also was observed in the point spread function (PSF) in the axial direction, indicating the existence of crosstalk. The relative amplitude of this tail with respect to the mainlobe was less than -20 dB.

Adipose Tissue↗
PubMed2002

Monitoring of temperature effects on animal cell metabolism in a packed bed process.

Animal cell (Chinese Hamster Ovary) concentration was determined on-line in a packed bed process using dielectric spectroscopy. This enabled the evaluation of the effect of temperature on specific metabolic rates during 3 months of continuous culture. The effect of low cultivation temperature on cell growth and metabolism was monitored, and the data were used for process development. At 37 degrees C cells grew exponentially with a specific growth rate of 0.038 d-1 and specific glucose uptake and lactate production rates increased continually. Reduction of the temperature to 33.5 degrees C resulted in a lowering of these metabolic rates while having no effect on cell proliferation. Subsequent reduction of the temperature to 32 degrees C resulted in stabilization of the cell concentration at a high density (3.6 x 10(7) cell per mL of packed bed). In addition, the specific production rate of the protein of interest increased by a factor of 6 compared to the value at 37 degrees C. During the stationary phase at 32 degrees C, all other specific metabolic rates could be controlled to low and constant levels.

Animals↗
PubMed2004

Zeta potential of microfluidic substrates: 1. Theory, experimental techniques, and effects on separations.

This paper summarizes theory, experimental techniques, and the reported data pertaining to the zeta potential of silica and silicon with attention to use as microfluidic substrate materials, particularly for microchip chemical separations. Dependence on cation concentration, buffer and cation type, pH, cation valency, and temperature are discussed. The Debye-Hückel limit, which is often correctly treated as a good approximation for describing the ion concentration in the double layer, can lead to serious errors if it is extended to predict the dependence of zeta potential on the counterion concentration. For indifferent univalent electrolytes (e.g., sodium and potassium), two simple scalings for the dependence of zeta potential on counterion concentration can be derived in high- and low-zeta limits of the nonlinear Poisson-Boltzman equation solution in the double layer. It is shown that for most situations relevant to microchip separations, the high-zeta limit is most applicable, leading to the conclusion that the zeta potential on silica substrates is approximately proportional to the logarithm of the molar counterion concentration. The zeta vs. pH dependence measurements from several experiments are compared by normalizing the zeta based on concentration.

Electric Capacitance↗
PubMed2004

Zeta potential of microfluidic substrates: 2. Data for polymers.

Zeta potential data are reviewed for a variety of polymeric microfluidic substrate materials. Many of these materials currently used for microchip fabrication have only recently been employed for generation of electroosmotic flow. Despite their recent history, polymeric microfluidic substrates are currently used extensively for microchip separations and other techniques, and understanding of the surface zeta potential is crucial for experimental design. This paper proposes the use of pC (the negative logarithm of the counterion concentration) as a useful normalization for the zeta potential on polymer substrates in contact with indifferent univalent counterions. Normalizing zeta by pC facilitates comparison of results from many investigators. The sparseness of available data for polymeric substrates prevents complete and rigorous justification for this normalization; however, it is consistent with double layer and adsorption theory. For buffers with indifferent univalent cations, normalization with the logarithm of the counterion concentration in general collapses data onto a single zeta/pC vs. pH curve, and (with the exception of PMMA) the repeatability of the data is quite encouraging. Normalization techniques should allow improved ability to predict zeta potential performance on microfluidic substrates and compare results observed with different parameters.

Electric Capacitance↗