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Equilibrium Potential (equilibrium + potential)
Selected AbstractsSynaptic stimulation of nicotinic receptors in rat sympathetic ganglia is followed by slow activation of postsynaptic potassium or chloride conductancesEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 8 2000Oscar Sacchi Abstract Two slow currents have been described in rat sympathetic neurons during and after tetanization of the whole preganglionic input. Both effects are mediated by nicotinic receptors activated by native acetylcholine (ACh). A first current, indicated as IAHPsyn, is calcium dependent and voltage independent, and is consistent with an IAHP -type potassium current sustained by calcium ions accompanying the nicotinic synaptic current. The conductance activated by a standard synaptic train was ,,3.6 nS per neuron; it was detected in isolation in 14 out of a 52-neuron sample. A novel current, IADPsyn, was described in 42/52 of the sample as a post-tetanic inward current, which increased in amplitude with increasing membrane potential negativity and exhibited a null-point close to the holding potential and the cell momentary chloride equilibrium potential. IADPsyn developed during synaptic stimulation and decayed thereafter according to a single exponential (mean ,,= 148.5 ms) in 18 neurons or according to a two-exponential time course (, = 51.8 and 364.9 ms, respectively) in 19 different neurons. The mean peak conductance activated was ,,20 nS per neuron. IADPsyn was calcium independent, it was affected by internal and external chloride concentration, but was insensitive to specific blockers (anthracene-9-carboxylic acid, 9AC) of the chloride channels open in the resting neuron. It is suggested that gADPsyn represents a specific chloride conductance activatable by intense nicotinic stimulation; in some neurons it is even associated with single excitatory postsynaptic potentials (EPSCs). Both IAHP and IADPsyn are apparently devoted to reduce neuronal excitability during and after intense synaptic stimulation. [source] Isolation of Solid Solution Phases in Size-Controlled LixFePO4 at Room TemperatureADVANCED FUNCTIONAL MATERIALS, Issue 3 2009Genki Kobayashi Abstract State-of-the-art LiFePO4 technology has now opened the door for lithium ion batteries to take their place in large-scale applications such as plug-in hybrid vehicles. A high level of safety, significant cost reduction, and huge power generation are on the verge of being guaranteed for the most advanced energy storage system. The room-temperature phase diagram is essential to understand the facile electrode reaction of LixFePO4 (0,<,x,<,1), but it has not been fully understood. Here, intermediate solid solution phases close to x,=,0 and x,=,1 have been isolated at room temperature. Size-dependent modification of the phase diagram, as well as the systematic variation of lattice parameters inside the solid-solution compositional domain closely related to the electrochemical redox potential, are demonstrated. These experimental results reveal that the excess capacity that has been observed above and below the two-phase equilibrium potential is largely due to the bulk solid solution, and thus support the size-dependent miscibility gap model. [source] Adenosine inhibits paraventricular pre-sympathetic neurons through ATP-dependent potassium channelsJOURNAL OF NEUROCHEMISTRY, Issue 2 2010De-Pei Li J. Neurochem. (2010) 113, 530,542. Abstract Adenosine produces cardiovascular depressor effects in various brain regions. However, the cellular mechanisms underlying these effects remain unclear. The pre-sympathetic neurons in the hypothalamic paraventricular nucleus (PVN) play an important role in regulating arterial blood pressure and sympathetic outflow through projections to the spinal cord and brainstem. In this study, we performed whole-cell patch-clamp recordings on retrogradely labeled PVN neurons projecting to the intermediolateral cell column of the spinal cord in rats. Adenosine (10,100 ,M) decreased the firing activity in a concentration-dependent manner, with a marked hyperpolarization in 12 of 26 neurons tested. Blockade of A1 receptors with the adenosine A1 receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine or intracellular dialysis of guanosine 5,- O -(2-thodiphosphate) eliminated the inhibitory effect of adenosine on labeled PVN neurons. Immunocytochemical labeling revealed that A1 receptors were expressed on spinally projecting PVN neurons. Also, blocking ATP-dependent K+ (KATP) channels with 100 ,M glibenclamide or 200 ,M tolbutamide, but not the G protein-coupled inwardly rectifying K+ channels blocker tertiapin-Q, abolished the inhibitory effect of adenosine on the firing activity of PVN neurons. Furthermore, glibenclamide or tolbutamide significantly decreased the adenosine-induced outward currents in labeled neurons. The reversal potential of adenosine-induced currents was close to the K+ equilibrium potential. In addition, adenosine decreased the frequency of both spontaneous and miniature glutamatergic excitatory post-synaptic currents and GABAergic inhibitory post-synaptic currents in labeled neurons, and these effects were also blocked by 8-cyclopentyl-1,3-dipropylxanthine. Collectively, our findings suggest that adenosine inhibits the excitability of PVN pre-sympathetic neurons through A1 receptor-mediated opening of KATP channels. [source] Regulation of membrane potential and fluid secretion by Ca2+ -activated K+ channels in mouse submandibular glandsTHE JOURNAL OF PHYSIOLOGY, Issue 2 2007Victor G. Romanenko We have recently shown that the IK1 and maxi-K channels in parotid salivary gland acinar cells are encoded by the KCa3.1 and KCa1.1 genes, respectively, and in vivo stimulated parotid secretion is severely reduced in double-null mice. The current study tested whether submandibular acinar cell function also relies on these channels. We found that the K+ currents in submandibular acinar cells have the biophysical and pharmacological footprints of IK1 and maxi-K channels and their molecular identities were confirmed by the loss of these currents in KCa3.1- and KCa1.1 -null mice. Unexpectedly, the pilocarpine-stimulated in vivo fluid secretion from submandibular glands was essentially normal in double-null mice. This result and the possibility of side-effects of pilocarpine on the nervous system, led us to develop an ex vivo fluid secretion assay. Fluid secretion from the ex vivo assay was substantially (about 75%) reduced in animals with both K+ channel genes ablated , strongly suggesting systemic complications with the in vivo assay. Additional experiments focusing on the membrane potential in isolated submandibular acinar cells revealed mechanistic details underlying fluid secretion in K+ channel-deficient mice. The membrane potential of submandibular acinar cells from wild-type mice remained strongly hyperpolarized (,55 ± 2 mV) relative to the Cl, equilibrium potential (,24 mV) during muscarinic stimulation. Similar hyperpolarizations were observed in KCa3.1- and KCa1.1 -null mice (,51 ± 3 and ,48 ± 3 mV, respectively), consistent with the normal fluid secretion produced ex vivo. In contrast, acinar cells from double KCa3.1/KCa1.1 -null mice were only slightly hyperpolarized (,35 ± 2 mV) also consistent with the ex vivo (but not in vivo) results. Finally, we found that the modest hyperpolarization of cells from the double-null mice was maintained by the electrogenic Na+,K+ -ATPase. [source] Quercetin as a novel activator of L-type Ca2+ channels in rat tail artery smooth muscle cellsBRITISH JOURNAL OF PHARMACOLOGY, Issue 7 2002Simona Saponara The aim of this study was to investigate the effects of quercetin, a natural polyphenolic flavonoid, on voltage-dependent Ca2+ channels of smooth muscle cells freshly isolated from the rat tail artery, using either the conventional or the amphotericin B-perforated whole-cell patch-clamp method. Quercetin increased L-type Ca2+ current [ICa(L)] in a concentration- (pEC50=5.09±0.05) and voltage-dependent manner and shifted the maximum of the current-voltage relationship by 10 mV in the hyperpolarizing direction, without, however, modifying the threshold and the equilibrium potential for Ca2+. Quercetin-induced ICa(L) stimulation was reversible upon wash-out. T-type Ca2+ current was not affected by quercetin. Quercetin shifted the voltage dependence of the steady-state inactivation and activation curves to more negative potentials by about 5.5 and 7.5 mV respectively, in the mid-potential of the curves as well as increasing the slope of activation. Quercetin slowed both the activation and the deactivation kinetics of the ICa(L). The inactivation time course was also slowed but only at voltages higher than 10 mV. Moreover quercetin slowed the rate of recovery from inactivation. These results prove quercetin to be a naturally-occurring L-type Ca2+ channel activator. British Journal of Pharmacology (2002) 135, 1819,1827; doi:10.1038/sj.bjp.0704631 [source] | ||||||||||