SUMMARY1. Single smooth muscle cells obtained by enzymic dispersion of the longitudinal muscle layer of guinea-pig ileum were used for recording membrane currents under whole-cell voltage clamp in response to carbachol (100 /bM, unless otherwise stated) or histamine (100 jam) applied extracellularly.2. At a holding potential of 0 mV, a transient outward current was evoked by carbachol and histamine. Responses to the two agonists were very similar in size and time course to the current response to caffeine (10 mM). The response to carbachol was virtually absent in the presence of histamine, and vice versa. Caffeine was without effect in the presence of either of these agonists. Inclusion of EGTA (10 or 20 mM) in the pipette abolished the responses to carbachol, histamine and caffeine. Thus, the outward current responses were considered to represent opening of Ca2+_ activated K+ channels in response to a massive release of Ca2+ from the same stores by these three agents.3. An inward current was evoked by carbachol and histamine, but not by caffeine at a holding potential of -40 mV, which was considered to represent opening of cationic channels. The carbachol-induced inward current was much longer in duration and larger in size than the histamine-induced inward current.4. Inclusion of GDPpJS (2 mm) in the pipette abolished the inward and outward current responses to histamine, but inhibited only part of those to carbachol.5. When the holding potential was held at 0 mV with inclusion of GTPyS (0'1-1 mM) in the pipette, spontaneous transient outward currents appeared immediately after break-through but disappeared a few minutes later. Under these conditions, caffeine (10 mM) was almost without effect, suggesting that GTPyS had released Ca2+ stores. When the holding potential was held at -40 mV and GTPyS (0-1 or 0-2 mm) was present in the pipette, an inward current developed a few minutes after break-through. During the GTPyS-induced inward current, application of carbachol or histamine produced no further inward current. However, when 0-01 mmGTPyS was included in the pipette solution, carbachol-and histamine-induced inward currents were potentiated.6. Pretreated with 2-5 gug/ml pertussis toxin (PTX) did not change noticeably the MS 9646 106 S. KOMORI, M. KA WAI, T. TAKEWAKI AND H. OHASHI outward current responses to carbachol and histamine, but abolished or markedly reduced the inward current responses.7. The results suggest that stimulation of muscarinic receptor or histamine receptor caused release of Ca2+ from storage sites and activation of cationic channels, and that regardless of the receptor type, calcium store release may be mediated via a PTX-insensitive G-protein, while the cation channels are activated via another G-protein which is sensitive to PTX.

We describe a novel polymer that exhibits a coordination of molecular recognition and actuation functionalities within itself. This coordination induces an autonomous polymer shrinking/swelling phase transition, accompanied by the complexation/decomplexation of a guest molecule. The artificial polymer exhibited autonomous behavior induced by molecular recognition, which is a unique function of the living body. We used β-cyclodextrin (CD) as the molecular recognition moiety, and poly(N-isopropylacrylamide) (NIPAM) as the actuation moiety in the polymer. Both these components affect each other: complexation between CD and its guest molecule 8-anilino-1-naphthalenesulfonic acid ammonium salt (ANS) induces a phase transition in the NIPAM chain. Meanwhile, the phase transition in the NIPAM chain affects CD/ANS complex formation. Coordination of these two phenomena induces an autonomous polymer shrinking/swelling behavior with CD/ANS complexation/decomplexation. We successfully observed this behavior using UV-vis and fluorescence spectroscopy.

We observed fast proton conduction in a material consisting of packed acids, the “packed-acid mechanism” resulting from acid–acid interactions.

In single cells isolated from guinea-pig ileal smooth muscle, held under voltage clamp at -40 mV or -50 mV by patch pipette in the whole-cell recording mode, carbachol (CCh) evoked an oscillatory inward cationic current. The frequency of current oscillations increased with increasing CCh concentration. CCh-evoked current oscillations were followed very closely by oscillations in intracellular free Ca2+ estimated from the Indo-1 signal, and were abolished by inclusion of EGTA in the pipette solution. Ryanodine and heparin, but not nifedipine, blocked the generation of current oscillations. CCh-evoked current oscillations were abolished upon withdrawal of extracellular calcium and restored upon its reintroduction. Inclusion of GTP[gamma S] in the pipette solution caused the generation of an oscillatory inward current, which was blocked by ryanodine. The present results are consistent with the hypothesis that CCh-evoked cationic current is gated by activation of a G protein and is steeply dependent on [Ca2+]i, fluctuations in the release of Ca2+ from stores during carbachol's action produce oscillations in [Ca2+]i which cause similar oscillations in the cationic current.

No abstract

A facile and one-pot method for the synthesis of Pt, Pd, and their alloy nanocrystals along with their exciting electrocatalytic activities toward methanol oxidation have been reported. Unique structures like truncated octahedrons of Pd, Pt, and their alloys like CoPt and PdPt have been synthesized in presence of a reducing solvent like N-methyl pyrrolidone (NMP) and stabilizer like polyvinyl pyrrolidone (PVP). Among these nanocrystals, Pd16Pt84 and Co5Pt95 show tremendous improvement in the electro-oxidation of methanol in acidic media with mass activities of 1790 and 1417 mA/mgPt, respectively (with lower onset potential compared to Pt alone), which is believed to be much higher compared to that of previous reports and state-of-art Pt/C and RuPt/C catalysts, indicating a better alloy formation and stable particle–support interactions.

Tetrodotoxin, at concentrations up to 5 x 10(-6) gram per milliliter, has no effect on the spontaneous discharge in the smooth muscle of taenia coli. However, the spontaneous discharge is abolished by Mn(++) at a concentration of 0.5 millimole per liter. The contraction induced by immersing the muscle in isotonic KCl solution is also suppressed in the presence of Mn(++). Because Mn(++) is a specific suppressor of the spike induced by Ca(++) and tetrodotoxin is an inhibitor of the spike induced by Na(+), we suggest that Ca(++) is a charge carrier in the production of spike potential in the smooth muscle and that the entry of intervening Ca(++) through the membrane acts as a trigger for the contraction of smooth muscle.

1 The eect on membrane currents of infection of mouse neuroblastoma NA cells with rabies virus was studied by using the whole-cell patch clamp technique. 2 Three types of membrane currents, namely voltage-dependent Na + current (I Na ), delayed recti®er K + current (I K-DR ) and inward recti®er K + current (I K-IR ) were elicited in uninfected cells. 3 In cells 3 days after infection with the virus, no detectable change was observed in morphology and membrane capacitance, but I Na and I K-IR were signi®cantly decreased in amplitude without any appreciable dierence in the time course of current activation and inactivation. The voltagedependence of I Na activation was signi®cantly shifted in the positive direction along the voltage axis with a decreased slope. I K-DR remained almost unaltered after the viral infection. 4 The resting membrane potential, measured with a physiological K + gradient across the cell membrane, was decreased (depolarized) after the viral infection. The depolarization was associated with the decreased amplitude of I K-IR . 5 These results suggest that infection of mouse neuroblastoma NA cells with rabies virus causes reduction of functional expression of ion channels responsible for I Na and I K-IR , and provide evidence for possible involvement of the change in membrane properties in the pathogenesis of rabies disease.