Polymer complexes consisting of polypyridinium, pyridinium and aluminium chloride are found to be a new class of highly conductive polymer electrolytes, which exhibit a high ionic conductivity of 10-3 S cm-1 at room temperature within range of the conductivity of electrolyte solutions, in spite of film-forming properties.

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Cooperative regulation of inosiol-1,4,5-trisphosphate receptors (IP(3)Rs) by Ca(2+) and IP(3) has been increasingly recognized, although its functional significance is not clear. The present experiments first confirmed that depolarization-induced Ca(2+) influx triggers an outward current in visual cortex pyramidal cells in normal medium, which was mediated by apamin-sensitive, small-conductance Ca(2+)-dependent K(+) channels (SK channels). With IP(3)-mobilizing neurotransmitters bath-applied, a delayed outward current was evoked in addition to the initial outward current and was mediated again by SK channels. Calcium turnover underlying this biphasic SK channel activation was investigated. By voltage-clamp recording, Ca(2+) influx through voltage-dependent Ca(2+) channels (VDCCs) was shown to be responsible for activating the initial SK current, whereas the IP(3)R blocker heparin abolished the delayed component. High-speed Ca(2+) imaging revealed that a biphasic Ca(2+) elevation indeed underlays this dual activation of SK channels. The first Ca(2+) elevation originated from VDCCs, whereas the delayed phase was attributed to calcium release from IP(3)Rs. Such enhanced SK currents, activated dually by incoming and released calcium, were shown to intensify spike-frequency adaptation. We propose that spike-induced calcium release from IP(3)Rs leads to SK channel activation, thereby fine tuning membrane excitability in central neurons.

For induction of long-term depression (LTD), mechanisms dependent on N-methyl-D-aspartate receptors (NMDARs) and on intracellular calcium stores have been separately known. How these two mechanisms coexist at the same synapses is not clear. Here, induction of LTD at hippocampal Schaffer collateral-to-CA1 pyramidal cell synapses was shown to depend on NMDARs throughout the theoretically predicted activation range for LTD induction. With stimulation at 1 Hz, the largest LTD was induced in a store-independent manner. With stimulation at 0.5 and 2.0 Hz the induced LTD was much smaller, and dependence on calcium stores appeared. Under caffeine application, an enlarged LTD was induced with 0.5 Hz stimulation. Postsynaptic blockade of ryanodine receptors prevented this caffeine-induced enhancement of LTD. It is therefore suggested that calcium release from calcium stores facilitated by caffeine contributed to the LTD enhancement, and that the caffeine effect was exerted on the postsynaptic side. Induction of this enhanced LTD was resistant to NMDAR blockade. We thus propose that the store-dependent mechanism for LTD induction is dormant at the centre of the theoretically predicted activation range for LTD induction, but operates at the fringes of this activation range, with its contribution more emphasized when ample calcium release occurs.

Appropriate dosages of cilostazol have not been studied in veterinary patients, and the degrees of heart rate (HR) increase have not been studied in dogs administered cilostazol. Therefore, this study aimed to investigate the degrees of HR increase in healthy dogs administered cilostazol. Thirty healthy beagle dogs (15 males and 15 females; age, 5–8 years) were divided into 3 groups of 10 dogs each and orally administered 2.5, 5, or 10 mg/kg cilostazol (twice a day at 8:00 AM and 8:00 PM for 10 days). Higher HR increases were seen in the 5 mg/kg group than in the 2.5 mg/kg group at all time points except 7:00 AM, 9:00 AM, 1:00 PM, and 4:00 PM (P<0.01). Higher HR increases were also observed in the 10 mg/kg group than in the 2.5 mg/kg group at all time points except 4:00 PM (P<0.01). The 10 mg/kg group showed higher HR increases than the 5 mg/kg group at all time points except 6:00 AM, 7:00 AM, 6:00 PM, and 7:00 PM (P<0.05 for 4:00 PM and 5:00 PM; P<0.01 for the other time points). These results together show that the HR of healthy dogs increased in a dose-dependent manner after cilostazol administration twice a day at doses of 5 to 10 mg/kg. These results provide a useful basis for choosing cilostazol in the treatment of bradyarrhythmia in dogs.