Decreased cardiac excitability secondary to reduction of sodium current may be a significant contributor to reduced contractility in a rat model of sepsis

Pembelajaran pada hakekatnya adalah proses interaksi antara peserta didik dengan lingkungannya. Pembelajaran merupakan aktualisasi kurikulum yang menuntut keaktifan guru dalam menciptakan dan menumbuhkan kegiatan peserta didik sesuai dengan rencana yang telah diprogramkan. Dalam pembelajaran matematika sering kita temui adanya siswa yang kesulitan dalam menerima materi yang diajarkan, untuk mengantisipasi hal itu pembelajaran matematika hendaknya dimulai dengan pengenalan masalah yang sesuai dengan situasi (contextual problem). Salah satu pendekatan yang sesuai untuk menunjang guru sebagai guru profesional adalah pendekatan PMRI, sehingga siswa bisa mengkonstruksi pengetahuannya sendiri. Rumusan masalah yang diteliti dalam penelitian ini adalah bagaimana mengembangkan bahan ajar yang valid dan praktis yang dikembangkan dengan pendekatan PMRI, dan bagaimana efek potensial bahan ajar yang dikembangkan dengan pendekatan PMRI terhadap hasil belajar siswa. Penelitian ini merupakan penelitian pengembangan (development research) yang bertujuan untuk menghasilkan bahan ajar yang valid, praktis dan efektif untuk pembelajaran matematika di kelas VII SMP Negeri 4 Pangkal Pinang. Subjek penelitian ini adalah siswa kelas VII.D sebanyak 36 siswa. Dengan kesimpulan bahwa bahan ajar yang dikembangkan dalam penelitian ini dikategorikan valid, praktis dan memiliki potential effect terhadap hasil belajar siswa di kelas VII.D SMP Negeri 4 Pangkal Pinang. Kata kunci : himpunan, pendekatan PMRI DOI: http://dx.doi.org/10.22342/jpm.8.1.1859.43-5

Muscle Nicotinic Acetylcholine Receptors May Mediate Trans-Synaptic Signaling at the Mouse Neuromuscular Junction

Block of neurotransmitter receptors at the neuromuscular junction (NMJ) has been shown to trigger upregulation of the number of synaptic vesicles released (quantal content, QC), a response termed homeostatic synaptic plasticity. The mechanism underlying this plasticity is not known. Here, we used selective toxins to demonstrate that block of α1-containing nicotinic acetylcholine receptors (nAChRs) at the NMJ of male and female mice triggers the upregulation of QC. Reduction of current flow through nAChRs, induced by drugs with antagonist activity, demonstrated that reduction in synaptic current per se does not trigger upregulation of QC. These data led to the remarkable conclusion that disruption of synaptic transmission is not sensed to trigger upregulation of QC. During studies of the effect of partial block of nAChRs on QC, we observed a small but reproducible increase in the decay kinetics of miniature synaptic currents. The change in kinetics was correlated with the increase in QC and raises the possibility that a change in postsynaptic nAChR conformation may be associated with the presynaptic increase in QC. We propose that, in addition to functioning in synaptic transmission, ionotropic muscle nicotonic nAChRs may serve as signaling molecules that participate in synaptic plasticity. Because nAChRs have been implicated in a number of disease states, the finding that nAChRs may be involved in triggering synaptic plasticity could have wide-reaching implications. SIGNIFICANCE STATEMENT The signals that initiate synaptic plasticity of the nervous system are still incompletely understood. Using the mouse neuromuscular junction as a model synapse, we studied how block of neurotransmitter receptors is sensed to trigger synaptic plasticity. Our studies led to the surprising conclusion that neither changes in synaptic current nor spiking of the presynaptic or postsynaptic cell are sensed to initiate synaptic plasticity. Instead, postsynaptic nicotinic acetylcholine receptors (nAChRs), in addition to functioning in synaptic transmission, may serve as signaling molecules that trigger synaptic plasticity. Because nAChRs have been implicated in a number of disease states, the finding that they may mediate synaptic plasticity has broad implications

Resting Potential–dependent Regulation of the Voltage Sensitivity of Sodium Channel Gating in Rat Skeletal Muscle In Vivo

Normal muscle has a resting potential of −85 mV, but in a number of situations there is depolarization of the resting potential that alters excitability. To better understand the effect of resting potential on muscle excitability we attempted to accurately simulate excitability at both normal and depolarized resting potentials. To accurately simulate excitability we found that it was necessary to include a resting potential–dependent shift in the voltage dependence of sodium channel activation and fast inactivation. We recorded sodium currents from muscle fibers in vivo and found that prolonged changes in holding potential cause shifts in the voltage dependence of both activation and fast inactivation of sodium currents. We also found that altering the amplitude of the prepulse or test pulse produced differences in the voltage dependence of activation and inactivation respectively. Since only the Nav1.4 sodium channel isoform is present in significant quantity in adult skeletal muscle, this suggests that either there are multiple states of Nav1.4 that differ in their voltage dependence of gating or there is a distribution in the voltage dependence of gating of Nav1.4. Taken together, our data suggest that changes in resting potential toward more positive potentials favor states of Nav1.4 with depolarized voltage dependence of gating and thus shift voltage dependence of the sodium current. We propose that resting potential–induced shifts in the voltage dependence of sodium channel gating are essential to properly regulate muscle excitability in vivo

Homeostatic Synaptic Plasticity of Miniature Excitatory Postsynaptic Currents in Mouse Cortical Cultures Requires Neuronal Rab3A

Following prolonged activity blockade, amplitudes of miniature excitatory postsynaptic currents (mEPSCs) increase, a form of homeostatic plasticity termed “synaptic scaling.” We previously showed that a presynaptic protein, the small GTPase Rab3A, is required for full expression of the increase in miniature endplate current amplitudes following prolonged blockade of action potential activity at the mouse neuromuscular junction in vivo (Wang et al., 2011), but it is unknown whether this form of Rab3A-dependent homeostatic plasticity shares any characteristics with central synapses. We show here that synaptic scaling of mEPSCs is impaired in mouse cortical neuron cultures prepared from Rab3A-/- and Rab3A Earlybird mutant mice. To determine if Rab3A is involved in the well-established homeostatic increase in postsynaptic AMPA-type receptors (AMPARs), we performed a series of experiments in which electrophysiological recordings of mEPSCs and confocal imaging of synaptic AMPAR immunofluorescence were assessed within the same cultures. We found that Rab3A is required for the increase in synaptic AMPARs following prolonged activity blockade, but the comparison of mEPSC amplitude and synaptic AMPARs in the same cultures revealed that mEPSC amplitude cannot solely be determined by postsynaptic AMPAR levels. Finally, we demonstrate that Rab3A is acting in neurons because selective loss of Rab3A in astrocytes did not disrupt homeostatic plasticity, whereas selective loss in neurons strongly reduced the homeostatic increase in mEPSC amplitudes. Taken together with the results at the neuromuscular junction, we propose that Rab3A is a presynaptic homeostatic regulator that controls quantal size on both sides of the synapse

On the Classification of UGC1382 as a Giant Low Surface Brightness Galaxy

We provide evidence that UGC1382, long believed to be a passive elliptical galaxy, is actually a giant low surface brightness (GLSB) galaxy which rivals the archetypical GLSB Malin 1 in size. Like other GLSB galaxies, it has two components: a high surface brightness disk galaxy surrounded by an extended low surface brightness (LSB) disk. For UGC1382, the central component is a lenticular system with an effective radius of 6 kpc. Beyond this, the LSB disk has an effective radius of ~38 kpc and an extrapolated central surface brightness of ~26 mag/arcsec^2. Both components have a combined stellar mass of ~8x10^10 M_sun, and are embedded in a massive (10^10 M_sun) low-density (<3 M_sun/pc^2) HI disk with a radius of 110 kpc, making this one of the largest isolated disk galaxies known. The system resides in a massive dark matter halo of at least 2x10^12 M_sun. Although possibly part of a small group, its low density environment likely plays a role in the formation and retention of the giant LSB and HI disks. We model the spectral energy distributions and find that the LSB disk is likely older than the lenticular component. UGC1382 has UV-optical colors typical of galaxies transitioning through the green valley. Within the LSB disk are spiral arms forming stars at extremely low efficiencies. The gas depletion time scale of ~10^11 yr suggests that UGC1382 may be a very long term resident of the green valley. We find that the formation and evolution of the LSB disk is best explained by the accretion of gas-rich LSB dwarf galaxies.Comment: 17 pages, 16 figures, 4 tables; accepted to the Astrophysical Journa

Nova Sagittarii 1994 #1 (V4332 Sagittarii): The Discovery and Evolution of an Unusual Luminous Red Variable Star

We report photometry and spectroscopy of the evolution of Nova Sagittarii 1994 #1 (V4332 Sagittarii) during outburst. We compare the photometric and spectral evolution of this outburst to known classes of outbursts -- including classical novae and outbursts occurring on symbiotic stars -- and find this object does NOT conform to any known class of outburst. The closest match to the behavior of this unusual object is M31 RV, an extremely luminous and red variable object discovered in the bulge of M31 in 1988. However, the temporal behavior and maximum luminosity of the two events differ by several orders of magnitude, requiring substantial intrinsic variation if these two events are members the same type of outburst. Our model of the spectroscopic evolution of this outburst shows that the effective temperature cooled from 4400 K to 2300 K over the three month span of our observations. In combination with line diagnostics in our later spectra, including [OI] lambda 5577 and the dramatic increase in the Halpha to Hbeta ratio, we infer the existence of a cool, dense (N_e ~ 10^{8-9} cm^{-3}) envelope that is optically thick in the Hydrogen Balmer recombination lines (case C). We suggest that a nuclear event in a single star, in which a slow shock drove the photosphere outwards, can power the observed luminosity evolution and the emission spectrum.Comment: Accepted for publication in AJ. 24 pages including 8 embedded postscript figures. Also available at http://www.astronomy.ohio-state.edu/~martini/pub

Shocked POststarbust Galaxy Survey I: Candidate Poststarbust Galaxies with Emission Line Ratios Consistent with Shocks

[Abridged] The Shocked POststarburst Galaxy Survey (SPOGS) aims to identify transforming galaxies, in which the nebular lines are excited via shocks instead of through star formation processes. Utilizing the OSSY measurements on the Sloan Digital Sky Survey Data Release 7 catalog, we applied Balmer absorption and shock boundary criteria to identify 1,067 SPOG candidates (SPOGs*) within z=0.2. SPOGs* represent 0.2% of the OSSY sample galaxies that exceed the continuum signal-to-noise cut (and 0.7% of the emission line galaxy sample). SPOGs* colors suggest that they are in an earlier phase of transition than OSSY galaxies that meet an E+A selection. SPOGs* have a 13% 1.4GHz detection rate from the Faint Images of the Radio Sky at Twenty centimeters survey, higher than most other subsamples, and comparable only to low-ionization nuclear emission line region hosts, suggestive of the presence of active galactic nuclei. SPOGs* also have stronger NaD absorption than predicted from the stellar population, suggestive of cool gas being driven out in galactic winds. It appears that SPOGs* represent an earlier phase in galaxy transformation than traditionally selected poststarburst galaxies, and that a large proportion of SPOGs* also have properties consistent with disruption of their interstellar media, a key component to galaxy transformation. It is likely that many of the known pathways to transformation undergo a SPOG phase. Studying this sample of SPOGs* further, including their morphologies, active galactic nuclei properties, and environments, has the potential for us to build a more complete picture of the initial conditions that can lead to a galaxy evolving.Comment: 19 pages, 19 figures, 3 tables, accepted to ApJ Supplements (Apr 13), full sample is available on www.spogs.or

Depressed Neuromuscular Transmission Causes Weakness in Mice Lacking BK Potassium Channels

Mice lacking functional large-conductance voltage- and Ca2+-activated K+ channels (BK channels) are viable but have motor deficits including ataxia and weakness. The cause of weakness is unknown. In this study, we discovered, in vivo, that skeletal muscle in mice lacking BK channels (BK−/−) was weak in response to nerve stimulation but not to direct muscle stimulation, suggesting a failure of neuromuscular transmission. Voltage-clamp studies of the BK−/− neuromuscular junction (NMJ) revealed a reduction in evoked endplate current amplitude and the frequency of spontaneous vesicle release compared with WT littermates. Responses to 50-Hz stimulation indicated a reduced probability of vesicle release in BK−/− mice, suggestive of lower presynaptic Ca2+ entry. Pharmacological block of BK channels in WT NMJs did not affect NMJ function, surprisingly suggesting that the reduced vesicle release in BK−/− NMJs was not due to loss of BK channel–mediated K+ current. Possible explanations for our data include an effect of BK channels on development of the NMJ, a role for BK channels in regulating presynaptic Ca2+ current or the effectiveness of Ca2+ in triggering release. Consistent with reduced Ca2+ entry or effectiveness of Ca2+ in triggering release, use of 3,4-diaminopyridine to widen action potentials normalized evoked release in BK−/− mice to WT levels. Intraperitoneal application of 3,4-diaminopyridine fully restored in vivo nerve-stimulated muscle force in BK−/− mice. Our work demonstrates that mice lacking BK channels have weakness due to a defect in vesicle release at the NMJ