Sodium current in ventricular myocardial fibers

Membrane currents were measured in thin bundles of dog ventricular myocardium under voltage-clamp conditions. A rather large initial inward current which had an equilibrium potential at about + 55 millivolts could be recorded. When the external sodium concentration was reduced, the equilibrium potential for this current was shifted by the amount predicted theoretically for a current carried solely by sodium ions. The size of the sodium inward current (I(Na)) was largely dependent on the preceding membrane potential. The I(Na) was completely inactivated if the membrane potential was as low as -45 millivolts. Sodium ions are the main carrier of charge during the rapid depolarization phase of the action potential.     

Membrane currents examined under voltage clamp in cultured neuroblastoma cells

Examination of ionic membrane currents in a voltage-clamped neuronal cell line derived from the mouse C1300 neuroblastoma disclosed four kinetically different components: sodium, potassium, calcium, and leakage current. The kinetics, voltage dependence, and pharmacological properties of the sodium and potassium currents qualitatively resemble those of the corresponding currents in squid giant axon and frog myelinated nerve fiber, suggesting that the molecular structures of the sodium and potassium channels in neuroblastoma are similar to those of the non-mammalian preparations.     

Autonomic regulation of a chloride current in heart

In isolated heart cells, beta-adrenergic receptor stimulation induced a background current that was suppressed by simultaneous muscarinic receptor stimulation. Direct activation of adenylate cyclase with forskolin also elicited this current, suggesting regulation by adenosine 3',5'-monophosphate (cAMP). This current could be recorded when sodium, calcium, and potassium currents were eliminated by channel antagonists or by ion substitution. Alteration of the chloride equilibrium potential produced changes in the reversal potential expected for a chloride current. Activation of this chloride current modulated action potential duration and altered the resting membrane potential in a chloride gradient-dependent manner.     

DDT: interaction with nerve membrane conductance changes

The falling phase of action potentials of lobster giant axons is prolonged by DDT; finally a plateau phase is produced like cardiac action potentials. In axons poisoned with DDT, peak transient (sodium) currents associated with step depolarizations are turned off very slowly, and steady-state (potassium) currents are markedly suppressed. These two changes would cause the prolongation of action potentials and are considered the major ionic mechanisms of DDT action.     

Tetraethylammonium ions: effect of presynaptic injection on synaptic transmission

Tetraethylammonium ions were injected into the presynaptic axon of the squid giant synapse. Injection of these ions caused prolongation of the action potential with decreased out ward current. The prolonged spike was associated with increased release and prolonged activity of the transmitter substance. Although the amplitude of the postsynaptic potential increased with presynaptic depolarization, strong depolarization blocked transmitter re lease. In the injected presynaptic axon, transmitter release was blocked by 10(-6) gram of tetrodotoxin per milliliter. Transmitter release appears to be under control of presynaptic potential levels.     

Tetrodotoxin does not block excitation from inside the nerve membrane

Tetrodotoxin does not block the action potential or membrane sodium current when internally perfused through the giant axon of a squid at much higher concentrations than those required for blocking by external application. It is suggested that the gate for the sodium channel is located on the exterior surface of the axon, because tetrodotoxin is not lipid soluble.     

Ionic basis of the photoresponse of Aplysia giant neuron: K + permeability increase

The giant neuron of the Aplysia abdominal ganglion hyperpolarizes during illumination. The light-initiated potential change is associated with an increase of membrane conductance. It reverses sign at the potassium equilibrium potential (about -83 millivolts), which was determined from direct measurements of internal potassium activity. The membrane hyperpolarization is produced entirely by a light-induced increase in potassium permeability.     

Synaptic transmission between dissociated adult mammalian neurons and attached synaptic boutons

In most studies of synaptic currents in mammalian central neurons, preparations have been used in which synaptic currents are recorded at some distance from the synapse itself. This procedure introduces problems in interpretation of the kinetics and voltage-dependent properties of the synaptic current. These problems have now been overcome by the development of a preparation in which presynaptic vesicle-containing boutons have been coisolated with the soma of individual neurons, thus providing the opportunity to study synaptic currents under conditions of both adequate voltage control and internal ionic perfusion. Spontaneous synaptic currents mediated by gamma-aminobutyric acid and excitatory amino acids were recorded from neurons isolated from a mammalian medial solitary tract nucleus. Calcium- and depolarization-dependent spontaneous currents of several to hundreds of picoamperes occurred with rapid rise times of 0.8 to 3 milliseconds and decays at least ten times as long.     

Beta-adrenergic inhibition of cardiac sodium channels by dual G-protein pathways

The signaling pathways by which beta-adrenergic agonists modulate voltage-dependent cardiac sodium currents are unknown, although it is likely that adenosine 3'5'-monophosphate (cAMP) is involved. Single-channel and whole-cell sodium currents were measured in cardiac myocytes and the signal transducing G protein Gs was found to couple beta-adrenergic receptors to sodium channels by both cytoplasmic (indirect) and membrane-delimited (direct) pathways. Hence, Gs can act on at least three effectors in the heart: sodium channels, calcium channels, and adenylyl cyclase. The effect on sodium currents was inhibitory and was enhanced by membrane depolarization. During myocardial ischemia the sodium currents of depolarized cells may be further inhibited by the accompanying increase in catecholamine levels.     

西沙群岛海域砗磲资源的调查

砗磲是珊瑚岛礁的构成物种,对维护珊瑚礁生态系统平衡起着重要作用。近年来,由于非法捕捞和海洋生态环境影响,对我国西沙砗磲资源造成严重威胁。为掌握西沙海域砗磲资源现状,笔者于2017年6—7月采用截线样带法,对西沙主要岛礁海域砗磲的种类、分布及其与环境相关性进行了分析。结果显示,调查海域共发现4种砗磲：鳞砗磲(Tridacna squamosa)、长砗磲(T.maxima)、番红砗磲(T.crocea)和砗蚝(Hippopus hippopus),分别占总数的71.9%、15.6%、9.4%和3.1%。西沙不同岛礁海域砗磲密度、物种多样性指数存在显著差异,砗磲平均密度为0.026个·m^-2。砗磲密度与珊瑚覆盖率呈显著正相关(P<0.05,R²=0.706 5),表明珊瑚覆盖率是影响砗磲分布的重要因素。     

Ca2+ and Ca2+-activated K+ currents in mammalian gastric smooth muscle cells

Inward movement of calcium through voltage-dependent channels in muscle is thought to initiate the action potential and trigger contraction. Calcium-activated potassium channels carry large outward potassium currents that may be responsible for membrane repolarization. Calcium and calcium-activated potassium currents were identified in enzymatically isolated mammalian gastric myocytes. These currents were blocked by cadmium and nifedipine but were not substantially affected by diltiazem or D600. No evidence for a tetrodotoxin-sensitive sodium current or an inwardly rectifying potassium current was found.     

Electrophysiological studies of chilean squid axons under internal perfusion with sodium-rich media

Electrophysiological properties of giant axons of Chilean squid were examined by intracellular perfusion combined with various recording techniques. The amplitude of the action potential of the axons perfused with equal sodium concentrations (0.35M) on both sides of the membrane was approximately 75 millivolts (glutamate salts being used internally); the resting potential recorded with a calomel electrode was roughly 45 mv. These observations confirm and extend previous data, obtained from Chilean squid axons, which show that the amplitude of the action-potential overshoot does not agree with the Nernst equation applied to sodium ion. The discrepancy between these results and those obtained by others is attributed to differences in the procedures used to determine the resting potential.     

Calcium transient in presynaptic terminal of squid giant synapse: detection with aequorin

Microinjection of aequorin, a bioluminescent protein sensitive tocalcium, into the presynaptic terminal of the squid giant synapse demnonstrated an increase in intracellular calcium ion concentration during repetitive synaptic transmission. Although no light flashes synchronous with individual presynaptic : tion potentials were detected, the results are considered consistent with the hypothesis that entry of calcium into the presynaptic terminal triggers release of e synaptic transmitter substance.     

The molecular basis of acid insensitivity in the African naked mole-rat

Acid evokes pain by exciting nociceptors; the acid sensors are proton-gated ion channels that depolarize neurons. The naked mole-rat (Heterocephalus glaber) is exceptional in its acid insensitivity, but acid sensors (acid-sensing ion channels and the transient receptor potential vanilloid-1 ion channel) in naked mole-rat nociceptors are similar to those in other vertebrates. Acid inhibition of voltage-gated sodium currents is more profound in naked mole-rat nociceptors than in mouse nociceptors, however, which effectively prevents acid-induced action potential initiation. We describe a species-specific variant of the nociceptor sodium channel Na(V)1.7, which is potently blocked by protons and can account for acid insensitivity in this species. Thus, evolutionary pressure has selected for an Na(V)1.7 gene variant that tips the balance from proton-induced excitation to inhibition of action potential initiation to abolish acid nociception.     

A voltage sensor-domain protein is a voltage-gated proton channel

Voltage-gated proton channels have been widely observed but have not been identified at a molecular level. Here we report that a four-transmembrane protein similar to the voltage-sensor domain of voltage-gated ion channels is a voltage-gated proton channel. Cells overexpressing this protein showed depolarization-induced outward currents accompanied by tail currents. Current reversal occured at equilibrium potentials for protons. The currents exhibited pH-dependent gating and zinc ion sensitivity, two features which are characteristic of voltage-gated proton channels. Responses of voltage dependence to sequence changes suggest that mouse voltage-sensor domain-only protein is itself a channel, rather than a regulator of another channel protein.     

Neuronal calcium sensor 1 and activity-dependent facilitation of P/Q-type calcium currents at presynaptic nerve terminals

P/Q-type presynaptic calcium currents (IpCa) undergo activity-dependent facilitation during repetitive activation at the calyx of the Held synapse. We investigated whether neuronal calcium sensor 1 (NCS-1) may underlie this phenomenon. Direct loading of NCS-1 into the nerve terminal mimicked activity-dependent IpCa facilitation by accelerating the activation time of IpCa in a Ca2+-dependent manner. A presynaptically loaded carboxyl-terminal peptide of NCS-1 abolished IpCa facilitation. These results suggest that residual Ca2+ activates endogenous NCS-1, thereby facilitating IpCa. Because both P/Q-type Ca2+ channels and NCS-1 are widely expressed in mammalian nerve terminals, NCS-1 may contribute to the activity-dependent synaptic facilitation at many synapses.     

Evidence for ectopic neurotransmission at a neuronal synapse

Neurotransmitter release is well known to occur at specialized synaptic regions that include presynaptic active zones and postsynaptic densities. At cholinergic synapses in the chick ciliary ganglion, however, membrane formations and physiological measurements suggest that release distant from postsynaptic densities can activate the predominantly extrasynaptic alpha7 nicotinic receptor subtype. We explored such ectopic neurotransmission with a novel model synapse that combines Monte Carlo simulations with high-resolution serial electron microscopic tomography. Simulated synaptic activity is consistent with experimental recordings of miniature excitatory postsynaptic currents only when ectopic transmission is included in the model, broadening the possibilities for mechanisms of neuronal communication.     

Spin-torque switching with the giant spin Hall effect of tantalum

Spin currents can apply useful torques in spintronic devices. The spin Hall effect has been proposed as a source of spin current, but its modest strength has limited its usefulness. We report a giant spin Hall effect (SHE) in β-tantalum that generates spin currents intense enough to induce efficient spin-torque switching of ferromagnets at room temperature. We quantify this SHE by three independent methods and demonstrate spin-torque switching of both out-of-plane and in-plane magnetized layers. We furthermore implement a three-terminal device that uses current passing through a tantalum-ferromagnet bilayer to switch a nanomagnet, with a magnetic tunnel junction for read-out. This simple, reliable, and efficient design may eliminate the main obstacles to the development of magnetic memory and nonvolatile spin logic technologies.     

Voltage-dependent sodium channels in an invertebrate striated muscle

Striated skeletal muscles from the planktonic arrowworm Sagitta elegans (phylum Chaetognatha) were voltage-clamped. The muscles displayed classical voltage-dependent sodium channels that (i) showed peak transient currents when the membrane was depolarized 90 millivolts from rest, (ii) opened rapidly with peak currents flowing within 0.4 milliseconds at 4 degrees C, (iii) showed voltage-dependent inactivation with 50 percent inactivation at +25 millivolts from rest, and (iv) were blocked by 500 nanomolar tetrodotoxin.     

Emergence of posttetanic potentiation as a distinct phase in the differentiation of an identified synapse in Aplysia

The developmental time course of posttetanic potentiation was studied at an identified chemical synapse. In stage 11 juveniles (3 weeks after metamorphosis), the synaptic connections made by cholinergic neuron L10 onto postsynaptic neurons L2 to L6 were present but showed no posttetanic potentiation. In stage 13 adults (12 weeks after metamorphosis), the same tetanus resulted in an increase of 300 percent in the synaptic potential. A similar pattern was observed at two other identified synapses in the abdominal ganglion. Thus, the initial steps in synapse formation do not include the expression of this plastic capability. Rather, at least 10 weeks is required between the onset of synaptic function and the final expression of mature synaptic properties.