Effects of EGTA on the calcium-activated afterhyperpolarization in hippocampal CA3 pyramidal cells

Intracellular recordings in the hippocampal slice preparation were made with electrodes filled with 0.2 molar potassium EGTA. The purpose was to investigate the role of calcium in mediating afterhyperpolarizations following bursts evoked by intracellular current pulses, arising spontaneously, or induced by the epileptogenic agent pencillin. In the first two cases the afterhyperpolarization was blocked and the associated conductance increase was reduced, suggesting that EGTA was blocking the calcium-activated potassium conductance during the hyperpolarization. In the third case the afterhyperpolarization and associated conductance increase persisted, implicating an alternative mechanism for the hyperpolarization. ?2Ns 04053     

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.     

Cyclic adenosine and guaosine monophosphates and gucagon: effect on liver membrane potentials

Cyclic adenosine monophosphate, cyclic guanosine monophosphate, glucagon, and isoproterenol each hyperpolarized perfused rat liver cells. The hyperpolarization followed a time course similar to the stimulated increase in potassium efflux and was preceded by the increase in calcium efflux. The hyperpolarization induced by cyclic adenosine monophosphate was blocked by tetracaine. The similarity of the action of the cyclic nucleotides to that of glucagon supports the hypothesis that cyclic adenosine monophosphate is the secondary messenger mediating the action of glucagon.     

External calcium ions are required for potassium channel gating in squid neurons

The effects of calcium removal on the voltage-dependent potassium channels of isolated squid neurons were studied with whole cell patch-clamp techniques. When the calcium ion concentration was lowered from 10 to 0 millimolar (that is, no added calcium), potassium channel activity, identified from its characteristic time course, disappeared within a few seconds and there was a parallel increase in resting membrane conductance and in the holding current. The close temporal correlation of the changes in the three parameters suggests that potassium channels lose their ability to close in the absence of calcium and simultaneously lose their selectivity. If potassium channels were blocked by barium ion before calcium ion was removed, the increases in membrane conductance and holding current were delayed or prevented. Thus calcium is an essential cofactor in the gating of potassium channels in squid neurons.     

Mechanism of the rapid effect of 17 beta-estradiol on medial amygdala neurons

The mechanism by which sex steroids rapidly modulate the excitability of neurons was investigated by intracellular recording of neurons in rat medial amygdala brain slices. Brief hyperpolarization and increased potassium conductance were produced by 17 beta-estradiol. This effect persisted after elimination of synaptic input and after suppression of protein synthesis. Thus, 17 beta-estradiol directly changes the ionic conductance of the postsynaptic membrane of medial amygdala neurons. In addition, a greater proportion of the neurons from females than from males responded to 17 beta-estradiol.     

Crayfish muscle fiber: ionic requirements for depolarizing synaptic electrogenesis

Presence of sodium in the bathing medium is not essential for the electrically excitable depolarizing electrogenesis of crayfish muscle fibers, production of action potentials being dependent on calcium. The depolarizing electrogenesis of the excitatory synaptic membrane component does require sodium, however, and this ion cannot be replaced by lithium as it can in spike electrogenesis of many cells. Ionophoretic applications of glutamate, which in the presence of sodium depolarize the cell by activating the excitatory synaptic membrane, are without effect in the absence of sodium. Not only is there no depolarization, but the membrane conductance also remains unchanged. Thus, in the absence of inward movement of sodium across the synaptic membrane there is also no outward movement of potassium. Accordingly, it seems that increased conductance for potassium is not an independent process in the synaptic membrane, whereas it is independent of sodium activation in spike electrogenesis. Chloride activation is independent, however; increase in conductance and the electrogenesis of the inhibitory synaptic component are not affected by the absence of sodium. Implications of these findings regarding the structure of differently excitable membrane components are discussed.     

Ionic mechanisms controlling behavioral responses of paramecium to mechanical stimulation

A mechanical stimulus applied to the anterior part of Paramecium causes a transient increase in membrane permeability to calcium. This permits a calcium current to flow into the cell, causing the membrane potential to approach the equilibrium level for calcium. The transient depolarization which results elicits a reversal in the direction of ciliary beat. When the organisms are free-swimming this is seen as the reversed locomotion of Jennings' "avoiding reaction." In contrast, a mechanical stimulus applied to the posterior part results in increased permeability to potassium ions, and hence an outward potassium current. The hyperpolarization which results causes an increase in the frequency of ciliary beat in the normal direction. In free-swimming specimens this is seen as an increase in the velocity of forward locomotion.     

Slow synaptic excitation in sympathetic ganglion cells: evidence for synaptic inactivation of potassium conductance

The slow excitatory postsynaptic potential (EPSP) was investigated in frog sympathetic ganglion cells. In contrast to the increased conductance associated with other known EPSP's, during the slow EPSP resting membrane conductance was decreased. Electrical depolarization of the membrane potentiated the slow EPSP, whereas progressive hyperpolarization decreased its size and then reversed it to a hyperpolarizing potential (the opposite of the effect of membrane polarization on other EPSP's). The reversal potential of the slow EPSP was close to the potassium equilibrium potential. We propose that the slow EPSP, in contrast to classical EPSP's, is generated by an inactivation of resting potassium conductance.     

In vivo Ca2+ dynamics in a cricket auditory neuron: an example of chemical computation

Fura-2 calcium imaging in the cricket omega neuron revealed increased intracellular free calcium ion concentration in response to simulated cricket calling songs and other sound stimuli. The time course of the increase and decrease in intracellular calcium coincided with the time course of forward masking, a time-dependent modulation of auditory sensitivity. The buffering of calcium transients with high concentrations of a kinetically fast calcium buffer eliminated the post-stimulus hyperpolarization associated with forward masking, whereas the uncaging of calcium inside the neuron produced a hyperpolarization. The results suggest that sound-stimulated intracellular calcium accumulation acts by means of a calcium-activated hyperpolarizing current to produce forward masking. These findings underscore the importance of chemical dynamics in neural computation by demonstrating a behaviorally relevant role of calcium dynamics in vivo.     

Control of membrane N+ permeability in a hyperpolarizing photoreceptor: similar effect of light and metabolic inhibitors

In the hyperpolarizing photoreceptors of the scallop Pecten irradians the metabolic inhibitors cyani 'e and 2,4-dinitrophenol cause a rapid hyperpolarization and increase in membrane permeability to potassium ions, similar to the effect of light. Cellular metabolism appears important in maintaining the low permeability to potassium ions necessary to keep the membrane depolarized in darkness, possibly by regulating the intracellular calcium ion concentration.     

Mediation of responses to calcium in taste cells by modulation of a potassium conductance

Calcium salts are strong taste stimuli in vertebrate animals. However, the chemosensory transduction mechanisms for calcium are not known. In taste buds of Necturus maculosus (mud puppy), calcium evokes depolarizing receptor potentials by acting extracellularly on the apical ends of taste cells to block a resting potassium conductance. Therefore, divalent cations elicit receptor potentials in taste cells by modulating a potassium conductance rather than by permeating the cell membrane, the mechanism utilized by monovalent cations such as sodium and potassium ions.     

Direct activation of mammalian atrial muscarinic potassium channels by GTP regulatory protein Gk

The mammalian heart rate is regulated by the vagus nerve, which acts via muscarinic acetylcholine receptors to cause hyperpolarization of atrial pacemaker cells. The hyperpolarization is produced by the opening of potassium channels and involves an intermediary guanosine triphosphate-binding regulatory (G) protein. Potassium channels in isolated, inside-out patches of membranes from atrial cells now are shown to be activated by a purified pertussis toxin-sensitive G protein of subunit composition alpha beta gamma, with an alpha subunit of 40,000 daltons. Thus, mammalian atrial muscarinic potassium channels are activated directly by a G protein, not indirectly through a cascade of intermediary events. The G protein regulating these channels is identified as a potent Gk; it is active at 0.2 to 1 pM. Thus, proteins other than enzymes can be under control of receptor coupling G proteins.     

不同形态氮素对玉米秸秆腐解与养分释放的影响

为研究不同形态氮素对玉米秸秆腐解和养分释放的影响,采用尼龙网袋法进行室内堆腐试验,通过外源添加碳酸氢铵、硫酸铵、硝酸钙、尿素和谷氨酸等不同形态氮素调节玉米秸秆C/N（25：1）,以不添加氮素处理为对照（CK）。结果表明,随着培养时间的延长,添加不同形态氮素处理的玉米秸秆质量残留率逐渐降低,谷氨酸、硫酸铵和碳酸氢铵均能促进玉米秸秆的降解,其中谷氨酸对玉米秸秆的促腐作用最强,腐解速率常数达到2.8×10^-2 d^-1。尿素对玉米秸秆腐解无明显影响,硝酸钙一定程度上减缓了玉米秸秆的腐解。玉米秸秆腐解过程中养分释放率呈钾>磷>氮的规律。随着培养时间的延长,添加不同形态氮素处理的玉米秸秆碳、氮、磷和钾素质量残留率逐渐降低。培养到180 d时,玉米秸秆残余物中碳、氮、磷和钾素残留质量分别是其初始质量的16.9%~24.8%、21.57%~51.27%、22.72%~59.00%和24.86%~54.48%,其中谷氨酸对玉米秸秆碳、氮和钾素释放促进作用最强,其释放速率常数分别为1.37×10^-2、7.15×10^-3 d^-1和5.62×10^-3 d^-1;而硫酸铵能够促进秸秆中磷的释放,其释放速率常数为7.94×10^-3 d^-1,高于CK处理（7.54×10^-3 d^-1）。研究表明,谷氨酸会提高玉米秸秆的腐解速率与碳、氮和钾素的释放,硫酸铵会提高玉米秸秆的腐解速率与碳、氮、磷素的释放,碳酸氢铵会提高玉米秸秆的腐解速率与氮素的释放,尿素和硝酸钙会促进碳、氮、钾养分的释放,谷氨酸和硫酸铵的促腐效应高于其他形态氮素处理。从还田秸秆快速腐解和养分释放及高效利用角度考虑,秸秆还田后施用谷氨酸和硫酸铵效果最佳。     

Stretch-inactivated ion channels coexist with stretch-activated ion channels

Stretch-activated ion channels of animal, plant, bacterial, and fungal cells are implicated in mechanotransduction and osmoregulation. A new class of channel has now been described that is stretch-inactivated. These channels occur in neurons, where they coexist with stretch-activated channels. Both channels are potassium selective. The differing stretch sensitivities of the two channels minimize potassium conductance over an intermediate range of tension, with the consequence that, over this same range, voltage-gated calcium channels are most readily opened. Thus, by setting the relation between membrane tension and transmembrane calcium fluxes, stretch-sensitive potassium channels may participate in the control of calcium-dependent motility in differentiating, regenerating, or migrating neurons.     

BKCa-Cav channel complexes mediate rapid and localized Ca2+-activated K+ signaling

Large-conductance calcium- and voltage-activated potassium channels (BKCa) are dually activated by membrane depolarization and elevation of cytosolic calcium ions (Ca2+). Under normal cellular conditions, BKCa channel activation requires Ca2+ concentrations that typically occur in close proximity to Ca2+ sources. We show that BKCa channels affinity-purified from rat brain are assembled into macromolecular complexes with the voltage-gated calcium channels Cav1.2 (L-type), Cav2.1 (P/Q-type), and Cav2.2 (N-type). Heterologously expressed BKCa-Cav complexes reconstitute a functional "Ca2+ nanodomain" where Ca2+ influx through the Cav channel activates BKCa in the physiological voltage range with submillisecond kinetics. Complex formation with distinct Cav channels enables BKCa-mediated membrane hyperpolarization that controls neuronal firing pattern and release of hormones and transmitters in the central nervous system.     

Increased numbers of ion channels promoted by an intracellular second messenger

The anomalous rectifier potassium current in Aplysia neurons was examined to determine the immediate cause of an increase in conductance induced by serotonin and mediated by adenosine 3',5'-monophosphate. Voltage-dependent cesium ion block and steady-state current power spectral density were measured under voltage clamp before and after application of serotonin. The amplitude of the anomalous rectifier conductance was increased by adding serotonin, but the shapes of the conductance-voltage curve and the power spectrum were not altered. Calculation of the number of functional channels and of the single-channel conductance from the power spectra indicates that the serotonin-induced increase in conductance resulted from an increase in the number of functional channels, while the single-channel conductance and the open-channel probability were unchanged.     

Long-term synaptic potentiation

Long-term synaptic potentiation (LTP) is a leading candidate for a synaptic mechanism of rapid learning in mammals. LTP is a persistent increase in synaptic efficacy that can be quickly induced. The biophysical process that controls one type of LTP is formally similar to a synaptic memory mechanism postulated decades ago by the psychologist Donald Hebb. A key aspect of the modification process involves the N-methyl-D-aspartate (NMDA) receptor-ionophore complex. This ionophore allows calcium influx only if the endogenous ligand glutamate binds to the NMDA receptor and if the voltage across the associated channel is also sufficiently depolarized to relieve a magnesium block. According to one popular hypothesis, the resulting increase in the intracellular calcium concentration activates protein kinases that enhance the postsynaptic conductance. Further biophysical and molecular understanding of the modification process should facilitate detailed explorations of the mnemonic functions of LTP.     

Residual calcium ions depress activation of calcium-dependent current

Calcium ions enter and accumulate during depolarization of some cells, activating a potassium current, IK(Ca), that depends on the cytoplasmic concentration of calcium ions, [Ca]i. However, elevation of [Ca]i can depress IK(Ca) elicited by a subsequent membrane depolarization. The depression of IK(Ca) is ascribed here to a [Ca]i-mediated inactivation of the voltage-gated calcium conductance, which causes a net reduction in calcium ions available for the activation of IK(Ca). This suggests that other processes dependent on gated calcium entry may also be depressed by small background elevations in cytosolic free calcium ions.     

A G protein couples serotonin and GABAB receptors to the same channels in hippocampus

Both serotonin and the selective gamma-aminobutyric acidB (GABAB) agonist, baclofen, increase potassium (K+) conductance in hippocampal pyramidal cells. Although these agonists act on separate receptors, the potassium currents evoked by the agonists are not additive, indicating that the two receptors share the same potassium channels. Experiments with hydrolysis-resistant guanosine triphosphate (GTP) and guanosine diphosphate analogs and pertussis toxin indicate that the opening of the potassium channels by serotonin and GABAB receptors involves a pertussis toxin-sensitive GTP-binding (G) protein, which may directly couple the two receptors to the potassium channel.     

Generation of adrenergic and cholinergic potentials in sympathetic ganglion cells

Norepinephrine elicited a hyperpolarizing response, and acetylcholine (during nicotinic blockade) elicited a depolarizing one. Both responses showed no increase in membrane conductance. The norepinephrine response was suppressed by initial depolarization; the acetylcholine response (frog cells); by hyperpolarization. These neurotransmitters apparently can activate electrogenic mechanisms which do not involve movement of ions down their electrochemical gradients.