UMLS:C0019829 - FACTA Search

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Query: UMLS:C0019829 (Hodgkin's disease)
30,247 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

High-resistance microelectrodes were used to measure membrane potential changes in response to increased extracellular K+ concentration ([K+]o; or a test cation X+ such as Li+, Rb+, Cs+, NH+4) in B cells from mouse islets of Langerhans. In the absence of glucose, a sudden increase in [K+]o (or [X+]o), keeping the sum [Na+]o + [K+]o constant (or [Na+]o + [K+]o + [X+]o), induced a rapid depolarization of the membrane. The membrane potential changes were essentially unchanged in the presence of 20 mM tetraethylammonium (TEA). The Goldman-Hodgkin-Katz equation was fitted to the experimental relationship between membrane potential and [K+]o (or [X+]o), and permeability (P) ratios were estimated. In the absence of TEA, P Na/PK was estimated to be approximately 0.046. In the presence of TEA the following ratios were estimated: P Rb/PK = 0.74, P Cs/PK = 0.62, and P NH4/PK = 0.36. From these ratios the following sequence of permeabilities was obtained, PK greater than P Rb greater than P Cs greater than P NH4 greater than P Na. It is proposed that this sequence reflects the selectivity of the intracellular [Ca2+]-activated K+ channel of the pancreatic B cell.
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PMID:Potassium channel selectivity in mouse pancreatic B cells. 241 95

This chapter reviews what is known of the voltage-dependent conductances of three classes of vertebrate nerve cell, as assessed by somatic voltage clamping. These classes are: (1) bullfrog paravertebral sympathetic ganglion cells; (2) rodent superior cervical sympathetic ganglion cells; and (3) rodent hippocampal pyramidal cells. Of these, bullfrog neurons are the most thoroughly characterized. They possess at least seven distinct voltage-activated conductances. Two of these, called GNa and GCa, carry inward, depolarizing current. They both activate rapidly, and can, under appropriate conditions, generate action potentials. The remaining five conductances are all potassium-mediated, and can thus in principle produce hyperpolarizations or repolarize the action potential. However, because each of these potassium conductances have different sizes, speeds, and voltage thresholds, they play a variety of hyperpolarizing, stabilizing, or braking roles. IC is large, fast, and voltage dependent. Action potentials trigger calcium influx, which rapidly turns on IC. This repolarizes the action potential and turns off IC. However another Ca-dependent current, IAHP, remains active even at negative potentials and leads to a prolonged hyperpolarization. If IC is blocked, spike repolarization slows somewhat, allowing the Hodgkin-Huxley delayed rectifier current IK to develop. This is also large enough to repolarize the spike rapidly, although it is normally preempted by IC. IA and IM are other small potassium currents that activate at more negative potentials than do IC, IK, and IAHP. IA is a transient outward current that mainly influences voltage trajectories following hyperpolarizing current pulses. IM activates progressively during prolonged depolarizing current pulses, and, together with IAHP, explains most of the adaptation seen in these cells. The harmonious counterpoint of this septet of currents explains most of the electrical excitability properties of these cells. However, several of the currents are also synaptically regulated, as a result of transmitters acting on muscarinic or peptide receptors. These slow synaptic actions can lead to dramatic changes in the electrical behavior of the cells. These currents all appear to be present in rat sympathetic ganglion cells also, although detailed analysis here has been hampered by the more complex geometry of these neurons. Furthermore, the roles of the various currents have not been completely defined. It seems possible that IA can contribute to spike repolarization, and clean separation of IC and IAHP has not yet been achieved.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Voltage-dependent currents of vertebrate neurons and their role in membrane excitability. 242 89

Action potentials, macroscopic ionic currents and single channel currents were recorded from growth cones of Aplysia right upper quadrant (r.u.q.) cells in culture, using the patch-clamp technique. Recordings were obtained from both intact growth cones and from growth cones that had been mechanically isolated from the rest of the neurone. In current-clamp mode, greater than half of the isolated growth cones display an all-or-none action potential when depolarized above 0 mV with outward current pulses. The remaining growth cones display only a graded depolarization that is unaffected by tetrodotoxin (TTX). In whole-cell voltage clamp almost all isolated growth cones display a rapidly activating and inactivating inward current followed by a delayed outward current in response to depolarizations positive to -20 mV. The rapid inward current reverses direction at around +70 to +80 mV and is completely suppressed by 100 microM-TTX, which suggests that this current is carried by the fast Hodgkin-Huxley sodium current channels. The delayed outward current appears to result from the activation of both the delayed rectifier potassium current, IK, and the calcium-activated potassium current, IC. The growth cones do not display any prominent early transient outward current, IA. The sodium current, INA, was studied in isolation by substituting caesium for potassium ions in the pipette solution. INa is half-inactivated at a holding potential of -36 mV, reaches half-maximal activation with a depolarization to 0 mV, and has a mean peak current density of 13 microA/cm2. The time course of inactivation is well described by a single exponential (tau = 3 ms at 0 mV). In cell-attached patches, a rapidly activating and inactivating inward current channel was recorded with an average unit conductance of 6.9 pS. The activation and inactivation parameters of the ensemble averaged current closely match the measured values from the macroscopic sodium current. At very positive potentials we recorded a voltage-dependent outward current channel with a conductance of around 35 pS. No significant inward calcium current was observed in whole-cell measurements and few single calcium channel currents were measured in cell-attached patches, suggesting a sparse distribution of calcium channels in the r.u.q. growth cones.
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PMID:Action potentials, macroscopic and single channel currents recorded from growth cones of Aplysia neurones in culture. 242 3

A quantitative description of the time-dependent and voltage-sensitive outward currents in heart has been hampered by the complications inherent to the multicellular preparations previously used. We have used the whole-cell patch-clamp technique to record the delayed outward K+ current, IK, in single cells dissociated from frog atrium. Na+ currents were blocked with tetrodotoxin and Ca2+ currents with Mn2+ or Cd2+. After depolarizations from -50 mV to potentials positive to -30 mV, a time-dependent outward current was observed. This current has been characterized according to its steady state activation, kinetics, and ion transfer function. The current is well described as a single Hodgkin-Huxley conductance. The deactivation of the current is a single exponential. Activation of the current is sigmoid and is fitted well by raising the activation variable to the second power. The reversal potential of IK is near EK and shifts by 57 mV/10-fold change in [K+]o. This suggests that the current is carried selectively by K ions. The threshold for activation is near -30 mV. IK is maximally activated positive to +20 mV and shows no inactivation. The fully activated current-voltage relationship is linear between -110 and +50 mV. Neither Ba2+ (250 microM) nor Cd2+ (100 microM) affects IK.
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PMID:A time-dependent and voltage-sensitive K+ current in single cells from frog atrium. 243 57

Individual myocytes were isolated from bullfrog atrium by enzymatic and mechanical dispersion, and a one-microelectrode voltage clamp was used to record the slow outward K+ currents. In normal [K+]o (2.5 mM), the slow outward current tails reverse between -95 and -100 mV. This finding, and the observed 51-mV shift of Erev/10-fold change in [K+]o, strongly suggest that the "delayed rectifier" in bullfrog atrial cells is a K+ current. This current, IK, plays an important role in initiating repolarization, and it is distinct from the quasi-instantaneous, inwardly rectifying background current, IK. In atrial cells, IK does not exhibit inactivation, and very long depolarizing clamp steps (20 s) can be applied without producing extracellular K+ accumulation. The possibility of [K+]o accumulation contributing to these slow outward current changes was assessed by (a) comparing reversal potentials measured after short (2 s) and very long (15 s) activating prepulses, and (b) studying the kinetics of IK at various holding potentials and after systematically altering [K+]o. In the absence of [K+]o accumulation, the steady state activation curve (n infinity) and fully activated current-voltage (I-V) relation can be obtained directly. The threshold of the n infinity curve is near -50 mV, and it approaches a maximum at +20 mV; the half-activation point is approximately -16 mV. The fully activated I-V curve of IK is approximately linear in the range -40 to +30 mV. Semilog plots of the current tails show that each tail is a single-exponential function, which suggests that only one Hodgkin-Huxley conductance underlies this slow outward current. Quantitative analysis of the time course of onset of IK and of the corresponding envelope of tails demonstrate that the activation variable, n, must be raised to the second power to fit the sigmoid onset accurately. The voltage dependence of the kinetics of IK was studied by recording and curve-fitting activating and deactivating (tail) currents. The resulting 1/tau n curve is U-shaped and somewhat asymmetric; IK exhibits strong voltage dependence in the diastolic range of potentials. Changes in the [Ca2+]o in the superfusing Ringer's, and/or addition of La3+ to block the transmembrane Ca2+ current, show that the time course and magnitude of IK are not significantly modulated by transmembrane Ca2+ movements, i.e., by ICa. These experimentally measured voltage- and time-dependent descriptors of IK strongly suggest an important functional role for IK in atrial tissue: it initiates repolarization and can be an important determinant of rate-induced changes in action potential duration.
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PMID:A time- and voltage-dependent K+ current in single cardiac cells from bullfrog atrium. 243 58

The development of the intracellular perfusion technique made isolated nerve cells an extremely convenient object for the detailed study of calcium channels, which allow the corresponding ions to enter the cell through the surface membrane during excitation. A wide range of investigations conducted in this object has shown that calcium channels, allowing the passage of bivalent cations in the order of preference Ba greater than Sr greater than Ca greater than Mg, bind these ions with the aid of a binding group located inside the channel. Other bivalent cations (Co, Ni, Mn, Cd), which bind too strongly with this group, become competitive channel blockers. In the absence of bivalent cations in the extracellular medium the calcium channels lose their selectivity and begin to transmit monovalent cations effectively; the reason for this transformation is detachment of the bound calcium ions from a special regulating group at the mouth of the calcium channels. Calcium channels can exist in two functional states: conducting and nonconducting. The transition between these states is accompanied by movement of charges inside the membrane ("gating currents"). The statistical kinetics of this transition, like the kinetics of gating currents, can be described by a modified Hodgkin-Huxley equation, with an activation variable raised to the power of 2. During long-term membrane depolarization the calcium channels pass into an inactivated state, which is connected with the recurrent blocking action of calcium ions, entering the cell, on the channels. Meanwhile, for some types of calcium channels, potential-dependent activation analogous to that in sodium or potassium channels is observed.
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PMID:Calcium channels in the cell membrane. 243 85

We have developed a model to predict the effects of temperature on the electrical activity of a hippocampal pyramidal cell. Four populations of membrane channels in the pyramidal cell were simulated. Equations for current through these ion channels are similar to those first developed by Hodgkin and Huxley for Na+ and K+ channels in the squid axon and more recently extended by Traub to include not only these channel types but, in addition, Ca2+ and Ca2+ mediated K+ channels in hippocampal cells. Voltage- and/or concentration-dependent rate functions are used to describe the kinetic behavior of each population of channels. A temperature-dependent term is included for each rate function to simulate the effect of changing temperature on neural activity. Model simulations correspond to experimental data over a range of temperature from 40 degrees C to 35 degrees C.
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PMID:A simulation of the effects of temperature on hippocampal neurons. 244 4

1. Ganglion cells were dissociated from the enzyme-treated rat retina, identified with specific fluorescent labels, and maintained in vitro. Electrophysiological properties of solitary retinal ganglion cells were investigated with both conventional intracellular and patch-clamp recordings. Although comparable results were obtained for most measurements some important differences were noted. 2. The input resistance of solitary retinal ganglion cells was considerably higher when measured with 'giga-seal' suction pipettes than with conventional intracellular electrodes. Under current-clamp conditions with both intracellular and patch pipettes, these central mammalian neurones maintained resting potentials of about -60 mV and displayed action potentials followed by an after-hyperpolarization in response to small depolarizations. The membrane currents during this activity, analysed under voltage clamp with patch pipettes, consisted of five components: Na+ current (INa), Ca2+ current (ICa), and currents with properties similar to the delayed outward, the transient (A-type), and the Ca2+-activated K+ currents (IK, IA and IK(Ca), respectively). 3. Ionic substitution, pharmacological agents, and voltage-clamp experiments revealed that the regenerative currents were carried by both Na+ and Ca2+. 100 nM-1 microM-tetradotoxin (TTX) reversibly blocked the fast spikes carried by the presumptive INa, which under voltage-clamp analysis had classical Hodgkin-Huxley-type activation and inactivation. 4. Single-channel recordings of the Na+ current (iNa) permitted comparison of these 'microscopic' events with the 'macroscopic' whole-cell current (INa). The inactivation time constant (tau h) fitted to the averaged single-channel recordings of iNa in outside-out patches was slower than the tau h obtained during whole-cell recordings of INa. 5. In the presence of 1-40 microM-TTX and 20 mM-TEA, slow action potentials appeared in intracellular recordings and were probably mediated by Ca2+. The potentials were abrogated by 3 mM-Co2+ or 200 microM-Cd2+; conversely, increasing the extracellular Ca2+ concentration from 2.5 to 10-25 mM or substitution of 1 mM-Ba2+ for 2.5 mM-Ca2+ enhanced their amplitude. ICa was measured directly in whole-cell recordings with patch pipettes after blocking INa with extracellular 1 microM-TTX and K+ currents with intracellular 120-mM Cs+ and 20 mM-TEA. 6. During whole-cell recordings with patch electrodes, extracellular 20 mM-TEA suppressed IK and, to a lesser extent, IA. Extracellular 5 mM-4-AP or a pre-pulse of the membrane potential to -40 mV prior to stronger depolarization completely blocked IA.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Voltage-dependent conductances of solitary ganglion cells dissociated from the rat retina. 244 69

1. Monovalent cation selectivity and divalent cation sensitivity of the tetrodotoxin (TTX)-resistant Na+ current in dissociated adult rat nodose ganglion neurones were investigated using the whole-cell patch-clamp technique. 2. The TTX-resistant Na+ current was isolated using ion substitution and pharmacological agents. Under these conditions, the current reversal potential shifted 52 mV per tenfold change in external [Na+]. 3. Inorganic and organic monovalent cation permeability ratios (Px/PNa) were determined from changes in reversal potential and the Goldman-Hodgkin-Katz equation. The Px/PNa values determined by the former method were HONH3+, 1.38; Li+, 1.00; H2NNH3+, 0.66; NH4+, 0.28; CH3NH3+, less than 0.13; K+, less than 0.13; Rb+, less than 0.12; Cs+, less than 0.10; (CH3)4N+, less than 0.10. The values determined by either method agreed within 10%. 4. The effects of Cd2+, Co2+, Mn2+ and Ni2+ on the TTX-resistant Na+ current were analysed from peak-conductance values. These ions shifted the activation of the current to more positive potentials and decreased the maximal conductance. At 3 mM concentrations, Cd2+, Ni2+, Co2+ and Mn2+ decreased the maximal conductance 64.6, 50.7, 25.0 and 20.3%, respectively. 5. The results indicate that: (a) the monovalent cation selectivity of the TTX-resistant Na+ current is similar to that of the TTX-sensitive Na+ current in other tissues; and (b) the TTX-resistant Na+ current is less sensitive to divalent cations than the Ca2+ current in these neurones. These observations suggest that the structure determining the monovalent cation permeability of the TTX-resistant Na+ current is similar to that of the TTX-sensitive Na+ current in other tissues, and that the channels carrying the TTX-resistant Na+ current are distinct from those responsible for the Ca2+ current.
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PMID:Tetrodotoxin-resistant sodium current of rat nodose neurones: monovalent cation selectivity and divalent cation block. 244 74

1. Neurones were isolated from the CA1 region of the guinea-pig hippocampus and subjected to the whole-cell mode of voltage clamping, to determine the kinetics of voltage-gated Ca2+ channel activation. 2. Isolated neurones had an abbreviated morphology, having lost most of the distal dendritic tree during the isolation procedure. The electrical compactness of the cells facilitates voltage clamp analysis. 3. Block of sodium and potassium currents revealed a persistent current activated on depolarization above -40 mV, which inactivated slowly when the intracellular medium contained EGTA. The current was blocked by Co2+ and Cd2+, augmented by increases in Ca2+ and could be carried by Ba2+, suggesting that the current is borne by Ca2+. 4. Steady-state activation of the Ca2+ current was found to be well described by the Boltzman equation raised to the second power. 5. The open channel's current-voltage (I-V) relationship rectified in the inward direction and was consistent with the constant-field equation. 6. The kinetics of Ca2+ current onset followed m2 kinetics throughout the range of its activation. Tail current kinetics were in accord with this model. A detailed Hodgkin-Huxley model was derived, defining the activation of this current. 7. The kinetics of the currents observed in this regionally and morphologically defined class of neurones were consistent with the existence of a single kinetic class of channels.
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PMID:Calcium current activation kinetics in isolated pyramidal neurones of the Ca1 region of the mature guinea-pig hippocampus. 245 32

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