Conductance Characteristics of Interactive Subunit Membranes

1975 ◽  
Vol 30 (7-8) ◽  
pp. 535-537 ◽  
Author(s):  
A. H. Bretag ◽  
D. I. B. Kerr
Keyword(s):  
Special Form ◽  
Potassium Conductance ◽  
Membrane Conductance ◽  
Membrane Channels ◽  
Subunit Interaction ◽  
Simple Basis

Abstract Membrane channels formed by groups of subunits with a special form of interaction between the subunits provide a simple basis for models of membrane conductance. It is shown how the subunit interaction can explain conductance kinetics; particular attention being paid to characteristics of the potassium conductance in the squid piant axon.

Serotonin has different effects on two classes of Betz cells from the cat

1994 ◽  
Vol 72 (4) ◽  
pp. 1925-1937 ◽  
Author(s):  
W. J. Spain
Keyword(s):  
Firing Rate ◽  
Potassium Conductance ◽  
Membrane Conductance ◽  
Constant Current ◽  
Repetitive Firing ◽  
Calcium Dependent ◽  
Constant Current Stimulation ◽  
Ionic Mechanisms ◽  
Betz Cells

1. Intracellular recording from cat Betz cells in vitro revealed a strong correlation between the dominant effect of serotonin (5-HT) and the Betz cell subtype in which it occurred. In large Betz cells that show posthyperpolarization excitation (termed PHE cells), 5-HT evoked a long-lasting membrane depolarization, whereas 5-HT evoked an initial hyperpolarization of variable duration in smaller Betz cells that show posthyperpolorization inhibition (termed PHI cells). 2. Voltage-clamp studies revealed that 5-HT caused a depolarizing shift of activation of the cation current Ih, which resulted in the depolarization in PHE cells, whereas the hyperpolarization in PHI cells is caused by an increase in a resting potassium conductance. 3. The effect of 5-HT on firing properties during constant current stimulation also differed consistently in the two types of Betz cells. In PHE cells the initial firing rate increased after 5-HT application, but the steady firing was unaffected. The depolarizing shift of Ih activation caused the increase of initial firing rate. 4. In PHI cells 5-HT caused a decrease in spike frequency adaptation. The decrease in adaptation was caused by a combination of two conductance changes. First, 5-HT caused a slow afterdepolarization in PHI cells that could trigger repetitive firing in the absence of further stimulation. The sADP depended on calcium entry through voltage-gated channels and was associated with a decrease in membrane conductance. Second, 5-HT caused reduction of a slow calcium-dependent potassium current that normally contributes to slow adaptation. 5. In conclusion, the effect of 5-HT on excitability differs systematically in Betz cell subtypes in part because they have different dominant ionic mechanisms that are modulated. If we assume that PHE cells and PHI cells represent fast and slow pyramidal tract (PT) neurons respectively, 5-HT will cause early recruitment of fast PT cells and delay recruitment of slow PT cells during low levels of synaptic excitation.

scholarly journals Cholecystokinin B-Type Receptors Mediate a G-Protein-Dependent Depolarizing Action of Sulphated Cholecystokinin Ocatapeptide (CCK-8s) on Rodent Neonatal Spinal Ventral Horn Neurons

2007 ◽  
Vol 98 (3) ◽  
pp. 1108-1114 ◽  
Author(s):  
Murat Oz ◽  
Keun-Hang Yang ◽  
Toni S. Shippenberg ◽  
Leo P. Renaud ◽  
Michael J. O'Donovan
Keyword(s):  
Spinal Cord ◽  
G Protein ◽  
Time Course ◽  
Neuronal Excitability ◽  
Potassium Conductance ◽  
Membrane Conductance ◽  
Ventral Horn ◽  
Similar Time ◽  
Inward Current ◽  
Cck Receptors

Reports of cholecystokinin (CCK) binding and expression of CCK receptors in neonatal rodent spinal cord suggest that CCK may influence neuronal excitability. In patch-clamp recordings from 19/21 ventral horn motoneurons in neonatal (PN 5–12 days) rat spinal cord slices, we noted a slowly rising and prolonged membrane depolarization induced by bath-applied sulfated CCK octapeptide (CCK-8s; 1 μM), blockable by the CCKB receptor antagonist L-365,260 (1 μM). Responses to nonsulfated CCK-8 or CCK-4 were significantly weaker. Under voltage clamp ( VH −65 mV), 22/24 motoneurons displayed a CCK-8s-induced tetrodotoxin-resistant inward current [peak: −136 ± 28 pA] with a similar time course, mediated via reduction in a potassium conductance. In 29/31 unidentified neurons, CCK-8s induced a significantly smaller inward current (peak: −42.8 ± 5.6 pA), and I-V plots revealed either membrane conductance decrease with net inward current reversal at 101.3 ± 4.4 mV ( n = 16), membrane conductance increase with net current reversing at 36.1 ± 3.8 mV ( n = 4), or parallel shift ( n = 9). Intracellular GTP-γ-S significantly prolonged the effect of CCK-8s ( n = 6), whereas GDP-β-S significantly reduced the CCK-8s response ( n = 6). Peak inward currents were significantly reduced after 5-min perfusion with N-ethylmaleimide. In isolated neonatal mouse spinal cord preparations, CCK-8s (30–300 nM) increased the amplitude and discharge of spontaneous depolarizations recorded from lumbosacral ventral roots. These observations imply functional postsynaptic G-protein-coupled CCKB receptors are prevalent in neonatal rodent spinal cord.

Analysis of decreased conductance serotonergic response in Aplysia ink motor neurons

1985 ◽  
Vol 53 (2) ◽  
pp. 590-602 ◽  
Author(s):  
J. P. Walsh ◽  
J. H. Byrne
Keyword(s):  
Cell Body ◽  
Motor Neurons ◽  
Potassium Conductance ◽  
Membrane Conductance ◽  
Resting Potential ◽  
Slow Inward Current ◽  
Equilibrium Potential ◽  
Voltage Sensitivity ◽  
Inward Current ◽  
Bath Application

Micropressure ejection of serotonin (5-hydroxytryptamine, 5-HT) produced excitatory responses in the L14 ink motor neurons of Aplysia that depended on the site of application. Ejection of 5-HT onto the cell body produced a slow response that showed variability in voltage sensitivity between preparations. In contrast, ejection of 5-HT onto the neuropil underneath the cell body produced a response whose amplitude was consistently a linear function of the holding potential, reversing near the predicted potassium equilibrium potential. Subsequent analyses focused on this second response. The neuropil response induced by 5-HT had a linear current-voltage relationship (reversing at ca. -80 mV), was associated with a decrease in input conductance, and was sensitive to changes in the concentration of extracellular K+. Serotonin application in artificial seawater (ASW) containing 30 mM K+ produced a response that reversed close to the altered Nernst potential for K+. The 5-HT response did not appear to be due to secondary activation of interneurons or to depend primarily on extracellular Ca2+, since ejection of 5-HT onto cells bathed in ASW containing 30 mM Co2+ produced responses comparable to, although somewhat attenuated from, those observed in ASW. Serotonin responses similar to those produced in ASW were obtained after perfusing the ganglion with ASW containing Co2+, 4-aminopyridine (4-AP), and tetraethylammonium (TEA). This suggests that the 5-HT-sensitive current is separate from the Ca2+-activated, fast, and delayed rectifying K+ currents. The 5-HT response appeared to be mediated by changes in levels of cAMP. Bath application of the phosphodiesterase inhibitors IBMX (3-isobutyl-1-methylxanthine) or Ro 20-1724, or the adenylate cyclase activator forskolin mimicked the 5-HT response by producing a slow inward current associated with a decrease in membrane conductance. Alteration of cellular cAMP metabolism modulated the response to 5-HT. Exposure of the ganglion to low concentrations of either Ro 20-1724 or forskolin potentiated the 5-HT response. Higher concentrations of these agents largely blocked the response to subsequent 5-HT applications. Bath application of the 8-bromo derivative of either cAMP or cGMP produced a slow inward current associated with a decrease in membrane conductance in cells voltage clamped at the resting potential. Responses to 5-HT were blocked, however, after exposure to 8-bromo-cAMP, but not to 8-bromo-cGMP. These results suggest that 5-HT produces a voltage-independent decrease in a steady-state potassium conductance that may be mediated by cAMP.(ABSTRACT TRUNCATED AT 400 WORDS)

Development of membrane conductance of chick skeletal muscle in culture

1980 ◽  
Vol 58 (6) ◽  
pp. 600-605 ◽  
Author(s):  
C. M. Thomson ◽  
W. F. Dryden
Keyword(s):  
Skeletal Muscle ◽  
Membrane Potential ◽  
Initial Level ◽  
Potassium Conductance ◽  
Membrane Conductance ◽  
Resting Membrane Potential ◽  
Membrane Conductances ◽  
Rapid Changes ◽  
Fibre Development

Resting membrane potentials and membrane conductances of chick skeletal muscle in culture were determined from the 3rd to the 10th day after plating. The effect of tetraethylammonium (TEA) and of replacement of potassium with caesium on these parameters was investigated. Resting membrane potential (Em) rises during myogenesis in vitro and resting membrane conductance (Gm) falls. The initial level of Gm was relatively high (1.2 mS cm−2) but this fell to a final level around 0.2 mS cm−2. The most rapid changes in both parameters occurred between days 3 and 5 of culture. Both TEA and caesium depressed Em and Gm at all stages of development. On the 3rd day of culture Gm was reduced by 0.2 mS cm−2 by both agents. Thereafter, Gm was depressed by about 0.1 mS cm−2. Caesium does not penetrate potassium channels and the reduction in Gm is attributed to block of these channels. This indicates that resting potassium conductance is relatively constant at 0.1 mS cm−2 throughout muscle fibre development. Because TEA produces changes in Gm similar to those produced by caesium, TEA is concluded to be acting at the potassium channel in a manner similar to caesium.

scholarly journals Multiple Serotonin-Activated Currents in Isolated, Neuronal Somata from Locust Thoracic Ganglia

1992 ◽  
Vol 165 (1) ◽  
pp. 43-60 ◽  
Author(s):  
ISABEL BERMUDEZ ◽  
DAVID J. BEADLE ◽  
JACK A. BENSON
Keyword(s):  
Membrane Potential ◽  
Potassium Conductance ◽  
Membrane Conductance ◽  
Membrane Potentials ◽  
Potential Range ◽  
Neuronal Somata ◽  
Sodium Permeability ◽  
Fast Kinetics ◽  
Thoracic Ganglia ◽  
Slow Kinetics

1. Three different responses were evoked by pressure micro-application of serotonin onto freshly dissociated, current- and voltage-clamped neuronal somata from the thoracic ganglia of the locust Locusta migratoria. 2. In some neurones, an inward current, I(5HT)K, resulting from a decrease in potassium conductance, with slow kinetics and maximum activation at membrane potentials of −60 to - 70 mV, was evoked by serotonin and by the 5-HT3 agonist 2-methyl serotonin. This current was completely abolished by either 10 mmoll−1 caesium or 5 mmoll−1 rubidium and partially blocked by 50 mmoll−1 tetraethylammonium or 5 mmoll−1 4-aminopyridine. The response was antagonised by the 5-HT2-specific compounds, ketanserin and ritanserin. 3. In other somata, serotonin, 2-methyl serotonin and the 5-HT3 antagonist ICS205 930 evoked a second current, I(5HT)Na, which was due to an increase in sodium permeability and had slow kinetics similar to that of I(5HT)K. This current was inward over the membrane potential range −30 to - 80 mV and increased with hyperpolarisation. The response was blocked by sodium-free saline and the 5-HT3 receptor antagonist MDL 72222. 4. In other neurones, at membrane potentials more positive than - 50 mV, serotonin pulses could activate a third current, I(5HT)X, which increased with depolarisation of the membrane potential and had comparatively fast kinetics. Activation of the current was accompanied by a decrease in membrane conductance. This response was completely blocked by 4-aminopyridine and weakly inhibited by both caesium and tetraethylammonium and is, therefore, probably a potassium current. 5. The three currents described here differ in their pharmacology, their ionic mechanisms and their dependence on membrane potential from the serotoninactivated currents reported for vertebrates and they provide evidence for the mechanism of action of serotonin as a neurotransmitter in insects. Note: Present address: Pharmacology Institute, University of Zurich, Gloriastrasse 32, CH-8006 Zurich, Switzerland.

Electrophysiological Evidence for Vasopressin V1Receptors on Neonatal Motoneurons, Premotor and Other Ventral Horn Neurons

2001 ◽  
Vol 86 (3) ◽  
pp. 1202-1210 ◽  
Author(s):  
Murat Oz ◽  
Miloslav Kolaj ◽  
Leo P. Renaud
Keyword(s):  
Spinal Cord ◽  
Potassium Conductance ◽  
Membrane Conductance ◽  
Ventral Horn ◽  
Rat Spinal Cord ◽  
Neural Excitability ◽  
Axon Terminals ◽  
Glutamatergic Neurons ◽  
Inward Currents ◽  
Developing Rat

Prominent arginine-vasopressin (AVP) binding and AVP V1 type receptors are expressed early in the developing rat spinal cord. We sought to characterize their influence on neural excitability by using patch-clamp techniques to record AVP-induced responses from a population of motoneurons and interneurons in neonatal (5–18 days) rat spinal cord slices. Data were obtained from 58 thoracolumbar (T7–L5) motoneurons and 166 local interneurons. A majority (>90%) of neurons responded to bath applied AVP (10 nM to 3 μM) and (Phe2, Orn8)-vasotocin, a V1receptor agonist, but not V2 or oxytocin receptor agonists. In voltage-clamp, postsynaptic responses in motoneurons were characterized by slowly rising, prolonged (7–10 min) and tetrodotoxin-resistant inward currents associated with a 25% reduction in a membrane potassium conductance that reversed near −100 mV. In interneurons, net AVP-induced inward currents displayed three patterns: decreasing membrane conductance with reversal near −100 mV, i.e., similar to that in motoneurons (24 cells); increasing conductance with reversal near −40 mV (21 cells); small reduction in conductance with no reversal within the current range tested (41 cells). A presynaptic component recorded in most neurons was evident as an increase in the frequency but not amplitude (in motoneurons) of inhibitory and excitatory postsynaptic currents (IPSCs and EPSCs), in large part due to AVP-induced firing in inhibitory (mainly glycinergic) and excitatory (glutamatergic) neurons synapsing on the recorded cells. An increase in frequency but not amplitude of miniature IPSCs and EPSCs also indicated an AVP enhancement of neurotransmitter release from axon terminals of inhibitory and excitatory interneurons. These observations provide support for a broad presynaptic and postsynaptic distribution of AVP V1 type receptors and indicate that their activation can enhance the excitability of a majority of neurons in neonatal ventral spinal cord.

Increase of membrane conductance by adrenaline in the smooth muscle of guinea-pig taenia coli

1969 ◽  
Vol 172 (1027) ◽  
pp. 89-102 ◽  
Keyword(s):  
Smooth Muscle ◽  
Potassium Concentration ◽  
Potassium Conductance ◽  
Membrane Conductance ◽  
Membrane Resistance ◽  
Taenia Coli ◽  
High Potassium ◽  
External Potassium ◽  
Sucrose Gap ◽  
Muscle Cell Membrane

(1) The double sucrose-gap method was used to record changes in membrane resistance in intestinal smooth muscle strips. (2) Adrenaline reduced the membrane resistance; it hyperpolarized the membrane and blocked spontaneous and evoked spikes. (3) When the membrane potential was shifted by applying conditioning current, the hyperpolarization produced by adrenaline was larger during depolarization and smaller during hyperpolarization. The hyperpolarization caused by adrenaline was converted into depolarization by 18 to 20 mV conditioning hyperpolarization. (4) The resting membrane resistance was increased in the absence of potassium and in low external chloride (replaced with benzene- or ethane-sulphonate); it was decreased by excess potassium and by nitrate substitution for chloride. (5) The reduction of the membrane resistance by adrenaline was potentiated by high external potassium and by replacement of chloride with nitrate; it was diminished by low external potassium and by replacement of chloride with benzene- or ethane-sulphonate. (6) The hyperpolarization by adrenaline was reduced by raising the external potassium concentration; it was increased by lowering the external potassium concentration. In a solution containing low chloride and high potassium (24 m M ), adrenaline often produced depolarization. (7) It was concluded that adrenaline increases mainly the potassium conductance and also the chloride conductance of the smooth muscle cell membrane. Sodium seemed to be less important for the adrenaline action.

GABAB and adenosine receptors mediate enhancement of the K+ current, IAHP, by reducing adenylyl cyclase activity in rat CA3 hippocampal neurons

1994 ◽  
Vol 72 (5) ◽  
pp. 2360-2367 ◽  
Author(s):  
U. Gerber ◽  
B. H. Gahwiler
Keyword(s):  
Adenylyl Cyclase ◽  
Voltage Clamp ◽  
Hippocampal Neurons ◽  
Potassium Conductance ◽  
Membrane Conductance ◽  
Pyramidal Cells ◽  
Gabab Receptors ◽  
Cyclase Activity ◽  
Adenylyl Cyclase Activity ◽  
Similar Reduction

1. Gamma-aminobuturic acid-B (GABAB) and adenosine A1 receptors, which are expressed in hippocampal pyramidal cells, are linked to pertussis toxin-sensitive G-proteins known to be coupled negatively to the enzyme adenylyl cyclase. This study investigates the electrophysiological consequences of adenylyl cyclase inhibition in response to stimulation of these receptors. 2. Single-electrode voltage-clamp recordings were obtained from CA3 pyramidal cells in rat hippocampal slice cultures in presence of tetrodotoxin. The calcium-dependent potassium current (IAHP), which is very sensitive to intracellular levels of adenosine 3',5'-cyclic monophosphate (cAMP), was used as an electrophysiological indicator of adenylyl cyclase activity. 3. Application of baclofen (10 microM), a selective agonist at GABAB receptors, or adenosine (50 microM) each resulted in a transient decrease followed by a significant enhancement in the amplitude of evoked IAHP. The initial reduction in amplitude of IAHP probably reflects inadequacies in voltage clamp of electronically distant dendritic sites, due to the shunting caused by concomitant activation of potassium conductance by baclofen/adenosine. Comparable increases in membrane conductance in response to the GABAA agonist, muscimol, caused a similar reduction in IAHP. The enhancement of IAHP is consistent with an inhibition of constitutively active adenylyl cyclase. 4. The receptor mediating the responses to adenosine was identified as belonging to the A1 subtype on the basis of its sensitivity to the selective antagonist 8-cyclopentyl-1,3-dipropylxanthine.(ABSTRACT TRUNCATED AT 250 WORDS)

The effects of L-glutamate and its analogues upon the membrane conductance of central murine neurones in culture

1982 ◽  
Vol 60 (3) ◽  
pp. 282-296 ◽  
Author(s):  
J. F. MacDonald ◽  
J. M. Wojtowicz
Keyword(s):  
Amino Acids ◽  
Membrane Potential ◽  
Divalent Cations ◽  
Potassium Conductance ◽  
Membrane Conductance ◽  
Multiple Receptors ◽  
Voltage Dependent ◽  
Apparent Decrease ◽  
Brain And Spinal Cord ◽  
Related Compounds

Neurones from brain and spinal cord of foetal mice were grown dissociated in monolayer cultures for 4–6 weeks prior to electropharmacological analysis. Neurones were immersed in a Hanks balanced salt solution while drugs and ions were applied by pressure microperfusion during intracellular recordings obtained by conventional techniques. L-Glutamate and its analogues, L-aspartate, DL-homocysteate, N-methyl-D-aspartate, and DL-ibotenate activated two distinct mechanisms of excitation. The primary effect was depolarization accomplished by an apparent decrease of neurone input conductance (Gm). However, in most instances an expected increase in Gm was also observed, especially if membrane potential was reduced by tonic depolarization. Another glutamate analogue, DL-kainate, never decreased Gm and invariably increased Gm at all membrane potentials tested. The decrease of Gm evoked by glutamate and related compounds was strongly dependent upon membrane potential. It was most pronounced at potentials near resting values (−40 to −60 mV) and diminished both with depolarization or hyperpolarization from this range. This apparent decrease favoured the electrogenesis of regenerative potentials that were insensitive to tetrodotoxin. A voltage-dependent increase in sodium and(or) calcium conductance (GNa, GCa) or a decrease in potassium conductance (GK) is suggested to account for this decrease in Gm. Divalent cations (Mg and Co) reduced the depolarizing actions of all amino acids except for those to kainate. The decrease in Gm was more sensitive to Mg than was the increase of Gm. However, the receptor antagonist DL-α-aminoadipate blocked both changes in conductance and responses to all amino acids with the exception of those to kainate. The possible existence of multiple receptors for glutamate is also discussed.

scholarly journals The Action of Certain Polyvalent Cations on the Voltage-Clamped Lobster Axon

1968 ◽  
Vol 51 (3) ◽  
pp. 279-291 ◽  
Author(s):  
M. P. Blaustein ◽  
D. E. Goldman
Keyword(s):  
Metal Ions ◽  
Potassium Conductance ◽  
Binding Constants ◽  
Membrane Conductance ◽  
Giant Axon ◽  
Transition Metal Ions ◽  
Cation Binding ◽  
Axon Membrane ◽  
High Calcium ◽  
Excitation Processes

Calcium appears to be an essential participant in axon excitation processes. Many other polyvalent metal ions have calcium-like actions on axons. We have used the voltage-clamped lobster giant axon to test the effect of several of these cations on the position of the peak initial (sodium) and steady-state (potassium) conductance vs. voltage curves on the voltage axis as well as on the rate parameters for excitation processes. Among the alkaline earth metals, Mg+2 is a very poor substitute for Ca+2, while Ba+2 behaves like "high calcium" when substituted for Ca+2 on a mole-for-mole basis. The transition metal ions, Ni+2, Co+2, and Cd+2 also act like high calcium when substituted mole-for-mole. Among the trivalent ions, La+3 is a very effective Ca+2 replacement. Al+3 and Fe+3 are extremely active and seem to have some similar effects. Al+3 is effective at concentrations as low as 10-5 M. The data suggest that many of these ions may interact with the same cation-binding sites on the axon membrane, and that the relative effects on the membrane conductance and rate parameters depend on the relative binding constants of the ions. The total amount of Na+ transferred during a large depolarizing transient is nearly independent of the kind or amount of polyvalent ion applied.

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