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Kinetic and pharmacological properties of the M‐current in rodent neuroblastoma x glioma hybrid cells.

Kinetic and pharmacological properties of the M‐current in rodent neuroblastoma x glioma hybrid... 1. The M‐like current IK(M,ng) in differentiated NG108‐15 mouse neuroblastoma x rat glioma hybrid cells has been studied using tight‐seal, whole‐cell patch‐clamp recording. 2. When calculated from steady‐state current‐voltage curves, the conductance underlying IK(M,ng) showed a Boltzmann dependence on voltage with half‐activation voltage Vo = ‐44 mV (in 3 mM (K+)) and slope factor (a) = 8.1 mV/e‐fold increase in conductance. In 12 mM (K+) Vo = ‐38 mV and a = 6.9 mV. The deactivation reciprocal time constant accelerated with hyperpolarization with slope factor 17 mV/e‐fold voltage change. 3. The reversal potential for deactivation tail currents varied with external (K+) as if PNa/PK were 0.005. 4. Steady‐state current was increased on removing external Ca2+. In the presence of external Ca2+, reactivation of IK(M, ng) after a hyperpolarizing step was delayed. This delay was preceded by an inward Ca2+ current, and coincided with an increase in intracellular (Ca2+) as measured with Indo‐1 fluorescence. Elevation of intracellular (Ca2+) with caffeine also reduced IK(M, ng). 5. IK(M, ng) was inhibited by external divalent cations in decreasing order of potency (mM IC50 in parentheses): Zn2+ (0.011) greater than Cu2+ (0.018) greater than Cd2+ (0.070) greater than Ni2+ (0.44) greater than Ba2+ (0.47) greater than Fe2+ (0.69) greater than Mn2+ (0.86) greater than Co2+ (0.92) greater than Ca2+ (5.6) greater than Mg2+ (16) greater than Sr2+ (33). This was not secondary to inhibition of ICa since: (i) inhibition persisted in Ca(2+)‐free solution; (ii) La3+ did not inhibit IK(M, ng) at concentrations which inhibited ICa; and (iii) organic Ca2+ channel blockers were ineffective. Inhibition comprised both depression of the maximum conductance and a positive shift of the activation curve. Addition of Ca2+ (10 microM free (Ca2+)) or Ba2+ (1 mM total (Ba2+)) to the pipette solution did not significantly change IK(M, ng). 6. IK(M, ng) was reduced by 9‐amino‐1,2,3,4‐tetrahydroacridine (IC50 8 microM) and quinine (30 microM) but was insensitive to tetraethylammonium (IC50 greater than 30 mM), 4‐aminopyridine (greater than 10 mM), apamin (greater than 3 microM) or dendrotoxin (greater than 100 nM). 7. IK(M, ng) was inhibited by bradykinin (1‐10 microM) or angiotensin II (1‐10 microM), but not by the following other receptor agonists: acetylcholine (10 mM), muscarine (10 microM), noradrenaline (100 microM), adrenaline (100 microM), dopamine (100 microM), histamine (100 microM), 5‐hydroxytryptamine (10 microM), Met‐enkephalin (1 microM), glycine (100 microM), gamma‐aminobutyric acid (100 microM) or baclofen (500 microM).(ABSTRACT TRUNCATED AT 400 WORDS) http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png The Journal of Physiology Wiley

Kinetic and pharmacological properties of the M‐current in rodent neuroblastoma x glioma hybrid cells.

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References (50)

Publisher
Wiley
Copyright
© 2014 The Physiological Society
ISSN
0022-3751
eISSN
1469-7793
DOI
10.1113/jphysiol.1992.sp019159
Publisher site
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Abstract

1. The M‐like current IK(M,ng) in differentiated NG108‐15 mouse neuroblastoma x rat glioma hybrid cells has been studied using tight‐seal, whole‐cell patch‐clamp recording. 2. When calculated from steady‐state current‐voltage curves, the conductance underlying IK(M,ng) showed a Boltzmann dependence on voltage with half‐activation voltage Vo = ‐44 mV (in 3 mM (K+)) and slope factor (a) = 8.1 mV/e‐fold increase in conductance. In 12 mM (K+) Vo = ‐38 mV and a = 6.9 mV. The deactivation reciprocal time constant accelerated with hyperpolarization with slope factor 17 mV/e‐fold voltage change. 3. The reversal potential for deactivation tail currents varied with external (K+) as if PNa/PK were 0.005. 4. Steady‐state current was increased on removing external Ca2+. In the presence of external Ca2+, reactivation of IK(M, ng) after a hyperpolarizing step was delayed. This delay was preceded by an inward Ca2+ current, and coincided with an increase in intracellular (Ca2+) as measured with Indo‐1 fluorescence. Elevation of intracellular (Ca2+) with caffeine also reduced IK(M, ng). 5. IK(M, ng) was inhibited by external divalent cations in decreasing order of potency (mM IC50 in parentheses): Zn2+ (0.011) greater than Cu2+ (0.018) greater than Cd2+ (0.070) greater than Ni2+ (0.44) greater than Ba2+ (0.47) greater than Fe2+ (0.69) greater than Mn2+ (0.86) greater than Co2+ (0.92) greater than Ca2+ (5.6) greater than Mg2+ (16) greater than Sr2+ (33). This was not secondary to inhibition of ICa since: (i) inhibition persisted in Ca(2+)‐free solution; (ii) La3+ did not inhibit IK(M, ng) at concentrations which inhibited ICa; and (iii) organic Ca2+ channel blockers were ineffective. Inhibition comprised both depression of the maximum conductance and a positive shift of the activation curve. Addition of Ca2+ (10 microM free (Ca2+)) or Ba2+ (1 mM total (Ba2+)) to the pipette solution did not significantly change IK(M, ng). 6. IK(M, ng) was reduced by 9‐amino‐1,2,3,4‐tetrahydroacridine (IC50 8 microM) and quinine (30 microM) but was insensitive to tetraethylammonium (IC50 greater than 30 mM), 4‐aminopyridine (greater than 10 mM), apamin (greater than 3 microM) or dendrotoxin (greater than 100 nM). 7. IK(M, ng) was inhibited by bradykinin (1‐10 microM) or angiotensin II (1‐10 microM), but not by the following other receptor agonists: acetylcholine (10 mM), muscarine (10 microM), noradrenaline (100 microM), adrenaline (100 microM), dopamine (100 microM), histamine (100 microM), 5‐hydroxytryptamine (10 microM), Met‐enkephalin (1 microM), glycine (100 microM), gamma‐aminobutyric acid (100 microM) or baclofen (500 microM).(ABSTRACT TRUNCATED AT 400 WORDS)

Journal

The Journal of Physiology – Wiley

Published: Jun 1, 1992

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