Contribution of a non‐inactivating potassium current to the resting membrane potential of fusion‐competent human myoblasts.

Bernheim, Laurent; Liu, J. H.; Hamann, Martine; Haenggeli, Charles-Antoine; Fischer-Lougheed, Jacqueline; Bader, Charles

doi:10.1113/jphysiol.1996.sp021369

Cited by 34 publications

(52 citation statements)

References 28 publications

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“…7). An ether-à-go-go K ϩ current is expressed first and hyperpolarizes fusioncompetent myoblasts to an intermediate resting potential of approximately Ϫ30 mV (12,29,30). Then, slightly before fusion, the expression of an inward rectifier K ϩ current causes fusioncompetent myoblasts to hyperpolarize further to approximately Ϫ65 mV (11).…”

Section: Discussionmentioning

confidence: 99%

T-type α1H Ca ²⁺ channels are involved in Ca ²⁺ signaling during terminal differentiation (fusion) of human myoblasts

Bijlenga¹,

Liu²,

Espinos³

et al. 2000

Proc. Natl. Acad. Sci. U.S.A.

177

194

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Mechanisms underlying Ca 2؉ signaling during human myoblast terminal differentiation were studied using cell cultures. We found that T-type Ca 2؉ channels (T-channels) are expressed in myoblasts just before fusion. Their inhibition by amiloride or Ni 2؉ suppresses fusion and prevents an intracellular Ca 2؉ concentration increase normally observed at the onset of fusion. The use of antisense oligonucleotides indicates that the functional T-channels are formed by ␣1H subunits. At hyperpolarized potentials, these channels allow a window current sufficient to increase [Ca 2؉ ]i. As hyperpolarization is a prerequisite to myoblast fusion, we conclude that the Ca 2؉ signal required for fusion is produced when the resting potential enters the T-channel window. A similar mechanism could operate in other cell types of which differentiation implicates membrane hyperpolarization.

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Section: Discussionmentioning

confidence: 99%

T-type α1H Ca ²⁺ channels are involved in Ca ²⁺ signaling during terminal differentiation (fusion) of human myoblasts

Bijlenga¹,

Liu²,

Espinos³

et al. 2000

Proc. Natl. Acad. Sci. U.S.A.

177

194

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“…The mean input conductance was 1-35 + 0 03 nS, with a range of 0-2-4-0 nS (n = 379), measured with an instantaneous current induced by a 10-20 mV hyperpolarizing step from -60 mV. The leak conductance was 0-2 + 0 04 nS (n = 10), estimated by the residual current response to a 20 mV test pulse in the presence of 1 SMITTX, 300 /M Co2+, 3 mm Cs+, 1 mm Ba2P and 100 mm TEA, with NaCl reduced to maintain the osmolarity (Bernheim, Liou, Hamann, Haenggeli, Fischer-Lougheed & Bader, 1996). Unless stated, the leak current or conductance was not deducted from the values shown in the text and figures.…”

Section: Membrane Conductances and Their Circadian Changesmentioning

confidence: 99%

Membrane properties and synaptic inputs of suprachiasmatic nucleus neurons in rat brain slices.

Jiang

Yang

Liu

et al. 1997

The Journal of Physiology

104

100

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1. Whole-cell recordings were made from 390 neurons of the suprachiasmatic nucleus (SCN) in horizontal brain slices during different portions of the circadian day. The locomotor activity of the rats was measured prior to the preparation of brain slices to insure that each rat was entrained to a 12 h-12 h light-dark cycle. 2. The mean input conductance was 42% higher (1 fi58 nS) in neurons recorded near the subjective dawn than those (1 11 nS) recorded near the subjective dusk. The current required to hold the neurons at -60 mV also showed a circadian variation with a peak in the middle of the subjective day and a nadir in the middle of the subjective night. Analysis of the variations in the input conductance and the holding current at -60 mV suggested that at least two ion conductances are involved in the pacemaking of the circadian rhythms.3. Voltage-clamped SCN neurons often had both outward and inward spontaneous postsynaptic currents. The outward currents were blocked by bicuculline but not by strychnine, and were identified as IPSCs mediated by GABAA receptors. The inward currents were blocked by 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) and were identified as EPSCs mediated by glutamate. Most spontaneous synaptic currents were miniature currents but action potentialdependent large events were seen more often in IPSCs than in EPSCs. 4. Stimulation of the optic nerve or chiasm usually evoked a monosynaptic EPSC which was mediated by both NMDA and non-NMDA receptors. In 13% of cells, optic nerve stimulation evoked an outward current or an inward current followed by an outward current; all the evoked currents were blocked by 4-aminophosphonovaleric acid (APV) and CNQX whereas the outward current only was blocked by bicuculline, suggesting involvement of an inhibitory interneuron. 5. SCN neurons sum the excitatory inputs from both optic nerves; on average each SCN cell receives innervation from at least 4 8 retinohypothalamic tract (RHT) axons. 6. Focal stimulation in the vicinity of the recorded neuron revealed that nearly all SCN neurons receive local or extranuclear GABAergic inputs operating via GABAA receptors. The EPSCs activated by such stimulation were not significantly different in amplitude and pharmacological properties from those induced by RHT stimulation. 7. One hundred and one neurons were labelled with neurobiotin during whole-cell recording.Based on the dendritic structures, four types of SCN neurons (monopolar, radial, simple bipolar and curly bipolar) were identified. The curly bipolar cells had a higher membrane conductance, holding current and hyperpolarization-activated current (Ih) amplitude than the other neuronal types. Radial neurons did not respond to optic nerve stimulation, which activated EPSCs in the other cell types.Behavioural and physiological functions of mammals show (SCN), a paired hypothalamic structure lying dorsal to the daily patterns, called circadian rhythms.

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“…Typical K ϩ currents that show no inactivation upon depolarization are M currents (3,4), S currents (5), the standing outward current, I K(SO) , recently reported in cerebellar granule cells (6), and resembling currents in myoblasts (7). These currents have a common feature in that they begin to be activated from deep membrane potentials and are inhibited by neurotransmitters such as muscarinic agonists (4,6), bradykinin (3), and serotonin (5).…”

mentioning

confidence: 99%

KCR1, a Membrane Protein That Facilitates Functional Expression of Non-inactivating K+ Currents Associates with Rat EAG Voltage-dependent K+Channels

Hoshi

Takahashi

Shahidullah

et al. 1998

Journal of Biological Chemistry

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Cerebellar granule neurons possess a non-inactivating K؉ current, which controls resting membrane potentials and modulates the firing rate by means of muscarinic agonists. kcr1 was cloned from the cerebellar cDNA library by suppression cloning. KCR1 is a novel protein with 12 putative transmembrane domains and enhances the functional expression of the cerebellar non-inactivating K ؉ current in Xenopus oocytes. KCR1 also accelerates the activation of rat EAG K ؉ channels expressed in Xenopus oocytes or in COS-7 cells. FarWestern blotting revealed that KCR1 and EAG proteins interacted with each other by means of their C-terminal regions. These results suggest that KCR1 is the regulatory component of non-inactivating K ؉ channels.K ϩ channels are essential components of the plasma membranes of both excitable and non-excitable cells. Three major classes have been described for voltage-gated K ϩ currents in mammalian neurons: A-type currents with rapid inactivation, delayed rectifier currents with slow inactivation, and non-inactivating outward currents (1, 2). The first two classes play an important role in shaping action potentials during repolarization and in determining the interval of an action potential. The non-inactivating outward currents can modulate firing frequency upon receptor stimulation by neurotransmitters or produce resting membrane potentials.Typical K ϩ currents that show no inactivation upon depolarization are M currents (3, 4), S currents (5), the standing outward current, I K(SO) , recently reported in cerebellar granule cells (6), and resembling currents in myoblasts (7). These currents have a common feature in that they begin to be activated from deep membrane potentials and are inhibited by neurotransmitters such as muscarinic agonists (4, 6), bradykinin (3), and serotonin (5). Except for the many important items of physiological relevance identified for such currents, molecular bases for the responsible channels are poorly understood. The cloned K ϩ channels that exhibit non-inactivating currents are the aKv5.1 (8) and ether à go-go (EAG) 1 K ϩ channels (9, 10).Recently, it has been reported that the expression of Drosophila EAG K ϩ channels in oocytes results in a slow relaxation current resembling M currents (11). However, whether a rat homologue of EAG (r-EAG) contributes to the M channel has been the subject of much debate (12, 13).To characterize low-threshold non-inactivating K ϩ currents, we measured K ϩ currents in Xenopus oocytes injected with the cerebellar poly(A) ϩ RNA, in accordance with the report by Hoger et al. (14). We realized that low-threshold non-inactivating K ϩ currents (I K(ni) ), which are similar to I K(SO) , are expressed in oocytes injected with cerebellar poly(A) ϩ RNA. To clarify the molecular information for I K(ni) , we isolated a cDNA clone required for the functional channel protein for I K(ni) by suppression cloning, which in turn is based on the capacity of antisense single strand DNA to block the expression of I K(ni) in oocytes. This strategy enabled us...

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Contribution of a non‐inactivating potassium current to the resting membrane potential of fusion‐competent human myoblasts.

Cited by 34 publications

References 28 publications

T-type α1H Ca ²⁺ channels are involved in Ca ²⁺ signaling during terminal differentiation (fusion) of human myoblasts

T-type α1H Ca ²⁺ channels are involved in Ca ²⁺ signaling during terminal differentiation (fusion) of human myoblasts

Membrane properties and synaptic inputs of suprachiasmatic nucleus neurons in rat brain slices.

KCR1, a Membrane Protein That Facilitates Functional Expression of Non-inactivating K+ Currents Associates with Rat EAG Voltage-dependent K+Channels

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Contribution of a non‐inactivating potassium current to the resting membrane potential of fusion‐competent human myoblasts.

Cited by 34 publications

References 28 publications

T-type α1H Ca 2+ channels are involved in Ca 2+ signaling during terminal differentiation (fusion) of human myoblasts

T-type α1H Ca 2+ channels are involved in Ca 2+ signaling during terminal differentiation (fusion) of human myoblasts

Membrane properties and synaptic inputs of suprachiasmatic nucleus neurons in rat brain slices.

KCR1, a Membrane Protein That Facilitates Functional Expression of Non-inactivating K+ Currents Associates with Rat EAG Voltage-dependent K+Channels

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T-type α1H Ca ²⁺ channels are involved in Ca ²⁺ signaling during terminal differentiation (fusion) of human myoblasts

T-type α1H Ca ²⁺ channels are involved in Ca ²⁺ signaling during terminal differentiation (fusion) of human myoblasts