Single calcium‐activated potassium channels recorded from cultured rat sympathetic neurones.

Smart, TG

doi:10.1113/jphysiol.1987.sp016660

Cited by 93 publications

(82 citation statements)

References 58 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…However, in hippocampal neurons, the Ca 2ϩ sensitivities of large-conductance (BK) Ca 2ϩ -gated K ϩ channels (EC 50 of 2-4 M) (Smart, 1987;Franciolini, 1988;Gong et al, 2001) and of small-conductance (SK) Ca 2ϩ -gated K ϩ channels (EC 50 of 0.6 M) (Hirschberg et al, 1999) are considerably smaller than that of K V 7/M channels (EC 50 of 100 -120 nM) (Selyanko and Brown, 1996;Selyanko and Sim, 1998). Therefore, a hyposmotic increase in [Ca 2ϩ ] i to ϳ150 nM, as measured in acutely dissociated pyramidal cells (Borgdorff et al, 2000), may inhibit K V 7/M channels without concurrently activating BK or SK channels.…”

Section: Role Of Internal Camentioning

confidence: 99%

K_V7/M Channels Mediate Osmotic Modulation of Intrinsic Neuronal Excitability

Caspi¹,

Benninger²,

Yaari³

2009

J. Neurosci.

View full text Add to dashboard Cite

Modest decreases in extracellular osmolarity induce brain hyperexcitability that may culminate in epileptic seizures. At the cellular level, moderate hyposmolarity markedly potentiates the intrinsic neuronal excitability of principal cortical neurons without significantly affecting their volume. The most conspicuous cellular effect of hyposmolarity is converting regular firing neurons to burst-firing mode. This effect is underlain by hyposmotic facilitation of the spike afterdepolarization (ADP), but its ionic mechanism is unknown. Because blockers of K V 7 (KCNQ) channels underlying neuronal M-type K ϩ currents (K V 7/M channels) also cause spike ADP facilitation and bursting, we hypothesized that lowering osmolarity inhibits these channels. Using current-and voltage-clamp recordings in CA1 pyramidal cells in situ, we have confirmed this hypothesis. Furthermore, we show that hyposmotic inhibition of K V 7/M channels is mediated by an increase in intracellular Ca 2ϩ concentration via release from internal stores but not via influx of extracellular Ca 2ϩ . Finally, we show that interfering with internal Ca 2ϩ -mediated inhibition of K V 7/M channels entirely protects against hyposmotic ADP facilitation and bursting, indicating the exclusivity of this novel mechanism in producing intrinsic neuronal hyperexcitability in hyposmotic conditions.

show abstract

Section: Role Of Internal Camentioning

confidence: 99%

K_V7/M Channels Mediate Osmotic Modulation of Intrinsic Neuronal Excitability

Caspi¹,

Benninger²,

Yaari³

2009

J. Neurosci.

View full text Add to dashboard Cite

show abstract

“…Superior cervical ganglia (typically 4-16) were obtained from foetal (E17-21), young post-natal (P1-6) and adult (>P90) Sprague-Dawley rats and dissociated by use of a combination of enzymatic and mechanical methods, as previously described in detail (Smart, 1987). Minor modifications to the protocol included: coating dishes with a 20pgmlP1 laminin solution (Flow Labs.)…”

Section: Sympathetic Neuronal Tissue Culturementioning

confidence: 99%

Differential effect of zinc on the vertebrate GABA_A‐receptor complex

Smart

Constanti

1990

British J Pharmacology

109

View full text Add to dashboard Cite

-39 Brunswick Square, London WC1N lAX 1 y-Aminobutyric acid (GABA) responses were recorded from rat superior cervical ganglia (SCG) in culture using the whole cell recording technique.2 Zinc (50-300pM) reversibly antagonized the GABA response in embryonic and young post-natal neurones, while neurones cultured from adult animals were far less sensitive and occasionally resistant to zinc blockade. Cadmium (100-300 gM) also antagonised the GABA response, while barium (100 pM-2 mM) was ineffective. 3 The differential blocking effect of zinc on cultured neurones of different ages also occurred in intact SCG tissue. 4 The GABA log dose-response curve constructed with foetal or adult cultured neurones was reduced in a non-competitive manner by zinc. This inhibition was minimally affected by the membrane potential. 5 The GABA response recorded intracellularly from guinea-pig pyriform cortical slices was enhanced by zinc (300-500jMm), which occurred concurrently with a decrease in the input conductance of the cell. The enhancement was unaffected by prior blockade of the GABA uptake carrier by 1 mm nipecotic acid. This phenomenon could be reproduced by barium (300 pM) and cadmium (300 M).6 We conclude that the vertebrate neuronal GABAA-receptor becomes less sensitive to zinc with neural (GABAA-receptor?) development, and the enhanced GABA response recorded in the CNS is a consequence of the reduction in the input conductance and not due to a direct effect on the receptor complex.

show abstract

“…The only class of Ca2+-activated K+ channel in mammalian autonomic neurons categorized according to its unitary conductance is a large-conductance (Ε200 pS; BK or maxi K) Ca2+-dependent K+ channel [17,41]. This large-conductance Ca2+-dependent K+ channel is activated by an elevation of the cytoplasmic free Ca2+ concentration and is modulated by membrane potential.…”

Section: Introductionmentioning

confidence: 99%

Large-conductance calcium-activated potassium channels in neonatal rat intracardiac ganglion neurons

Franciolini

Hogg

Catacuzzeno

et al. 2000

Pflügers Arch - Eur J Physiol

View full text Add to dashboard Cite

The properties of single Ca2+-activated K+ (BK) channels in neonatal rat intracardiac neurons were investigated using the patch-clamp recording technique. In symmetrical 140 mM K+, the single-channel slope conductance was linear in the voltage range -60/+60 mV, and was 207±19 pS. Na+ ions were not measurably permeant through the open channel. Channel activity increased with the cytoplasmic free Ca2+ concentration ([Ca2+]i) with a Hill plot giving a halfsaturating [Ca2+] (K0.5) of 1.35 μM and slope of Ε3. The BK channel was inhibited reversibly by external tetraethylammonium (TEA) ions, charybdotoxin, and quinine and was resistant to block by 4-aminopyridine and apamin. Ionomycin (1-10 μM) increased BK channel activity in the cell-attached recording configuration. The resting activity was consistent with a [Ca2+]i <100 nM and the increased channel activity evoked by ionomycin was consistent with a rise in [Ca2+]i to ε0.3 μM. TEA (0.2-1 mM) increased the action potential duration Ε1.5-fold and reduced the amplitude and duration of the afterhyperpolarization (AHP) by 26%. Charybdotoxin (100 nM) did not significantly alter the action potential duration or AHP amplitude but reduced the AHP duration by Ε40%. Taken together, these data indicate that BK channel activation contributes to the action potential and AHP duration in rat intracardiac neurons.

show abstract

Single calcium‐activated potassium channels recorded from cultured rat sympathetic neurones.

Cited by 93 publications

References 58 publications

K_V7/M Channels Mediate Osmotic Modulation of Intrinsic Neuronal Excitability

K_V7/M Channels Mediate Osmotic Modulation of Intrinsic Neuronal Excitability

Differential effect of zinc on the vertebrate GABA_A‐receptor complex

Large-conductance calcium-activated potassium channels in neonatal rat intracardiac ganglion neurons

Contact Info

Product

Resources

About

Single calcium‐activated potassium channels recorded from cultured rat sympathetic neurones.

Cited by 93 publications

References 58 publications

KV7/M Channels Mediate Osmotic Modulation of Intrinsic Neuronal Excitability

KV7/M Channels Mediate Osmotic Modulation of Intrinsic Neuronal Excitability

Differential effect of zinc on the vertebrate GABAA‐receptor complex

Large-conductance calcium-activated potassium channels in neonatal rat intracardiac ganglion neurons

Contact Info

Product

Resources

About

K_V7/M Channels Mediate Osmotic Modulation of Intrinsic Neuronal Excitability

K_V7/M Channels Mediate Osmotic Modulation of Intrinsic Neuronal Excitability

Differential effect of zinc on the vertebrate GABA_A‐receptor complex