M‐currents and other potassium currents in bullfrog sympathetic neurones

Adams, Patrick W.; Da, Brown; Constanti, Andrew

doi:10.1113/jphysiol.1982.sp014357

Cited by 498 publications

(372 citation statements)

References 41 publications

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“…The characteristics of I Kx shown in Figures 1-3 resemble those of M-current, a class of K + current found in a variety of cell types (Adams et al, 1982;Brown, 1988). In addition, we have found I Kx to be blocked about 40% by bath-applied 10 mM tetraethylammonium (TEA) (n = 4), but less than 10% by 5 mM 4-aminopyridine (4-AP) at -60 mV (n = 4) (data not shown).…”

Section: Extracellular Ba 2+ Shifts the Activation Range Of I Kx Stromentioning

confidence: 80%

“…This pharmacology compares well with that of M-current (Brown and Adams, 1980). To further this comparison, we examined the effect of external Ba 2+ on I Kx , since Ba 2+ is known to block M-current in the millimolar concentration range (Adams et al, 1982).…”

Section: Extracellular Ba 2+ Shifts the Activation Range Of I Kx Stromentioning

confidence: 93%

“…We compared I Kx with known types of K + current (Adams et al, 1982;Hille, 1984). I Kx seems most similar to M-current because both currents are activated by depolarization over about the same voltage range, they do not inactivate, and they show simple, first-order kinetics.…”

Section: Properties Of I Kxmentioning

confidence: 99%

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Characterization of a voltage-gated K+ channel that accelerates the rod response to dim light

Beech

Barnes

1989

Neuron

102

100

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SummaryIn this study a K + current, I Kx , in isolated salamander rod photoreceptors was characterized and its role in shaping small photovoltages was examined. I Kx is a standing outward current of about 40 pA at -30 mV that deactivates slowly when the cell is hyperpolarized (τ max = 0.25 s). The voltage and time dependence of I Kx are similar to that of M-current, but I Kx can be distinguished from Mcurrent because it is not suppressed by acetylcholine and is "blocked" by external Ba 2+ in a surprising manner: the activation range of I Kx is shifted strongly in the positive direction. Using current-clamp recordings and a computer simulation of the photoresponse, we show that I Kx figures prominently in setting the dark resting potential and accelerates the voltage response to small photocurrents.

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Section: Extracellular Ba 2+ Shifts the Activation Range Of I Kx Stromentioning

confidence: 80%

Section: Extracellular Ba 2+ Shifts the Activation Range Of I Kx Stromentioning

confidence: 93%

See 1 more Smart Citation

Characterization of a voltage-gated K+ channel that accelerates the rod response to dim light

Beech

Barnes

1989

Neuron

102

100

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“…Upon returning to the holding potential, an instantaneous current jump (corresponding to leak current) followed by a slowly developing outward relaxation (corresponding to the opening of the M-channels) was recorded. The size of the outward relaxation before and after the + 100 mV jump was used to estimate the effect of Dr-VSP activation on M-current size [48,49]. The data were acquired and analyzed using pCLAMP software (version 8.2), normalized in Excel (Microsoft Corp.) and plotted in Sigmaplot 12 (SPSS Corp.).…”

Section: Methodsmentioning

confidence: 99%

Lack of correlation between surface expression and currents in epileptogenic AB-calmodulin binding domain Kv7.2 potassium channel mutants

et al. 2018

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Heteromers of Kv7.2/Kv7.3 subunits constitute the main substrate of the neuronal M-current that limits neuronal hyper-excitability and firing frequency. Calmodulin (CaM) binding is essential for surface expression of Kv7 channels, and disruption of this interaction leads to diseases ranging from mild epilepsy to early onset encephalopathy. In this study, we addressed the impact of a charge neutralizing mutation located at the periphery of helix B (K526N). We found that, CaM binding and surface expression was impaired, although current amplitude was not altered. Currents were reduced at a faster rate after activation of a voltage-dependent phosphatase, suggesting that phosphatidylinositol-4,5-bisphosphate (PIP2) binding was weaker. In contrast, a charge neutralizing mutation located at the periphery of helix A (R333Q) did not affect CaM binding, but impaired trafficking and led to a reduction in current amplitude. Taken together, these results suggest that disruption of CaM-dependent or CaM-independent trafficking of Kv7.2/Kv7.3 channels can lead to pathology regardless of the consequences on the macroscopic ionic flow through the channel.

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“…Activation of muscarinic receptors blocks the K + channels responsible for the M current (Adams et al, 1982;Brown and Adams, 1980) but also induces a Ca 2+ -activated, nonselective cation current that causes depolarizing plateau potentials that are intrinsically generated by principal cells in the hippocampus and subiculum (Caeser et al, 1993;Fraser and MacVicar, 1996;Kawasaki et al, 1999). These mechanisms contribute to increased neuronal excitability and, in vivo, the muscarinic agonist pilocarpine represents a valuable tool for inducing status epilepticus thus establishing a chronic epileptic condition that is regarded as a useful experimental model of temporal lobe epilepsy (Curia et al, 2008).…”

Section: Muscarinic Agonistsmentioning

confidence: 99%

Models of drug-induced epileptiform synchronization in vitro

Avoli

Jefferys

2016

Journal of Neuroscience Methods

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Models of epileptiform activity in vitro have many advantages for recording and experimental manipulation. Neural tissues can be maintained in vitro for hours, and in neuronal or organotypic slice cultures for several weeks. A variety of drugs and other agents increase activity in these in vitro conditions, in many cases resulting in epileptiform activity, thus providing a direct model of symptomatic seizures. We review these preparations and the experimental manipulations used to induce epileptiform activity. The most common of drugs used are GABA A receptor antagonists and potassium channel blockers (notably 4-aminopyridine). Muscarinic agents also can induce epileptiform synchronization in vitro, and include potassium channel inhibition amongst their cellular actions. Manipulations of extracellular ions are reviewed in another paper in this special issue, as are ex vivo slices prepared from chronically epileptic animals and from people with epilepsy. More complex slices including extensive networks and/or several connected brain structures can provide insights into the dynamics of long range connections during epileptic activity. Visualization of slices also provides opportunities for identification of living neurons and for optical recording/stimulation and manipulation. Overall, the analysis of the epileptiform activity induced in brain tissue in vitro has played a major role in advancing our understanding of the cellular and network mechanisms of epileptiform synchronization, and it is expected to continue to do so in future.

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M‐currents and other potassium currents in bullfrog sympathetic neurones

Cited by 498 publications

References 41 publications

Characterization of a voltage-gated K+ channel that accelerates the rod response to dim light

Characterization of a voltage-gated K+ channel that accelerates the rod response to dim light

Lack of correlation between surface expression and currents in epileptogenic AB-calmodulin binding domain Kv7.2 potassium channel mutants

Models of drug-induced epileptiform synchronization in vitro

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