Activation of calcium-dependent chloride channels causes post-tetanic depolarization in rabbit parasympathetic neurons

Nishimura, Toshihiko

doi:10.1016/0165-1838(94)00134-6

Cited by 6 publications

(3 citation statements)

References 27 publications

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“…Neither the amplitude nor the duration of the spike changed when CaCCs were blocked with 9AC, suggesting that this current does not play a substantial part in generating single APs. This is in agreement with data obtained from rabbit parasympathetic ganglia, where modifications of both external and internal Cl - concentrations do not significantly alter the properties of individual APs in cells with a Ca 2+ -activated Cl - current ( Nishimura, 1995 ), as demonstrated more recently in cardiac ventricular cells ( Váczi et al, 2015 ). The firing of excitable cells is not only affected by the characteristics of the AP but also, by the R input and rheobase.…”

Section: Discussionsupporting

confidence: 92%

“…A post-tetanic depolarization produced by activation of CaCCs in parasympathetic neurons has been proposed to cause a slow EPSP ( Nishimura, 1995 ). The same function could be attributed to this current in sympathetic neurons, stronger activation of CaCCs at high frequencies depolarizing the cell until the firing threshold is again reached, and its blockade would prolong the predominant effect of I K(Ca) , delaying the generation of the next spike.…”

Section: Discussionmentioning

confidence: 99%

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A Calcium-Dependent Chloride Current Increases Repetitive Firing in Mouse Sympathetic Neurons

et al. 2018

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Ca2+-activated ion channels shape membrane excitability in response to elevations in intracellular Ca2+. The most extensively studied Ca2+-sensitive ion channels are Ca2+-activated K+ channels, whereas the physiological importance of Ca2+-activated Cl- channels has been poorly studied. Here we show that a Ca2+-activated Cl- currents (CaCCs) modulate repetitive firing in mouse sympathetic ganglion cells. Electrophysiological recording of mouse sympathetic neurons in an in vitro preparation of the superior cervical ganglion (SCG) identifies neurons with two different firing patterns in response to long depolarizing current pulses (1 s). Neurons classified as phasic (Ph) made up 67% of the cell population whilst the remainders were tonic (T). When a high frequency train of spikes was induced by intracellular current injection, SCG sympathetic neurons reached an afterpotential mainly dependent on the ratio of activation of two Ca2+-dependent currents: the K+ [IK(Ca)] and CaCC. When the IK(Ca) was larger, an afterhyperpolarization was the predominant afterpotential but when the CaCC was larger, an afterdepolarization (ADP) was predominant. These afterpotentials can be observed after a single action potential (AP). Ph and T neurons had similar ADPs and hence, the CaCC does not seem to determine the firing pattern (Ph or T) of these neurons. However, inhibition of Ca2+-activated Cl- channels with anthracene-9′-carboxylic acid (9AC) selectively inhibits the ADP, reducing the firing frequency and the instantaneous frequency without affecting the characteristics of single- or first-spike firing of both Ph and T neurons. Furthermore, we found that the CaCC underlying the ADP was significantly larger in SCG neurons from males than from females. Furthermore, the CaCC ANO1/TMEM16A was more strongly expressed in male than in female SCGs. Blocking ADPs with 9AC did not modify synaptic transmission in either Ph or T neurons. We conclude that the CaCC responsible for ADPs increases repetitive firing in both Ph and T neurons, and it is more relevant in male mouse sympathetic ganglion neurons.

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Section: Discussionsupporting

confidence: 92%

Section: Discussionmentioning

confidence: 99%

A Calcium-Dependent Chloride Current Increases Repetitive Firing in Mouse Sympathetic Neurons

et al. 2018

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“…CaCC currents are also observed in a subpopulation of DRG neurons [113] and the spinal cord neurons where they would repolarize membrane during action potentials [114]. Furthermore, activation of CaCCs in rabbit parasympathetic neurons causes the after-depolarization [115]. Interestingly, high ANO1 immunoreactivity is detected in most of DRG neurons in mouse [100].…”

Section: Introductionmentioning

confidence: 99%

Anoctamin 1 Mediates Thermal Pain as a Heat Sensor

Cho¹,

Oh²

2013

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Vertebrates can sense and avoid noxious heat that evokes pain. Many thermoTRP channels are associated with temperature sensation. TRPV1 is a representative ion channel that is activated by noxious heat. Anoctamin 1 (ANO1) is a Cl- channel activated by calcium that is highly expressed in small sensory neurons, colocalized with markers for nociceptors, and most surprisingly, activated by noxious heat over 44oC. Although ANO1 is a Cl- channel, opening of this channel leads to depolarization of sensory neurons, suggesting a role in nociception. Indeed, the functional deletion of ANO1 in sensory neurons triggers the reduction in thermal pain sensation. Thus, it seems clear that ANO1 is a heat sensor in a nociceptive pathway. Since ANO1 modulators are developed for the purpose of treating chronic diseases such as cystic fibrosis, this finding is likely to predict unwanted effects and provide a guide for better developmental strategy

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Purinergic cation channels in neurons of rabbit vesical parasympathetic ganglia

Nishimura

Tokimasa

1996

Neuroscience Letters

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Activation of calcium-dependent chloride channels causes post-tetanic depolarization in rabbit parasympathetic neurons

Cited by 6 publications

References 27 publications

A Calcium-Dependent Chloride Current Increases Repetitive Firing in Mouse Sympathetic Neurons

A Calcium-Dependent Chloride Current Increases Repetitive Firing in Mouse Sympathetic Neurons

Anoctamin 1 Mediates Thermal Pain as a Heat Sensor

Purinergic cation channels in neurons of rabbit vesical parasympathetic ganglia

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