Role of K2P channels in stimulus-secretion coupling

Kim, Dong‐Hee; Kang, Dawon

doi:10.1007/s00424-014-1663-3

Cited by 16 publications

(10 citation statements)

References 69 publications

(78 reference statements)

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“…Also, only TREK and TASK channels have been reported to be expressed in the rodent adrenal medullary tissue (Inoue et al . 2008; Kim & Kang, 2015; Guarina et al . 2017).…”

Section: Discussionmentioning

confidence: 99%

A sodium background conductance controls the spiking pattern of mouse adrenal chromaffin cells in situ

Milman

Ventéo

Bossu

et al. 2021

The Journal of Physiology

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Key points Mouse chromaffin cells in acute adrenal slices exhibit two distinct spiking patterns, a repetitive mode and a bursting mode. A sodium background conductance operates at rest as demonstrated by the membrane hyperpolarization evoked by a low Na+‐containing extracellular saline. This sodium background current is insensitive to TTX, is not blocked by Cs+ ions and displays a linear I‐V relationship at potentials close to chromaffin cell resting potential. Its properties are reminiscent of those of the sodium leak channel NALCN. In the adrenal gland, Nalcn mRNA is selectively expressed in chromaffin cells. The study fosters our understanding of how the spiking pattern of chromaffin cells is regulated and adds a sodium background conductance to the list of players involved in the stimulus‐secretion coupling of the adrenomedullary tissue. Abstract Chromaffin cells (CCs) are the master neuroendocrine units for the secretory function of the adrenal medulla and a finely‐tuned regulation of their electrical activity is required for appropriate catecholamine secretion in response to the organismal demand. Here, we aim at deciphering how the spiking pattern of mouse CCs is regulated by the ion conductances operating near the resting membrane potential (RMP). At RMP, mouse CCs display a composite firing pattern, alternating between active periods composed of action potentials spiking with a regular or a bursting mode, and silent periods. RMP is sensitive to changes in extracellular sodium concentration, and a low Na+‐containing saline hyperpolarizes the membrane, regardless of the discharge pattern. This RMP drive reflects the contribution of a depolarizing conductance, which is (i) not blocked by tetrodotoxin or caesium, (ii) displays a linear I‐V relationship between −110 and −40 mV, and (iii) is carried by cations with a conductance sequence gNa > gK > gCs. These biophysical attributes, together with the expression of the sodium‐leak channel Nalcn transcript in CCs, state credible the contribution of NALCN. This inaugural report opens new research routes in the field of CC stimulus‐secretion coupling, and extends the inventory of tissues in which NALCN is expressed to neuroendocrine glands.

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“…Also, only TREK and TASK channels have been reported to be expressed in the rodent adrenal medullary tissue (Inoue et al . 2008; Kim & Kang, 2015; Guarina et al . 2017).…”

Section: Discussionmentioning

confidence: 99%

A sodium background conductance controls the spiking pattern of mouse adrenal chromaffin cells in situ

Milman

Ventéo

Bossu

et al. 2021

The Journal of Physiology

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“…Figure summarizes a proposed model illustrating how crosstalk might contribute to sensory processing at the CB ‘tripartite’ synapse via purinergic signalling pathways. There is a consensus that during hypoxia and acid hypercapnia rat type I cells depolarize due to the closing of TASK1/3 background K + channels (Buckler, ; Kim & Kang, ). This leads to voltage‐gated Ca 2+ entry and release of multiple neurotransmitters including ATP and adenosine (Prasad et al .…”

Section: Discussionmentioning

confidence: 99%

“…There is a consensus that during hypoxia and acid hypercapnia rat type I cells depolarize due to the closing of TASK1/3 background K + channels (Buckler, 2015;Kim & Kang, 2015). This leads to voltage-gated Ca 2+ entry and release of multiple neurotransmitters including ATP and adenosine (Prasad et al 2001;Buttigieg & Nurse, 2004;Conde et al 2012;Nurse & Piskuric, 2013;Nurse, 2014).…”

Section: Is There a Physiological Role For Bidirectional Crosstalk Bementioning

confidence: 99%

Purinergic signalling mediates bidirectional crosstalk between chemoreceptor type I and glial‐like type II cells of the rat carotid body

Murali

Nurse

2015

The Journal of Physiology

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Key pointsr Carotid body chemoreceptors are organized in clusters containing receptor type I and contiguous glial-like type II cells.r While type I cells depolarize and release ATP during chemostimulation, the role of type II cells which express purinergic P2Y2 receptors (P2Y2Rs) and ATP-permeable pannexin-1 (Panx-1) channels, is unclear. r We propose that reciprocal crosstalk between type I and type II cells contributes to sensory processing in the carotid body via purinergic signalling pathways. AbstractThe mammalian carotid body (CB) is excited by blood-borne stimuli including hypoxia and acid hypercapnia, leading to respiratory and cardiovascular reflex responses. This chemosensory organ consists of innervated clusters of receptor type I cells, ensheathed by processes of adjacent glial-like type II cells. ATP is a major excitatory neurotransmitter released from type I cells and type II cells express purinergic P2Y2 receptors (P2Y2Rs), the activation of which leads to the opening of ATP-permeable, pannexin-1 (Panx-1) channels. While these properties support crosstalk between type I and type II cells during chemotransduction, direct evidence is lacking. To address this, we first exposed isolated rat chemoreceptor clusters to acute hypoxia, isohydric hypercapnia, or the depolarizing stimulus high K + , and monitored intracellular [Ca 2+ ] using Fura-2. As expected, these stimuli induced intracellular [Ca 2+ ] elevations ( [Ca 2+ ] i ) in type I cells. Interestingly, however, there was often a delayed, secondary [Ca 2+ ] i in nearby type II cells that was reversibly inhibited by the P2Y2R antagonist suramin, or by the nucleoside hydrolase apyrase. By contrast, type II cell stimulation with the P2Y2R agonist uridine-5 -triphosphate (100 μM) often led to a delayed, secondary [Ca 2+ ] i response in nearby type I cells that was reversibly inhibited by the Panx-1 blocker carbenoxolone (5 μM). This [Ca 2+ ] i response was also strongly inhibited by blockers of either the adenosine A 2A receptor (SCH 58261) or of the 5 -ectonucleotidase (AOPCP), suggesting it was due to adenosine arising from breakdown of ATP released through Panx-1 channels. Collectively, these data strongly suggest that purinergic signalling mechanisms mediate crosstalk between CB chemoreceptor and glial cells during chemotransduction.

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“…Indeed, insulin granule exocytosis is induced by membrane depolarization that is a direct consequence of the inhibition of ATP dependent potassium channels by the increased ATP production from glucose metabolism. Other types of K+ channels including TREK-1, a two-pore-domain (K 2 P) background potassium channel are known to be involved in the control of the resting membrane potential and the regulation of depolarizing stimulus (Kim and Kang, 2015).…”

Section: Sortilin Acting On Trek-1 Channel Regulates Cell Excitabilitymentioning

confidence: 99%

Sortilin in Glucose Homeostasis: From Accessory Protein to Key Player?

et al. 2019

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The pharmacological properties and physiological roles of the type I receptor sortilin, also called neurotensin receptor-3, are various and complex. Sortilin is involved in important biological functions from neurotensin and pro-Nerve Growth Factor signaling in the central nervous system to regulation of glucose and lipid homeostasis in the periphery. The peripheral functions of sortilin being less extensively addressed, the focus of the current review is to discuss recent works describing sortilin-induced molecular mechanisms regulating blood glucose homeostasis and insulin signaling. Thus, an overview of several roles ascribed to sortilin in diabetes and other metabolic diseases are presented. Investigations on crucial cellular pathways involved in the protective effect of sortilin receptor on beta cells, including recent discoveries about regulation of cell fate, are also detailed. In addition, we provide a special focus on insulin secretion regulation involving complexes between sortilin and neurotensin receptors. The last section comments on the future research areas which should be developed to address the function of new effectors of the sortilin system in the endocrine apparatus.

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Role of K2P channels in stimulus-secretion coupling

Cited by 16 publications

References 69 publications

A sodium background conductance controls the spiking pattern of mouse adrenal chromaffin cells in situ

A sodium background conductance controls the spiking pattern of mouse adrenal chromaffin cells in situ

Purinergic signalling mediates bidirectional crosstalk between chemoreceptor type I and glial‐like type II cells of the rat carotid body

Sortilin in Glucose Homeostasis: From Accessory Protein to Key Player?

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