Mechanisms and roles of muscarinic activation in guinea-pig adrenal medullary cells

Inoue, Masumi; Harada, Kensuke; Matsuoka, Hiroaki; Nakamura, Jun; Warashina, Akira

doi:10.1152/ajpcell.00147.2012

Cited by 21 publications

(26 citation statements)

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“…These isoforms, which are divided into 6 subfamilies, form a homodimeric or heterodimeric channel with isoforms in the same or different subfamilies (2), and they contribute to the resting membrane potential. We have elucidated that TASK1 proteins, which belong to the TASK subfamily of K 2P channels, are expressed in adrenal medullary (AM) cells of rats (3) and guinea pigs (4), and a decrease in external pH induces catecholamine secretion by inhibiting TASK1-like channels (3). Moreover, muscarinic M 1 receptor activation (5) produces suppression of TASK1like channel activity with consequent depolarization in rat AM cells (3,6).…”

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confidence: 99%

“…Moreover, muscarinic M 1 receptor activation (5) produces suppression of TASK1like channel activity with consequent depolarization in rat AM cells (3,6). Thus, TASK1-like channels in AM cells not only function as acidic pH sensors but also are located downstream of muscarinic receptors, which are involved in neuronal transmission from the sympathetic preganglionic nerve fiber (4,7,8). However, the molecular identity of TASK1-like channels in AM cells remains an open question.…”

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Lack of p11 expression facilitates acidity‐sensing function of TASK1 channels in mouse adrenal medullary cells

et al. 2018

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External acidity induces catecholamine secretion by inhibiting TASK1-like channels in rat adrenal medullary (AM) cells. TASK channels can function as a heteromer or homomer in the TASK subfamily. In this study, we elucidate the molecular identity of TASK1-like channels in mouse AM cells using gene knockout. Genetic deletion of TASK1, but not TASK3, abolished the depolarizing inward current and catecholamine secretion in response to acidity, whereas it did not affect the resting current level. Immunocytochemistry revealed that AM cells exhibited predominantly TASK1-like and little TASK3-like immunoreactivity. A proximity ligation assay showed that TASK1/3 heteromeric channels were not formed in AM cells or PC12 cells. However, the exogenous expression of p11 in PC12 cells resulted in the heteromeric formation of TASK isoforms, which were mainly located in the cytoplasm, and p11 was not expressed in rat adrenal medullae or PC12 cells. In AM cells, genetic deletion of TASK1 resulted in enhancement of the immunoreactivity of the TALK2 channel, but not TASK3. The results indicate that TASK1 homomeric channels function as acidity sensors in AM cells, and that function is facilitated by the lack of p11 expression.-Inoue, M., Matsuoka, H., Lesage, F., Harada, K. Lack of p11 expression facilitates acidity-sensing function of TASK1 channels in mouse adrenal medullary cells.

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Lack of p11 expression facilitates acidity‐sensing function of TASK1 channels in mouse adrenal medullary cells

et al. 2018

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“…These results indicate that G q ‐PLC signalling was not altered by M 1 receptor ablation. Furthermore, a decrease in the external pH to 6.8 induced secretion, probably via inhibition of TASK channel activity (Inoue et al ., 2008; 2012), in 38% ( n = 3), 38% ( n = 6) and 60% ( n = 18) of the cells examined in wild‐type, M 1 M 4 KO and M 1 M 2 M 4 KO mice respectively (Figure B, D and E). These results suggest that the expression of TASK1 channels was not affected by the lack of M 1 receptors.…”

Section: Resultsmentioning

confidence: 94%

“…Embryonic rat chromaffin cells, just before birth, exhibited an increase in intracellular Ca 2+ concentration in response to stimulation of nAChRs, but not of muscarinic receptors, whereas cells after birth responded to muscarinic receptor stimulation as well. Muscarinic receptors are responsible for part of neuronal transmission in guinea pig chromaffin cells (Inoue et al ., ; Warashina and Inoue, ). Taken together with phylogenic and ontogenic considerations, this result suggests that muscarinic signalling in chromaffin cells develops to help animals cope with life‐threatening stress.…”

Section: Discussionmentioning

confidence: 97%

“…However, the expression of muscarinic receptors has been detected biochemically and/or functionally in chromaffin cells of almost every, if not all, mammalian animals (Olivos and Artalejo, ; Harada et al ., ). We have recently reported that catecholamine secretion electrically evoked in perfused guinea pig adrenal medullae is partly blocked by retrograde application of hexamethonium, a nAChR blocker, and the remaining component is abolished by atropine, a muscarinic receptor antagonist (Inoue et al ., ), indicating that muscarinic receptors are involved in synaptic transmission at least in guinea pig chromaffin cells. To further elucidate the physiological functions of muscarinic receptors in chromaffin cells, it would be necessary to identify the muscarinic receptor subtypes involved in catecholamine secretion.…”

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confidence: 98%

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Identification of muscarinic receptor subtypes involved in catecholamine secretion in adrenal medullary chromaffin cells by genetic deletion

Harada

Matsuoka

Miyata

et al. 2015

British J Pharmacology

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BACKGROUND AND PURPOSEActivation of muscarinic receptors results in catecholamine secretion in adrenal chromaffin cells in many mammals, and muscarinic receptors partly mediate synaptic transmission from the splanchnic nerve, at least in guinea pigs. To elucidate the physiological functions of muscarinic receptors in chromaffin cells, it is necessary to identify the muscarinic receptor subtypes involved in excitation. EXPERIMENTAL APPROACHTo identify muscarinic receptors, pharmacological tools and strains of mice where one or several muscarinic receptor subtypes were genetically deleted were used. Cellular responses to muscarinic stimulation in isolated chromaffin cells were studied with the patch clamp technique and amperometry. KEY RESULTSMuscarinic M1, M4 and M5 receptors were immunologically detected in mouse chromaffin cells, and these receptors disappeared after the appropriate gene deletion. Mouse cells secreted catecholamines in response to muscarinic agonists, angiotensin II and a decrease in external pH. Genetic deletion of M1, but not M3, M4 or M5, receptors in mice abolished secretion in response to muscarine, but not to other stimuli. The muscarine-induced secretion was suppressed by MT7, a snake peptide toxin specific for M1 receptors. Similarly, muscarine failed to induce an inward current in the presence of MT7 in mouse and rat chromaffin cells. The binding affinity of VU0255035 for the inhibition of muscarine-induced currents agreed with that for the M1 receptor. CONCLUSIONS AND IMPLICATIONSBased upon the effects of genetic deletion of muscarinic receptors and MT7, it is concluded that the M1 receptor alone is responsible for muscarine-induced catecholamine secretion. AbbreviationsHA, haemagglutinin; IR, immunoreactivity; KO, knockout; nAChR, nicotinic ACh receptor BJP British Journal of Pharmacology

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Nerve growth factor-induced endocytosis of TWIK-related acid-sensitive K+ 1 channels in adrenal medullary cells and PC12 cells

Matsuoka

Harada

Nakamura

et al. 2013

Pflugers Arch - Eur J Physiol

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TWIK-related acid-sensitive K(+) (TASK) channels belong to a family of two-pore domain K(+) channels which produce background K(+) currents and are involved in important physiological functions, such as acidosis detection. We have recently elucidated that TASK1-like channels function as a sensor of acidosis in rat adrenal medullary (AM) cells and thus are indispensable for the endocrine function of AM cells. Here, using pharmacological, electrophysiological and biochemical methods, we studied how the expression and localisation of TASK1 channels are regulated in rat AM cells and PC12 cells. PC12 cells were found to express not only TASK1 but also TASK3 channels, and they did not constitute a heterodimer. The exposure of AM cells and PC12 cells to nerve growth factor (NGF) induced endocytosis of TASK1, but not TASK3 channels, in a clathrin-dependent manner. Mutation analysis of the TASK1 channel revealed that the dileucine motif (LL263/264) was involved in at least part of the endocytosis. Plating GFP-TASK1-expressing PC12 cells onto a sheet of fibroblasts, which produced NGF, resulted in the endocytosis of GFP-TASK1 channels. Additionally, the expression of TASK1 channels at the protein and mRNA levels was suppressed in PC12 cells treated with NGF for 2 weeks. These results indicate that NGF suppresses the expression of TASK1 channels in the plasma membrane via not only endocytosis but also the inhibition of gene transcription. Thus, no access to NGF may play a major role for the maintenance of TASK1 channels in the cell membrane in AM cells.

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Mechanisms and roles of muscarinic activation in guinea-pig adrenal medullary cells

Cited by 21 publications

References 59 publications

Lack of p11 expression facilitates acidity‐sensing function of TASK1 channels in mouse adrenal medullary cells

Lack of p11 expression facilitates acidity‐sensing function of TASK1 channels in mouse adrenal medullary cells

Identification of muscarinic receptor subtypes involved in catecholamine secretion in adrenal medullary chromaffin cells by genetic deletion

Nerve growth factor-induced endocytosis of TWIK-related acid-sensitive K+ 1 channels in adrenal medullary cells and PC12 cells

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