Histamine promotes excitability in bovine adrenal chromaffin cells by inhibiting an M-current

Wallace, Damian J.; Chen, Chen; Marley, Philip D.

doi:10.1111/j.1469-7793.2002.00921.x

Cited by 8 publications

(9 citation statements)

References 15 publications

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“…The cells had mean resting potentials (V r ) of −49.0±1.5 mV (n=24) that, after correction for the liquid junction potential (−15.8 mV), resulted to be more negative and in good agreement (after appropriate compensation) with other V r estimated using patch pipettes (from −50 to −70 mV [13,27,61]). The average input resistance measured using small hyperpolarizing current pulses (5-10 pA) was very high (1.2±0.2 GΩ; n=7) and in good agreement with previously reported values in other chromaffin cell types (0.6 to 5 GΩ) [13,27,35].…”

Section: Effect Of Rolipram On Action Potential Firing Frequencymentioning

confidence: 85%

PDE type-4 inhibition increases L-type Ca2+ currents, action potential firing, and quantal size of exocytosis in mouse chromaffin cells

Marcantoni

Carabelli

Vandael

et al. 2008

Pflugers Arch - Eur J Physiol

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We studied the effects of the cAMP-hydrolyzing enzyme phosphodiesterase type-4 (PDE4) on the L-type Ca(2+) channels (LTCCs) and Ca(2+)-dependent secretion in mouse chromaffin cells (MCCs). The selective PDE4 inhibitor rolipram (3 microM) had a specific potentiating action on Ca(2+) currents of MCCs (40% increase within 3 min). A similar effect was produced by the selective beta(1)-AR agonist denopamine (1 microM) and by the unselective PDEs inhibitor IBMX (100 microM). Rolipram and denopamine actions were selective for LTCCs, and the Ca(2+) current increase remained unchanged if the two compounds were applied simultaneously. This suggests that at rest, LTCCs in MCCs are down-regulated by the low levels of cAMP determined by PDE4 activity and that LTCCs can be up-regulated by either inhibiting PDE4 or activating beta(1)-AR. No other PDEs are likely involved in this specific action. PDE4 inhibition had also a marked effect on the spontaneous firing of resting MCCs and catecholamine secretion. Rolipram up-regulated the LTCCs contributing to the "pace-maker" current underlying action potential (AP) discharges and accelerated the firing rate, with no significant effects on AP waveform. Acceleration of AP firing was also induced by the LTCC-agonist Bay K (1 microM), while nifedipine (3 microM) reduced the firing frequency, suggesting that LTCCs and intracellular cAMP play a key role in setting the pace-maker current regulating MCCs excitability. Rolipram increased also the size of the ready-releasable pool and the quantal content of secretory vesicles without affecting their probability of release. Thus, rolipram acts on MCCs by up-regulating both exocytosis and AP firings. These two processes are effectively down-regulated by PDE4 at rest and can dramatically increase the quantity of released catecholamines when PDE4 is inhibited and/or cAMP is raised.

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Section: Effect Of Rolipram On Action Potential Firing Frequencymentioning

confidence: 85%

PDE type-4 inhibition increases L-type Ca2+ currents, action potential firing, and quantal size of exocytosis in mouse chromaffin cells

Marcantoni

Carabelli

Vandael

et al. 2008

Pflugers Arch - Eur J Physiol

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“…1 could be at the basis of the adrenal gland response to increased blood levels of histamine, acetylcholine, angiotensin II (ATII), and K + ions. Histamine and acetylcholine (muscarine) are shown to increase the firing rate of spontaneous APs [57,59,60] and the same is likely to occur during postprandial hyperkaliemia and enhanced blood levels of ATII that is known to increase the amount of circulating catecholamines. These physiological responses coming from the periphery (adrenal medulla capillaries) could occur independently of the central sympathetic control of chromaffin cell activity and could be regulated by the electrical synchronism of firing cells coupled by gap junctions [63].…”

Section: Ca V 13 As Pacemaker Channel Of Adrenal Chromaffin Cellsmentioning

confidence: 98%

“…Bovine, rat, mouse, and human adrenal chromaffin cells fire spontaneously when cultured in vitro [16][17][18][53][54][55][56][57][58][59][60][61] or prepared in slices of the adrenal gland [62,63]. Spontaneous firing is not observed in all chromaffin cells, a feature that may point to a different function of the cells.…”

Section: Ca V 13 As Pacemaker Channel Of Adrenal Chromaffin Cellsmentioning

confidence: 99%

Cav1.3 and BK Channels for Timing and Regulating Cell Firing

et al. 2010

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L-type Ca(2+) channels (LTCCs, Ca(v)1) open readily during membrane depolarization and allow Ca(2+) to enter the cell. In this way, LTCCs regulate cell excitability and trigger a variety of Ca(2+)-dependent physiological processes such as: excitation-contraction coupling in muscle cells, gene expression, synaptic plasticity, neuronal differentiation, hormone secretion, and pacemaker activity in heart, neurons, and endocrine cells. Among the two major isoforms of LTCCs expressed in excitable tissues (Ca(v)1.2 and Ca(v)1.3), Ca(v)1.3 appears suitable for supporting a pacemaker current in spontaneously firing cells. It has steep voltage dependence and low threshold of activation and inactivates slowly. Using Ca(v)1.3(-/-) KO mice and membrane current recording techniques such as the dynamic and the action potential clamp, it has been possible to resolve the time course of Ca(v)1.3 pacemaker currents that regulate the spontaneous firing of dopaminergic neurons and adrenal chromaffin cells. In several cell types, Ca(v)1.3 is selectively coupled to BK channels within membrane nanodomains and controls both the firing frequency and the action potential repolarization phase. Here we review the most critical aspects of Ca(v)1.3 channel gating and its coupling to large conductance BK channels recently discovered in spontaneously firing neurons and neuroendocrine cells with the aim of furnishing a converging view of the role that these two channel types play in the regulation of cell excitability.

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“…Denervated cells in primary cell culture fire spontaneous action potentials at less than 0.2 Hz [33]. When challenged with action potential trains of frequencies between 0.02 and 20 Hz, chromaffin cells respond with a biphasic exocytosis-coupled endocytosis.…”

Section: Introductionmentioning

confidence: 99%

Calcium dependence of action potential-induced endocytosis in chromaffin cells

Chan

Chow

Smith

2003

Pflugers Arch - Eur J Physiol

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Exocytosis occurs via fusion of transmitter-containing granules with the cell membrane, whereupon the granule contents are released and the cell membrane surface area increases. Exocytosis is followed by endocytosis to maintain proper cell membrane surface area and composition. We have shown that adrenal chromaffin cells internalize membrane in a biphasic manner following action potential stimulation. At basal firing rates (single - 0.5 Hz trains) endocytosis occurs by a rapid retrieval of membrane (termed Phase I) that is independent of the activity of the protein phosphatase calcineurin and wanes in efficiency with cell activity. At intermediate firing frequencies (>6 Hz) a second, calcineurin-sensitive, form of activity-enhanced endocytosis emerges (Phase II). In this study, we employ electrophysiological, electrochemical, and computational techniques to estimate intracellular Ca(2+) at the site of endocytosis by measuring secretion rates. The measured rates of secretion yield estimates of [Ca(2+)](i) based on a kinetic scheme for exocytosis calibrated under highly controlled [Ca(2+)](i). Based on this analysis, we propose that Phase I endocytosis is inhibited by cytosolic Ca(2+) with a K(inh)=605 nM, while Phase II endocytosis is activated by Ca(2+) with a K(act)=1.46 micro M. Molecular processes that may be consistent with the measured behaviors are discussed.

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Histamine promotes excitability in bovine adrenal chromaffin cells by inhibiting an M-current

Cited by 8 publications

References 15 publications

PDE type-4 inhibition increases L-type Ca2+ currents, action potential firing, and quantal size of exocytosis in mouse chromaffin cells

PDE type-4 inhibition increases L-type Ca2+ currents, action potential firing, and quantal size of exocytosis in mouse chromaffin cells

Cav1.3 and BK Channels for Timing and Regulating Cell Firing

Calcium dependence of action potential-induced endocytosis in chromaffin cells

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