Control of Secretion by Temporal Patterns of Action Potentials in Adrenal Chromaffin Cells

Duan, Kailai; Yu, Xiao; Zhang, Chen; Zhou, Zhuan

doi:10.1523/jneurosci.23-35-11235.2003

Cited by 40 publications

(56 citation statements)

References 44 publications

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“…Cultured bovine (Fenwick et al, 1982;Wallace et al, 2002), rat (Brandt et al, 1976;Gullo et al, 2003), and mouse (NassarGentina et al, 1988;Marcantoni et al, 2009) chromaffin cells undergo spontaneous firing, but little is known about the ion currents regulating their resting activity. AP-induced secretion in chromaffin cells occurs under basal firing conditions, set by the sympathetic tone, and varies remarkably by changes in AP firing patterns (Duan et al, 2003;Fulop et al, 2005). Our data showing the presence of net inward Cav1.3 and Cav1.2 currents during interspike intervals highlights the role that LTCCs play in regulating AP firing and secretion.…”

Section: Cav13 As Pacemaker Channels In Neurons and Role In Chromaffmentioning

confidence: 59%

Loss of Cav1.3 Channels Reveals the Critical Role of L-Type and BK Channel Coupling in Pacemaking Mouse Adrenal Chromaffin Cells

Marcantoni

Vandael²,

Mahapatra³

et al. 2010

J. Neurosci.

162

325

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We studied wild-type (WT) and Cav1.3 ؊/؊ mouse chromaffin cells (MCCs) with the aim to determine the isoform of L-type Ca 2ϩ channel (LTCC) and BK channels that underlie the pacemaker current controlling spontaneous firing. Most WT-MCCs (80%) were spontaneously active (1.5 Hz) and highly sensitive to nifedipine and BayK-8644 (1,4-dihydro-2,6-dimethyl-5-nitro-4-[2-(trifluoromethyl)phenyl]-3-pyridinecarboxylic acid, methyl ester). Nifedipine blocked the firing, whereas BayK-8644 increased threefold the firing rate. The two dihydropyridines and the BK channel blocker paxilline altered the shape of action potentials (APs), suggesting close coupling of LTCCs to BK channels. WT-MCCs expressed equal fractions of functionally active Cav1.2 and Cav1.3 channels. Cav1.3 channel deficiency decreased the number of normally firing MCCs (30%; 2.0 Hz), suggesting a critical role of these channels on firing, which derived from their slow inactivation rate, sizeable activation at subthreshold potentials, and close coupling to fast inactivating BK channels as determined by using EGTA and BAPTA Ca 2ϩ buffering. By means of the action potential clamp, in TTX-treated WT-MCCs, we found that the interpulse pacemaker current was always net inward and dominated by LTCCs. Fast inactivating and non-inactivating BK currents sustained mainly the afterhyperpolarization of the short APs (2-3 ms) and only partially the pacemaker current during the long interspike (300 -500 ms). Deletion of Cav1.3 channels reduced drastically the inward Ca 2ϩ current and the corresponding Ca 2ϩ -activated BK current during spikes. Our data highlight the role of Cav1.3, and to a minor degree of Cav1.2, as subthreshold pacemaker channels in MCCs and open new interesting features about their role in the control of firing and catecholamine secretion at rest and during sustained stimulations matching acute stress.

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Section: Cav13 As Pacemaker Channels In Neurons and Role In Chromaffmentioning

confidence: 59%

Loss of Cav1.3 Channels Reveals the Critical Role of L-Type and BK Channel Coupling in Pacemaking Mouse Adrenal Chromaffin Cells

Marcantoni

Vandael²,

Mahapatra³

et al. 2010

J. Neurosci.

162

325

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“…Synaptic facilitation requires two preconditions: (1) terminal [Ca 2 þ ] i accumulation during a burst of stimulation; and (2) sufficient releasable vesicles remaining in the presynaptic terminals after the first of paired stimuli 13,31,32 . Actually, facilitation is usually masked by depression and becomes evident only when the depression is relieved by reducing the amount of vesicular transmitter release 33 .…”

Section: Discussionmentioning

confidence: 99%

Modulation of dopamine release in the striatum by physiologically relevant levels of nicotine

et al. 2014

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Striatal dopamine (DA) release can be independently triggered not only by action potentials (APs) in dopaminergic axons but also APs in cholinergic interneurons (ChIs). Nicotine causes addiction by modulating DA release, but with paradoxical findings. Here, we investigate how physiologically relevant levels of nicotine modulate striatal DA release. The optogenetic stimulation of ChIs elicits DA release, which is potently inhibited by nicotine with an IC 50 of 28 nM in the dorsal striatum slice. This ChI-driven DA release is predominantly mediated by a6b2* nAChRs. Local electrical stimulus (Estim) activates both dopaminergic axons and ChIs. Nicotine does not affect the AP DA -dependent DA release (AP DA , AP of dopaminergic axon). During burst Estim, nicotine permits the facilitation of DA release by prevention of DA depletion. Our work indicates that cholinergic stimulation-induced DA release is profoundly modulated by physiologically relevant levels of nicotine and resolves the paradoxical observation of nicotine's effects on striatal DA release.

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“…Cell dissociation. Adrenal chromaffin cells were isolated from Wistar rats and cultured as previously described (7,31). Cells were used in experiments after 2-6 days in culture.…”

Section: Methodsmentioning

confidence: 99%

Calcium influx through I_f channels in rat ventricular myocytes

Yu¹,

Chen²,

Zhou³

et al. 2007

American Journal of Physiology-Cell Physiology

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The hyperpolarization-activated, cyclic nucleotide-gated (HCN) channels, or cardiac ( If)/neuronal ( Ih) time- and voltage-dependent inward cation current channels, are conventionally considered as monovalent-selective channels. Recently we discovered that calcium ions can permeate through HCN4 and Ih channels in neurons. This raises the possibility of Ca2+ permeation in If, the Ih counterpart in cardiac myocytes, because of their structural homology. We performed simultaneous measurement of fura-2 Ca2+ signals and whole cell currents produced by HCN2 and HCN4 channels (the 2 cardiac isoforms present in ventricles) expressed in HEK293 cells and by If in rat ventricular myocytes. We observed Ca2+ influx when HCN/ If channels were activated. Ca2+ influx was increased with stronger hyperpolarization or longer pulse duration. Cesium, an If channel blocker, inhibited If and Ca2+ influx at the same time. Quantitative analysis revealed that Ca2+ flux contributed to ∼0.5% of current produced by the HCN2 channel or If. The associated increase in Ca2+ influx was also observed in spontaneously hypertensive rat (SHR) myocytes in which If current density is higher than that of normotensive rat ventricle. In the absence of EGTA (a Ca2+ chelator), preactivation of If channels significantly reduced the action potential duration, and the effect was blocked by another selective If channel blocker, ZD-7288. In the presence of EGTA, however, preactivation of If channels had no effects on action potential duration. Our data extend our previous discovery of Ca2+ influx in Ih channels in neurons to If channels in cardiac myocytes.

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Control of Secretion by Temporal Patterns of Action Potentials in Adrenal Chromaffin Cells

Cited by 40 publications

References 44 publications

Loss of Cav1.3 Channels Reveals the Critical Role of L-Type and BK Channel Coupling in Pacemaking Mouse Adrenal Chromaffin Cells

Loss of Cav1.3 Channels Reveals the Critical Role of L-Type and BK Channel Coupling in Pacemaking Mouse Adrenal Chromaffin Cells

Modulation of dopamine release in the striatum by physiologically relevant levels of nicotine

Calcium influx through I_f channels in rat ventricular myocytes

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Control of Secretion by Temporal Patterns of Action Potentials in Adrenal Chromaffin Cells

Cited by 40 publications

References 44 publications

Loss of Cav1.3 Channels Reveals the Critical Role of L-Type and BK Channel Coupling in Pacemaking Mouse Adrenal Chromaffin Cells

Loss of Cav1.3 Channels Reveals the Critical Role of L-Type and BK Channel Coupling in Pacemaking Mouse Adrenal Chromaffin Cells

Modulation of dopamine release in the striatum by physiologically relevant levels of nicotine

Calcium influx through If channels in rat ventricular myocytes

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Calcium influx through I_f channels in rat ventricular myocytes