Carbachol-stimulated chloride secretion in mouse colon: evidence of a role for autocrine prostaglandin E2 release

Carew, Mark; Thorn, Peter

doi:10.1017/s0958067000019473

Cited by 9 publications

(8 citation statements)

References 16 publications

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“…cAMP and Ca 2+ induced Cl − secretion mechanisms are both critically dependent on the presence of active apical CFTR channels. Because CFTR channels are gated by an increase in intracellular cAMP, Ca 2+ -mediated Cl − secretion requires pre-activation of the CFTR channel by cAMP 13 . Considering the dependence of the Ca 2+ -mediated process on intracellular cAMP, Ussing chambers experiments to examine Cl − secretion in EDC and LDC used a sequential cAMP and then Ca 2+ mobilization protocol.…”

Section: Resultsmentioning

confidence: 99%

“…The solution bathing the apical and basolateral hemi-chambers consisted of (in mM): 115 NaCl, 5 KCl, 25 NaHCO 3 , 1 CaCl 2 and 2 MgCl 2 , at pH 7.4. Indomethacin (5 μM) was added to the serosal side to prevent endogenous cAMP production via prostaglandin E 2 release 13, 14 . Solutions were gassed with 95% O 2 /5% CO 2 .…”

Section: Methodsmentioning

confidence: 99%

“…It appears that activation of the basolateral Ca 2+ -activated K + channel KCNN4 during Ca 2+ -activated intestinal secretion hyperpolarizes intestinal epithelial cells, and consequently, generates a greater driving force for CFTR-mediated Cl − efflux 12 . Indeed, if CFTR is not first activated, a rise in intracellular Ca 2+ does not cause Cl − secretion 11, 13, 14 .…”

Section: Introductionmentioning

confidence: 99%

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Severe Defects in Absorptive Ion Transport in Distal Colons of Mice That Lack ClC-2 Channels

et al. 2012

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Background & Aims The fluid secretion model predicts that intestinal obstruction disorders can be alleviated by promoting epithelial Cl− secretion. The cAMP-activated anion channel CFTR mediates Cl−-dependent fluid secretion in the intestine. Although the role of the ClC-2 channel has not been determined in the intestine, this voltage-gated Cl− channel might compensate for the secretory defects observed in patients with cystic fibrosis and other chronic constipation disorders. We investigated whether mice that lack ClC-2 channels (Clcn2−/−) have defects in intestinal ion transport. Methods Immunolocalization and immunoblot analyses were used to determine the cellular localization and the amount of ClC-2 expressed in mouse early (EDC) and late distal colon (LDC). Colon sheets from wildtype and Clcn2−/− littermates were mounted in Ussing chambers to determine transepithelial bioelectrical parameters and Na+, K+ and Cl− flux. Results Expression of ClC-2 was higher in the basolateral membrane of surface cells in the EDC, compared to the LDC, with little expression in crypts. Neither cAMP nor Ca2+-induced secretion of Cl− was affected in the EDC or LDC of Clcn2−/− mice, whereas the amiloride-sensitive short circuit current (ISC) was increased approximately 3-fold in Clcn2−/− EDC, compared to that of control littermates. Conversely, electroneutral Na+, K+ and Cl− absorption were dramatically reduced in colons of Clcn2−/− mice. Conclusions Basolateral ClC-2 channels are required for colonic electroneutral absorption of NaCl and KCl. The increase in the amiloride-sensitive ISC in Clcn2−/− mice revealed a compensatory mechanism that is activated in the colons of mice that lack the ClC-2 channel.

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Section: Resultsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Severe Defects in Absorptive Ion Transport in Distal Colons of Mice That Lack ClC-2 Channels

et al. 2012

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“…The exact reason why specific frequency stimulations optimize neuropeptide secretion is still under intense study (Lemos & Wang, 2000). Various possible explanations for this phenomenon have been proposed.…”

Section: Discussionmentioning

confidence: 99%

“…However, a yet unexplained residual frequency-dependent facilitation of action potential-induced rise in the intracellular Ca 2+ concentration, unrelated to action potential broadening, remain to be explained (Jackson et al, 1991). Furthermore, biophysical properties of the VGCC present in isolated terminals cannot account for the observed frequency-dependent facilitation (Wang et al, 1997b; Wang et al, 1999; Lemos & Wang, 2000). …”

Section: Discussionmentioning

confidence: 99%

Voltage‐dependent κ‐opioid modulation of action potential waveform‐elicited calcium currents in neurohypophysial terminals

Velázquez-Marrero

Marrero

Lemos

2010

Journal Cellular Physiology

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Release of neurotransmitter is activated by the influx of calcium. Inhibition of Ca2+ channels results in less calcium influx into the terminal and presumably a reduction in transmitter release. In the neurohypophysis (NH), Ca2+ channel kinetics, and the associated Ca2+ influx, is primarily controlled by membrane voltage and can be modulated, in a voltage-dependent manner, by G-protein subunits interacting with voltage-gated calcium channels (VGCC). In this series of experiments we test whether the κ- and μ-opioid inhibition of Ca2+ currents in NH terminals is voltage-dependent. Voltage-dependent relief of G-protein inhibition of VGCC can be achieved with either a depolarizing square pre-pulse or by action potential waveforms. Both protocols were tested in the presence and absence of opioid agonists targeting the κ- and μ-receptors in neurohypophysial terminals. The κ-opioid VGCC inhibition is relieved by such pre-pulses, suggesting that this receptor is involved in a voltage-dependent membrane delimited pathway. In contrast, μ-opioid inhibition of VGCC is not relieved by such pre-pulses, indicating a voltage-independent diffusible second-messenger signaling pathway. Furthermore, relief of κ-opioid inhibition during a physiological action potential burst stimulation indicates the possibility of activity-dependent modulation in vivo. Differences in the facilitation of Ca2+ channels due to specific G-protein modulation during a burst of action potentials may contribute to the fine-tuning of Ca2+-dependent neuropeptide release in other CNS terminals, as well.

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An Inositol Phosphate Analog, INO-4995, Normalizes Electrophysiology in CF Airway Epithelia

Traynor‐Kaplan

Moody

Schultz

2005

Advances in Experimental Medicine and Biology

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Carbachol-stimulated chloride secretion in mouse colon: evidence of a role for autocrine prostaglandin E2 release

Cited by 9 publications

References 16 publications

Severe Defects in Absorptive Ion Transport in Distal Colons of Mice That Lack ClC-2 Channels

Severe Defects in Absorptive Ion Transport in Distal Colons of Mice That Lack ClC-2 Channels

Voltage‐dependent κ‐opioid modulation of action potential waveform‐elicited calcium currents in neurohypophysial terminals

An Inositol Phosphate Analog, INO-4995, Normalizes Electrophysiology in CF Airway Epithelia

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