Neuropeptide inhibition of voltage-gated calcium channels mediated by mobilization of intracellular calcium

Neuron ◽  
1991 ◽  
Vol 6 (4) ◽  
pp. 557-563 ◽  
Author(s):  
Richard H. Kramer ◽  
Leonard K. Kaczmarek ◽  
Edwin S. Levitan
Keyword(s):  
Calcium Channels ◽  
Intracellular Calcium ◽  
Voltage Gated ◽  
Voltage Gated Calcium Channels

Glutamatergic Calcium Responses in the Developing Lateral Superior Olive: Receptor Types and Their Specific Activation by Synaptic Activity Patterns

2003 ◽  
Vol 90 (4) ◽  
pp. 2581-2591 ◽  
Author(s):  
F. Aura Ene ◽  
Paul H. M. Kullmann ◽  
Deda C. Gillespie ◽  
Karl Kandler
Keyword(s):  
Calcium Channels ◽  
Intracellular Calcium ◽  
Glutamate Receptors ◽  
Cochlear Nucleus ◽  
Metabotropic Glutamate Receptors ◽  
Lateral Superior Olive ◽  
Voltage Gated ◽  
Superior Olive ◽  
Metabotropic Glutamate ◽  
Voltage Gated Calcium Channels

The lateral superior olive (LSO) is a binaural auditory brain stem nucleus that plays a central role in sound localization. Survival and maturation of developing LSO neurons critically depend on intracellular calcium signaling. Here we investigated the mechanisms by which glutamatergic afferents from the cochlear nucleus increase intracellular calcium concentration in LSO neurons. Using fura-2 calcium imaging in slices prepared from neonatal mice, we found that cochlear nucleus afferents can activate all major classes of ionotropic and metabotropic glutamate receptors, each of which contributes to an increase in intracellular calcium. The specific activation of different glutamate receptor classes was dependent on response amplitudes and afferent stimulus patterns. Low-amplitude responses elicited by single stimuli were entirely mediated by calcium-impermeable AMPA/kainate receptors that activated voltage-gated calcium channels. Larger-amplitude responses elicited by either single stimuli or stimulus trains resulted in additional calcium influx through N-methyl-d-aspartate receptors. Finally, high-frequency stimulation also recruited group I and group II metabotropic glutamate receptors, both of which mobilized intracellular calcium. This calcium release in turn activated a strong influx of extracellular calcium through a membrane calcium channel that is distinct from voltage-gated calcium channels. Together, these results indicate that before hearing onset, distinct patterns of afferent activity generate qualitatively distinct types of calcium responses, which likely serve in guiding different aspects of LSO development.

scholarly journals Inhibitory Effect of Somatostatin-14 on L-Type Voltage-Gated Calcium Channels in Cultured Cone Photoreceptors Requires Intracellular Calcium

2009 ◽  
Vol 102 (3) ◽  
pp. 1801-1810 ◽  
Author(s):  
Kuihuan Jian ◽  
Rola Barhoumi ◽  
Michael L. Ko ◽  
Gladys Y.-P. Ko
Keyword(s):  
Calcium Channels ◽  
Intracellular Calcium ◽  
G Protein ◽  
Inhibitory Effect ◽  
Calcium Stores ◽  
Dependent Effect ◽  
Voltage Gated ◽  
Circadian Phase ◽  
Voltage Gated Calcium Channels ◽  
Somatostatin 14

The inhibitory effects of somatostatin have been well documented for many physiological processes. The action of somatostatin is through G-protein-coupled receptor-mediated second-messenger signaling, which in turn affects other downstream targets including ion channels. In the retina, somatostatin is released from a specific class of amacrine cells. Here we report that there was a circadian phase-dependent effect of somatostatin-14 (SS14) on the L-type voltage-gated calcium channels (L-VGCCs) in cultured chicken cone photoreceptors, and our study reveals that this process is dependent on intracellular calcium stores. Application of 500 nM SS14 for 2 h caused a decrease in L-VGCC currents only during the subjective night but not the subjective day. We then explored the cellular mechanisms underlying the circadian phase-dependent effect of SS14. The inhibitory effect of SS14 on L-VGCCs was mediated through the pertussis-toxin-sensitive G-protein-dependent somatostatin receptor 2 (sst2). Activation of sst2 by SS14 further activated downstream signaling involving phospholipase C and intracellular calcium stores. Mobilization of intracellular Ca2+ was required for somatostatin induced inhibition of photoreceptor L-VGCCs, suggesting that somatostatin plays an important role in the modulation of photoreceptor physiology.

scholarly journals Trafficking of neuronal calcium channels

2017 ◽  
Vol 1 (1) ◽  
Author(s):  
Norbert Weiss ◽  
Gerald W. Zamponi
Keyword(s):  
Plasma Membrane ◽  
Calcium Channels ◽  
Intracellular Calcium ◽  
Dynamic Control ◽  
Surface Expression ◽  
Regulatory Mechanisms ◽  
Signalling Pathways ◽  
Physiological Functions ◽  
Voltage Gated ◽  
Voltage Gated Calcium Channels

Neuronal voltage-gated calcium channels (VGCCs) serve complex yet essential physiological functions via their pivotal role in translating electrical signals into intracellular calcium elevations and associated downstream signalling pathways. There are a number of regulatory mechanisms to ensure a dynamic control of the number of channels embedded in the plasma membrane, whereas alteration of the surface expression of VGCCs has been linked to various disease conditions. Here, we provide an overview of the mechanisms that control the trafficking of VGCCs to and from the plasma membrane, and discuss their implication in pathophysiological conditions and their potential as therapeutic targets.

Dependency of hypoxic chemotransduction in cat carotid body on voltage-gated calcium channels

1991 ◽  
Vol 71 (3) ◽  
pp. 1062-1069 ◽  
Author(s):  
M. Shirahata ◽  
R. S. Fitzgerald
Keyword(s):  
Calcium Channels ◽  
Calcium Channel ◽  
Intracellular Calcium ◽  
Carotid Body ◽  
Calcium Ions ◽  
Extracellular Calcium ◽  
Bay K 8644 ◽  
Voltage Gated ◽  
Voltage Gated Calcium Channels ◽  
Selective Perfusion

The hypothesis that the entry of extracellular calcium ions into some compartment, quite possibly the type I cells, through voltage-gated calcium channels (VGCC) is essential for hypoxic chemotransduction in the cat carotid body was tested using an in situ perfusion technique. The neural output of the carotid body of anesthetized, paralyzed, and artificially ventilated cats in response to perfusions with Krebs-Ringer bicarbonate solution (KRB), calcium-free KRB, KRB containing calcium channel blockers, or KRB containing BAY K 8644 was recorded. Selective perfusion of the carotid body with hypoxic calcium-free KRB significantly decreased carotid chemoreceptor activity, suggesting that extracellular calcium is essential for hypoxic chemotransduction. Selective perfusion of the carotid body with hypoxic KRB containing verapamil (10–100 microM), diltiazem (10–100 microM), or nifedipine (10–100 microM) dose dependently attenuated the increase in chemoreceptor activity produced by hypoxia, suggesting that VGCC need to be activated for hypoxic chemotransduction. The carotid body response to hyperoxic KRB containing the calcium channel agonist BAY K 8644 (10 microM) was 267 +/- 87% of hyperoxic control KRB, suggesting that an enhanced influx of calcium ions through VGCC stimulates carotid chemoreceptor activity. Selective perfusion of the carotid body with severely hypoxic KRB containing BAY K 8644 did not increase chemoreceptor activity above that produced by severe hypoxia alone. This suggests that severe hypoxia increases intracellular calcium in some compartment of the carotid body to achieve stimulatory maximum response and that further increase in intracellular calcium does not produce further elevation of neural activity.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Histamine causes influx via T-type voltage-gated calcium channels in an enterochromaffin tumor cell line: potential therapeutic target in adverse food reactions

2019 ◽  
Vol 316 (2) ◽  
pp. G291-G303 ◽  
Author(s):  
Beatrix Pfanzagl ◽  
Victor F. Zevallos ◽  
Detlef Schuppan ◽  
Roswitha Pfragner ◽  
Erika Jensen-Jarolim
Keyword(s):  
Calcium Channels ◽  
Intracellular Calcium ◽  
Tumor Cells ◽  
Molecular Mechanisms ◽  
Trypsin Inhibitors ◽  
Enterochromaffin Cells ◽  
Neuroendocrine Cells ◽  
Voltage Gated ◽  
Voltage Gated Calcium Channels ◽  
Tnf Α

The P-STS human ileal neuroendocrine tumor cells, as a model for gut enterochromaffin cells, are strongly and synergistically activated by histamine plus acetylcholine (ACh), presumably via histamine 4 receptors, and weakly activated by histamine alone. Sensing these signals, enterochromaffin cells could participate in intestinal intolerance or allergic reactions to food constituents associated with elevated histamine levels. In this study we aimed to analyze the underlying molecular mechanisms. Inhibition by mepyramine and mibefradil indicated that histamine alone caused a rise in intracellular calcium concentration ([Ca2+]i) via histamine 1 receptors involving T-type voltage-gated calcium channels (VGCCs). Sensitivity to histamine was enhanced by pretreatment with the inflammatory cytokine tumor necrosis factor-α (TNF-α). In accordance with the relief it offers some inflammatory bowel disease patients, otilonium bromide, a gut-impermeable inhibitor of T-type (and L-type) VGCCs and muscarinic ACh receptors, efficiently inhibited the [Ca2+]i responses induced by histamine plus ACh or by histamine alone in P-STS cells. It will take clinical studies to show whether otilonium bromide has promise for the treatment of adverse food reactions. The cells did not react to the nutrient constituents glutamate, capsaicin, cinnamaldehyde, or amylase-trypsin inhibitors and the transient receptor potential channel vanilloid 4 agonist GSK-1016790A. The bacterial product butyrate evoked a rise in [Ca2+]i only when added together with ACh. Lipopolysaccharide had no effect on [Ca2+]i despite the presence of Toll-like receptor 4 protein. Our results indicate that inflammatory conditions with elevated levels of TNF-α might enhance histamine-induced serotonin release from intestinal neuroendocrine cells. NEW & NOTEWORTHY We show that histamine synergistically enhances the intracellular calcium response to the physiological agonist acetylcholine in human ileal enterochromaffin tumor cells. This synergistic activation and cell activation by histamine alone largely depend on T-type voltage-gated calcium channels and are inhibited by the antispasmodic otilonium bromide. The cells showed no response to wheat amylase-trypsin inhibitors, suggesting that enterochromaffin cells are not directly involved in nongluten wheat sensitivity.

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