Acetylcholine Increases Intracellular Calcium of Arterial Chemoreceptor Cells of Adult Cats

1997 ◽  
Vol 78 (5) ◽  
pp. 2388-2395 ◽  
Author(s):  
Machiko Shirahata ◽  
Robert S. Fitzgerald ◽  
James S. K. Sham
Keyword(s):  
Intracellular Calcium ◽  
Carotid Body ◽  
Calcium Concentration ◽  
Similar Response ◽  
Muscarinic Agonists ◽  
High K ◽  
Chemoreceptor Cells ◽  
Adult Cats ◽  
Kinetics Of ◽  
Arterial Chemoreceptor

Shirahata, Machiko, Robert S. Fitzgerald, and James S. K. Sham. Acetylcholine increases intracellular calcium of arterial chemoreceptor cells of adult cats. J. Neurophysiol. 78: 2388–2395, 1997. Several neurotransmitters have been reported to play important roles in the chemoreception of the carotid body. Among them acetylcholine (ACh) appears to be involved in excitatory processes in the cat carotid body. As one of the steps to elucidate possible roles of ACh in carotid body chemoreception in the cat, we examined the effect of ACh on intracellular calcium concentration ([Ca2+]i) of cultured carotid body cells. The carotid body from adult cats was dissociated and cultured for up to 2 wk. [Ca2+]i was measured from clusters of cells with a microfluorometric technique using Indo-1 AM. Experiments were performed at 37°C, and cells were continuously superfused with modified Krebs solutions equilibrated with 5% CO2-16% O2-79% N2. ACh (100 μM) caused a marked increase in [Ca2+]i in ∼70% of clusters, and the responses to 1–300 μM of ACh were concentration dependent. The magnitude and kinetics of the ACh response were mimicked by the application of nicotine, whereas muscarinic agonists, pilocarpine, and muscarine failed to evoke a similar response. ACh-induced increase in [Ca2+]i was dependent on extracellular Ca2+: it was greatly reduced or completely abolished by a transient removal of extracellular Ca2+. The response was consistently but only partially reduced by caffeine (5 mM) or nifedipine (10 μM). The effect of mecamylamine (100 μM) was inhibitory but small. Moreover, the increase in [Ca2+]i in response to ACh was also observed in some clusters that did not respond to high K (100 mM) Krebs. These results suggest that ACh increases [Ca2+]i of cultured carotid body cells by activating neuronal nicotinic ACh receptors, leading to Ca2+ influx via nicotinic channels. In addition, other pathways such as Ca2+ influx through L-type calcium channels, perhaps secondary to membrane depolarization, and Ca2+ release from intracellular stores may participate in increasing [Ca2+]i in response to ACh. Muscarinic receptors appear to play only a small role, if any.

scholarly journals Hydroxycobalamin Reveals the Involvement of Hydrogen Sulfide in the Hypoxic Responses of Rat Carotid Body Chemoreceptor Cells

Antioxidants ◽  
2019 ◽  
Vol 8 (3) ◽  
pp. 62
Author(s):  
Teresa Gallego-Martin ◽  
Jesus Prieto-Lloret ◽  
Philip Aaronson ◽  
Asuncion Rocher ◽  
Ana Obeso
Keyword(s):  
Hydrogen Sulfide ◽  
Carotid Body ◽  
Oxygen Sensor ◽  
Catecholamine Release ◽  
Glomus Cells ◽  
Arterial Blood ◽  
Carotid Bodies ◽  
High K ◽  
Chemoreceptor Cells ◽  
Ca2 Channels

Carotid body (CB) chemoreceptor cells sense arterial blood PO2, generating a neurosecretory response proportional to the intensity of hypoxia. Hydrogen sulfide (H2S) is a physiological gaseous messenger that is proposed to act as an oxygen sensor in CBs, although this concept remains controversial. In the present study we have used the H2S scavenger and vitamin B12 analog hydroxycobalamin (Cbl) as a new tool to investigate the involvement of endogenous H2S in CB oxygen sensing. We observed that the slow-release sulfide donor GYY4137 elicited catecholamine release from isolated whole carotid bodies, and that Cbl prevented this response. Cbl also abolished the rise in [Ca2+]i evoked by 50 µM NaHS in enzymatically dispersed CB glomus cells. Moreover, Cbl markedly inhibited the catecholamine release and [Ca2+]i rise caused by hypoxia in isolated CBs and dispersed glomus cells, respectively, whereas it did not alter these responses when they were evoked by high [K+]e. The L-type Ca2+ channel blocker nifedipine slightly inhibited the rise in CB chemoreceptor cells [Ca2+]i elicited by sulfide, whilst causing a somewhat larger attenuation of the hypoxia-induced Ca2+ signal. We conclude that Cbl is a useful and specific tool for studying the function of H2S in cells. Based on its effects on the CB chemoreceptor cells we propose that endogenous H2S is an amplifier of the hypoxic transduction cascade which acts mainly by stimulating non-L-type Ca2+ channels.

scholarly journals Changes in Intracellular Calcium Concentration Affect Desensitization of GABAA Receptors in Acutely Dissociated P2–P6 Rat Hippocampal Neurons

1998 ◽  
Vol 79 (3) ◽  
pp. 1321-1328 ◽  
Author(s):  
Jerzy W. Mozrzymas ◽  
Enrico Cherubini
Keyword(s):  
Intracellular Calcium ◽  
Hippocampal Neurons ◽  
Calcium Concentration ◽  
Intracellular Calcium Concentration ◽  
Potential Range ◽  
Patch Clamp Technique ◽  
Whole Cell ◽  
Cell Configuration ◽  
High Calcium ◽  
Kinetics Of

Mozrzymas, Jerzy W. and Enrico Cherubini. Changes in intracellular calcium concentration affect desensitization of GABAA receptors in acutely dissociated P2–P6 rat hippocampal neurons. J. Neurophysiol. 79: 1321–1328, 1998. The whole cell configuration of the patch-clamp technique was used to study the effects of different cytosolic calcium concentrations [Ca2+]i on desensitization kinetics of γ-aminobutyric acid (GABA)-activated receptors in acutely dissociated rat hippocampal neurons. Two different intrapipette concentrations of the calcium chelator 1,2-bis(2-aminophenoxy)ethane- N, N, N′, N′-tetraacetic acid (BAPTA; 11 and 0.9 mM, respectively) were used to yield a low (1.2 × 10−8 M) or a high (2.2 × 10−6 M) [Ca2+]i. In low [Ca2+]i, peak values of GABA-evoked currents (20 μM) evoked at −30 mV, were significantly larger than those recorded in high calcium [2,970 ± 280 (SE) pA vs. 1,870 ± 150 pA]. The extent of desensitization, assessed from steady-state to peak ratio was significantly higher in high calcium conditions (0.14 ± 0.007 vs. 0.11 ± 0.008). Similar effects of [Ca2+]i on desensitization were observed with GABA (100 μM). Recovery from desensitization, measured at 30 s interval with double pulse protocol was significantly slower in high [Ca2+]i than in low [Ca2+]i (54 ± 3% vs. 68 ± 2%). The current-voltage relationship of GABA-evoked currents was linear in the potential range between −50 and 50 mV. The kinetics of desensitization process including the rate of onset, extent of desensitization, and recovery were voltage independent. The run down of GABA-evoked currents was faster with the higher intracellular calcium concentration. The run down process was accompanied by changes in desensitization kinetics: in both high and low [Ca2+]i desensitization rate was progressively increasing with time as the slow component of the desensitization onset was converted into the fast one. In excised patches, the desensitization kinetics was much faster and more profound than in the whole cell configuration, indicating the involvement of intracellular factors in regulation of this process. In conclusion, [Ca2+]i affects the desensitization of GABAA receptors possibly by activating calcium-dependent enzymes that regulate their phosphorylation state. This may lead to modifications in cell excitability because of changes in GABA-mediated synaptic currents.

scholarly journals Electrophysiological study of Drosophila rhodopsin mutants.

1986 ◽  
Vol 88 (5) ◽  
pp. 651-673 ◽  
Author(s):  
E C Johnson ◽  
W L Pak
Keyword(s):  
Intracellular Calcium ◽  
Calcium Concentration ◽  
Electrophysiological Study ◽  
Noise Analysis ◽  
Intracellular Calcium Concentration ◽  
Wild Type ◽  
Light Responses ◽  
Kinetics Of

Electrophysiological investigations were carried out on several independently isolated mutants of the ninaE gene, which encodes opsin in R1-6 photoreceptors, and a mutant of the ninaD gene, which is probably important in the formation of the rhodopsin chromophore. In these mutants, the rhodopsin content in R1-6 photoreceptors is reduced by 10(2)-10(6)-fold. Light-induced bumps recorded from even the most severely affected mutants are physiologically normal. Moreover, a detailed noise analysis shows that photoreceptor responses of both a ninaE mutant and a ninaD mutant follow the adapting bump model. Since any extensive rhodopsin-rhodopsin interactions are not likely in these mutants, the above results suggest that such interactions are not needed for the generation and adaptation of light-induced bumps. Mutant bumps are strikingly larger in amplitude than wild-type bumps. This difference is observed both in ninaD and ninaE mutants, which suggests that it is due to severe depletion of rhodopsin content, rather than to any specific alterations in the opsin protein. Lowering or buffering the intracellular calcium concentration by EGTA injection mimics the effects of the mutations on the bump amplitude, but, unlike the mutations, it also affects the latency and kinetics of light responses.

Intracellular Ca2+ stores in chemoreceptor cells of the rabbit carotid body: significance for chemoreception

2000 ◽  
Vol 279 (1) ◽  
pp. C51-C61 ◽  
Author(s):  
I. Vicario ◽  
A. Obeso ◽  
A. Rocher ◽  
J. R. López-Lopez ◽  
C. González
Keyword(s):  
Significant Role ◽  
Carotid Body ◽  
Time Course ◽  
Cyclopiazonic Acid ◽  
Structural Identity ◽  
High K ◽  
Intracellular Ca ◽  
Intact Rabbit ◽  
Chemoreceptor Cells

The notion that intracellular Ca2+ (Cai 2+) stores play a significant role in the chemoreception process in chemoreceptor cells of the carotid body (CB) appears in the literature in a recurrent manner. However, the structural identity of the Ca2+ stores and their real significance in the function of chemoreceptor cells are unknown. To assess the functional significance of Cai 2+ stores in chemoreceptor cells, we have monitored 1) the release of catecholamines (CA) from the cells using an in vitro preparation of intact rabbit CB and 2) the intracellular Ca2+ concentration ([Ca2+]i) using isolated chemoreceptor cells; both parameters were measured in the absence or the presence of agents interfering with the storage of Ca2+. We found that threshold [Ca2+]i for high extracellular K+ (Ke +) to elicit a release response is ≈250 nM. Caffeine (10–40 mM), ryanodine (0.5 μM), thapsigargin (0.05–1 μM), and cyclopiazonic acid (10 μM) did not alter the basal or the stimulus (hypoxia, high Ke +)-induced release of CA. The same agents produced Cai 2+transients of amplitude below secretory threshold; ryanodine (0.5 μM), thapsigargin (1 μM), and cyclopiazonic acid (10 μM) did not alter the magnitude or time course of the Cai 2+responses elicited by high Ke +. Several potential activators of the phospholipase C system (bethanechol, ATP, and bradykinin), and thereby of inositol 1,4,5-trisphosphate receptors, produced minimal or no changes in [Ca2+]i and did not affect the basal release of CA. It is concluded that, in the rabbit CB chemoreceptor cells, Cai 2+ stores do not play a significant role in the instant-to-instant chemoreception process.

Culture of arterial chemoreceptor cells from adult cats in defined medium

1994 ◽  
Vol 658 (1-2) ◽  
pp. 60-66 ◽  
Author(s):  
Machiko Shirahata ◽  
Brian Schofield ◽  
Beek Y. Chin ◽  
Tomas R. Guilarte
Keyword(s):  
Defined Medium ◽  
Chemoreceptor Cells ◽  
Adult Cats ◽  
Arterial Chemoreceptor

scholarly journals Orientia tsutsugamushi Inhibits Apoptosis of Macrophages by Retarding Intracellular Calcium Release

2002 ◽  
Vol 70 (8) ◽  
pp. 4692-4696 ◽  
Author(s):  
Mee-Kyung Kim ◽  
Seung-Yong Seong ◽  
Ju-Young Seoh ◽  
Tae-Hee Han ◽  
Hyeon-Je Song ◽  
...  
Keyword(s):  
Intracellular Calcium ◽  
Calcium Concentration ◽  
Calcium Release ◽  
Cytosolic Calcium ◽  
Orientia Tsutsugamushi ◽  
Cytosolic Calcium Concentration ◽  
Infected Cells ◽  
Intracellular Calcium Release ◽  
Calcium Redistribution ◽  
In Cells

ABSTRACT Orientia tsutsugamushi shows both pro- and antiapoptotic activities in infected vertebrate cells. Apoptosis of THP-1 cells induced by beauvericin was inhibited by O. tsutsugamushi infection. Beauvericin-induced calcium redistribution was significantly reduced and retarded in cells infected with O. tsutsugamushi. Antiapoptotic activities of O. tsutsugamushi in infected cells are most probably due to inhibition of the increase in the cytosolic calcium concentration.

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