scholarly journals A temperature-sensitive TRP ion channel, Painless, functions as a noxious heat sensor in fruit flies

2009 ◽  
Vol 2 (2) ◽  
pp. 170-173 ◽  
Author(s):  
Takaaki Sokabe ◽  
Makoto Tominaga
Keyword(s):  
Ion Channel ◽  
Fruit Flies ◽  
Temperature Sensitive ◽  
Noxious Heat ◽  
Heat Sensor ◽  
Trp Ion Channel

A cell-based impedance assay for monitoring transient receptor potential (TRP) ion channel activity

2011 ◽  
Vol 26 (5) ◽  
pp. 2376-2382 ◽  
Author(s):  
Oliver Pänke ◽  
Winnie Weigel ◽  
Sabine Schmidt ◽  
Anja Steude ◽  
Andrea A. Robitzki
Keyword(s):  
Ion Channel ◽  
Transient Receptor Potential ◽  
Receptor Potential ◽  
Channel Activity ◽  
A Cell ◽  
Transient Receptor ◽  
Trp Ion Channel

scholarly journals Building a Temperature-Sensitive Ion Channel

Cell ◽  
2014 ◽  
Vol 158 (5) ◽  
pp. 977-979 ◽  
Author(s):  
Ming-Feng Tsai ◽  
Christopher Miller
Keyword(s):  
Ion Channel ◽  
Temperature Sensitive

scholarly journals Synthesis and biological activity study of the retro-isomer of RhTx against TRPV1

RSC Advances ◽  
2020 ◽  
Vol 10 (4) ◽  
pp. 2141-2145
Author(s):  
Rilei Yu ◽  
Huijie Liu ◽  
Baishi Wang ◽  
Peta J. Harvey ◽  
Ningning Wei ◽  
...  
Keyword(s):  
Biological Activity ◽  
Ion Channel ◽  
Noxious Heat ◽  
Trpv1 Antagonist

TRPV1 is a ligand-gated ion channel and plays an important role in detecting noxious heat and pain. A new TRPV1 antagonist RL-RhTx was discovered.

scholarly journals The Temperature-Sensitive Ion Channel TRPV2 is Endogenously Expressed and Functional in the Primary Sensory Cell Line F-11

2005 ◽  
Vol 15 (1-4) ◽  
pp. 183-194 ◽  
Author(s):  
Florian Bender ◽  
Michael Mederos y Schnitzler ◽  
Yanzhang Li ◽  
Ailing Ji ◽  
Eberhard Weihe ◽  
...  
Keyword(s):  
Ion Channel ◽  
Cell Line ◽  
Sensory Cell ◽  
Temperature Sensitive

scholarly journals Rapid characterisation of hERG channel kinetics II: temperature dependence

2019 ◽  
Author(s):  
Chon Lok Lei ◽  
Michael Clerx ◽  
Kylie A. Beattie ◽  
Dario Melgari ◽  
Jules C. Hancox ◽  
...  
Keyword(s):  
Ion Channel ◽  
Temperature Dependence ◽  
Kinetic Parameters ◽  
Room Temperature ◽  
Herg Channel ◽  
Rate Theory ◽  
Temperature Sensitive ◽  
Channel Kinetics ◽  
Voltage Dependent ◽  
The Many

ABSTRACTIon channel behaviour can depend strongly on temperature, with faster kinetics at physiological temperatures leading to considerable changes in currents relative to room temperature. These temperature-dependent changes in voltage-dependent ion channel kinetics (rates of opening, closing and inactivating) are commonly represented with Q10coefficients or an Eyring relationship. In this paper we assess the validity of these representations by characterising channel kinetics at multiple temperatures. We focus on the hERG channel, which is important in drug safety assessment and commonly screened at room temperature, so that results require extrapolation to physiological temperature. In Part I of this study we established a reliable method for high-throughput characterisation of hERG1a (Kv11.1) kinetics, using a 15 second information-rich optimised protocol. In this Part II, we use this protocol to study the temperature dependence of hERG kinetics using CHO cells over-expressing hERG1a on the Nanion SyncroPatch 384PE, a 384-well automated patch clamp platform, with temperature control. We characterise the temperature dependence of hERG gating by fitting the parameters of a mathematical model of hERG kinetics to data obtained at five distinct temperatures between 25 and 37 °C, and validate the models using different protocols. Our models reveal that activation is far more temperature sensitive than inactivation, and we observe that the temperature dependency of the kinetic parameters is not represented well by Q10coefficients: it broadly follows a generalised, but not the standardly-used, Eyring relationship. We also demonstrate that experimental estimations of Q10coefficients are protocol-dependent. Our results show that a direct fit using our 15 second protocol best represents hERG kinetics at any given temperature, and suggests that predictions from the Generalised Eyring theory may be preferentially used if no experimentally-derived data are available.Statement of SignificanceIon channel currents are highly sensitive to temperature changes. Yet because many experiments are performed more easily at room temperature, it is common to extrapolate findings to physiological temperatures through the use of Q10coefficients or Eyring rate theory. By applying short, information-rich protocols that we developed in Part I of this study we identify how kinetic parameters change over temperature. We find that the commonly-used Q10and Eyring formulations are incapable of describing the parameters’ temperature dependence, a more Generalised Eyring relationship works well, but remeasuring kinetics and refitting a model is optimal. The findings have implications for the accuracy of the many applications of Q10coefficients in electrophysiology, and suggest that care is needed to avoid misleading extrapolations in their many scientific and industrial pharmaceutical applications.

scholarly journals Single nucleotide polymorphisms and genotypes of transient receptor potential ion channel and acetylcholine receptor genes from isolated B lymphocytes in myalgic encephalomyelitis/chronic fatigue syndrome patients

2016 ◽  
Vol 44 (6) ◽  
pp. 1381-1394 ◽  
Author(s):  
Sonya Marshall-Gradisnik ◽  
Samantha Johnston ◽  
Anu Chacko ◽  
Thao Nguyen ◽  
Peter Smith ◽  
...  
Keyword(s):  
B Cells ◽  
Chronic Fatigue Syndrome ◽  
Single Nucleotide Polymorphisms ◽  
Ion Channel ◽  
B Cell ◽  
Chronic Fatigue ◽  
Nucleotide Polymorphisms ◽  
Single Nucleotide ◽  
Fatigue Syndrome ◽  
Trp Ion Channel

Objective The pathomechanism of chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME) is unknown; however, a small subgroup of patients has shown muscarinic antibody positivity and reduced symptom presentation following anti-CD20 intervention. Given the important roles of calcium (Ca2+) and acetylcholine (ACh) signalling in B cell activation and potential antibody development, we aimed to identify relevant single nucleotide polymorphisms (SNPs) and genotypes in isolated B cells from CFS/ME patients. Methods A total of 11 CFS/ME patients (aged 31.82 ± 5.50 years) and 11 non-fatigued controls (aged 33.91 ± 5.06 years) were included. Flow cytometric protocols were used to determine B cell purity, followed by SNP and genotype analysis for 21 mammalian TRP ion channel genes and nine mammalian ACh receptor genes. SNP association and genotyping analysis were performed using ANOVA and PLINK analysis software. Results Seventy-eight SNPs were identified in nicotinic and muscarinic acetylcholine receptor genes in the CFS/ME group, of which 35 were in mAChM3. The remaining SNPs were identified in nAChR delta (n = 12), nAChR alpha 9 (n = 5), TRPV2 (n = 7), TRPM3 (n = 4), TRPM4 (n = 1) mAChRM3 2 (n = 2), and mAChRM5 (n = 3) genes. Nine genotypes were identified from SNPs in TRPM3 (n = 1), TRPC6 (n = 1), mAChRM3 (n = 2), nAChR alpha 4 (n = 1), and nAChR beta 1 (n = 4) genes, and were located in introns and 3′ untranslated regions. Odds ratios for these specific genotypes ranged between 7.11 and 26.67 for CFS/ME compared with the non-fatigued control group. Conclusion This preliminary investigation identified a number of SNPs and genotypes in genes encoding TRP ion channels and AChRs from B cells in patients with CFS/ME. These may be involved in B cell functional changes, and suggest a role for Ca2+ dysregulation in AChR and TRP ion channel signalling in the pathomechanism of CFS/ME.

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