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Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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1

Sherkheli, Muhammad Azhar, Guenter Gisselmann, and Hanns Hatt. "Supercooling Agent Icilin Blocks a Warmth-Sensing Ion Channel TRPV3." Scientific World Journal 2012 (2012): 1–8. http://dx.doi.org/10.1100/2012/982725.

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Transient receptor potential vanilloid subtype 3 (TRPV3) is a thermosensitive ion channel expressed in a variety of neural cells and in keratinocytes. It is activated by warmth (33–39°C), and its responsiveness is dramatically increased at nociceptive temperatures greater than 40°C. Monoterpenoids and 2-APB are chemical activators of TRPV3 channels. We found that Icilin, a known cooling substance and putative ligand of TRPM8, reversibly inhibits TRPV3 activity at nanomolar concentrations in expression systems likeXenopus laevesoocytes, HEK-293 cells, and in cultured human keratinocytes. Our data show that icilin's antagonistic effects for the warm-sensitive TRPV3 ion channel occurs at very low concentrations. Therefore, the cooling effect evoked by icilin may at least in part be due to TRPV3 inhibition in addition to TRPM8 potentiation. Blockade of TRPV3 activity by icilin at such low concentrations might have important implications for overall cooling sensations detected by keratinocytes and free nerve endings in skin. We hypothesize that blockage of TRPV3 might be a signal for cool-sensing systems (like TRPM8) to beat up the basal activity resulting in increased cold perception when warmth sensors (like TRPV3) are shut off.

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2

Vahabi, Bahareh, Brian A. Parsons, Olena Doran, Anthony Rhodes, Sarah Dean, and Marcus J. Drake. "TRPM8 agonists modulate contraction of the pig urinary bladder." Canadian Journal of Physiology and Pharmacology 91, no. 7 (July 2013): 503–9. http://dx.doi.org/10.1139/cjpp-2012-0406.

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The transient receptor potential melastin-8 (TRPM8) channel is activated by the “cooling” compounds menthol and icilin. Pathophysiologically, it is implicated in the overactive bladder and bladder cooling reflex, but the activity of TRPM8 in normal bladder physiology is poorly understood. We investigated the distribution of TRPM8 channels and the effect of TRPM8 agonists on the contractile function of pig bladder (n = 35) strips and whole bladders. The distribution of TRPM8 was examined by immunohistochemistry. The effect of vesical or intravascular menthol (0.1–0.3 mmol/L) or icilin (50 μmol/L) on carbachol-induced isolated whole bladder contractions was monitored by recording vesical pressure. Strips of denuded detrusor or mucosa were mounted in organ baths to study the effect of TRPM8 agonists on the contractile responses to 10 μmol/L carbachol. TRPM8-like immunoreactivity was detected on pig urothelium. Intravascular menthol (0.3 mmol/L) and icilin (50 μmol/L) significantly decreased the magnitude of carbachol-induced whole bladder contraction, whereas vesical administration significantly increased the response. In detrusor and mucosal strips, both menthol (0.3 mmol/L) and icilin (50 μmol/L) inhibited carbachol-induced contractions. We conclude that the TRPM8 channel is expressed on the urothelium of pig bladder. In the whole organ, exposure of the urothelium to menthol or icilin increases the contractile response to carbachol. Where detrusor muscle is exposed directly to these compounds, the contractile response to carbachol is reduced.

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3

De Petrocellis, Luciano, Giorgio Ortar, Aniello Schiano Moriello, Eric M. Serum, and David B. Rusterholz. "Structure–activity relationships of the prototypical TRPM8 agonist icilin." Bioorganic & Medicinal Chemistry Letters 25, no. 11 (June 2015): 2285–90. http://dx.doi.org/10.1016/j.bmcl.2015.04.032.

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4

Kim, Jae, Alan Cowan, Renata Lisek, Natalie Raymondi, Aaron Rosenthal, Daniel D. Hirsch, and Scott M. Rawls. "Icilin-evoked behavioral stimulation is attenuated by alpha2-adrenoceptor activation." Brain Research 1384 (April 2011): 110–17. http://dx.doi.org/10.1016/j.brainres.2011.02.002.

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5

Gao, Tianle, Jingxia Hao, Zsuzsanna Wiesenfeld-Hallin, and Xiao-Jun Xu. "Activation of TRPM8 cold receptor triggers allodynia-like behavior in spinally injured rats." Scandinavian Journal of Pain 4, no. 1 (January 1, 2013): 33–37. http://dx.doi.org/10.1016/j.sjpain.2012.09.007.

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AbstractAimsPain in response to innocuous cold stimulation (cold allodynia) is a common symptom in patients with neuropathic pain. Cold allodynia is difficult to treat and its mechanisms are poorly understood. Several transient receptor potential (TRP) channels have been shown to be the molecular sensors for cold stimulation in a temperature-dependent manner, but the contribution of various TRP channels in mediating cold allodynia in neuropathic pain is unclear. We have previously shown that spinally injured rats developed neuropathic pain-like behaviors, including marked cold allodynia. We now assessed the role of TRP channels in mediating cold allodynia in rats after ischemic spinal cord injury.Methods Methods: Spinal cord injury was produced using a photochemical method. The mechanical allodynia was assessed by examining the vocalization thresholds to graded mechanical touch/pressure applied with von Frey hairs. Temperature controlled cold stimulation was produced by a Peltier thermode (active surface 25 mm × 50 mm) connected to a MSA Thermal Simulator (Somedic, Sweden) with baseline temperature of 32 °C. The rate of temperature change was 0.5 °C/s. The temperature required to elicit cold allodynia was examined. The responses of the rats to topical application of icilin or menthol, agonists of transient receptor potential melastain 8 (TRPM8), were also studied.ResultsNormal rats did not exhibit nociceptive responses to cooling stimulation to the trunk and back area (minimal temperature +6°C) and they also did not react aversively to topical application of icilin or menthol. After spinal cord injury, the rats developed mechanical allodynia at the trunk and back just rostral to the dermatome of the injured spinal segments. In the same area, rats exhibited significant nociceptive responses to cooling from day 1 after injury, lasting for at least 70 days which is the longest time of observation. For the first two weeks after injury, the majority of spinally injured rats had a nociceptive response to cooling above 17°C. At day 70, about 50% of rats responded to cooling above 17 °C. Topical application of 400 μM icilin or 4mM menthol also elicited pain-like responses in spinally injured rats and these two cold mimetics also significantly exacerbated existing mechanical allodynia.ConclusionOur results showed that activation of the TRPM8 channel by menthol or icilin triggers allodynia in spinally injured rats and increases, rather than decreases, mechanical allodynia. TRPM8 channels which respond to cooling above 17 ° C may be involved at least in part in mediating cold allodynia in the rat model of neuropathic spinal cord injury pain.ImplicationsThe work introduced a method of quantitative testings of responses of rats to cold stimulation and may contribute to the understanding of mechanisms of cold allodynia after injury to the nervous system.

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6

Yamamura, Hisao, Shinya Ugawa, Takashi Ueda, Masataka Nagao, and Shoichi Shimada. "Icilin Activates the δ-Subunit of the Human Epithelial Na+ Channel." Molecular Pharmacology 68, no. 4 (July 20, 2005): 1142–47. http://dx.doi.org/10.1124/mol.104.010850.

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7

Lee, Sanghoon, Jung Nyeo Chun, Su-Hwa Kim, Insuk So, and Ju-Hong Jeon. "Icilin inhibits E2F1-mediated cell cycle regulatory programs in prostate cancer." Biochemical and Biophysical Research Communications 441, no. 4 (November 2013): 1005–10. http://dx.doi.org/10.1016/j.bbrc.2013.11.015.

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8

Burgos-Vega, Carolina C., David Dong-Uk Ahn, Christina Bischoff, Weiya Wang, Dan Horne, Judy Wang, Narender Gavva, and Gregory Dussor. "Meningeal transient receptor potential channel M8 activation causes cutaneous facial and hindpaw allodynia in a preclinical rodent model of headache." Cephalalgia 36, no. 2 (May 5, 2015): 185–93. http://dx.doi.org/10.1177/0333102415584313.

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Background Migraine headache is a neurological disorder affecting millions worldwide. However, little is known about the mechanisms contributing to migraine. Recent genome-wide association studies have found single nucleotide polymorphisms in the gene encoding transient receptor potential channel M8. Transient receptor potential channel M8 is generally known as a cold receptor but it has been implicated in pain signaling and may play a role in migraine pain. Methods In order to investigate whether transient receptor potential channel M8 may contribute to the pain of migraine, the transient receptor potential channel M8 activator icilin was applied to the dura mater using a rat behavioral model of headache. Cutaneous allodynia was measured for 5 hours using Von Frey filaments. Results : Dural application of icilin produced cutaneous facial and hind paw allodynia that was attenuated by systemic pretreatment with the transient receptor potential channel M8-selective antagonist AMG1161 (10 mg/kg p.o.). Further, the anti-migraine agent sumatriptan (0.6 mg/kg s.c.) or the non-selective NOS inhibitor L-NAME (20 mg/kg i.p.) also attenuated allodynia when given as a pretreatment. Conclusions These data indicate that transient receptor potential channel M8 activation in the meninges produces behaviors in rats that are consistent with migraine and that are sensitive to pharmacological mechanisms known to have efficacy for migraine in humans. The findings suggest that activation of meningeal transient receptor potential channel M8 may contribute to the pain of migraine.

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9

Han, J., H. Choi, and S. Kim. "Topical TRPM8 Agonist (Icilin) Relieved Vulva Pruritus Originating From Lichen Sclerosus et Atrophicus." Acta Dermato Venereologica 92, no. 5 (2012): 561–62. http://dx.doi.org/10.2340/00015555-1244.

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10

Anand, Uma, William R. Otto, and Praveen Anand. "Sensitization of Capsaicin and Icilin Responses in Oxaliplatin Treated Adult Rat DRG Neurons." Molecular Pain 6 (January 2010): 1744–8069. http://dx.doi.org/10.1186/1744-8069-6-82.

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11

Andersson, D. A. "TRPM8 Activation by Menthol, Icilin, and Cold Is Differentially Modulated by Intracellular pH." Journal of Neuroscience 24, no. 23 (June 9, 2004): 5364–69. http://dx.doi.org/10.1523/jneurosci.0890-04.2004.

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12

Rawls, Scott M., Teresa Gomez, Zhe Ding, and Robert B. Raffa. "Differential behavioral effect of the TRPM8/TRPA1 channel agonist icilin (AG-3-5)." European Journal of Pharmacology 575, no. 1-3 (December 2007): 103–4. http://dx.doi.org/10.1016/j.ejphar.2007.07.060.

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13

Wu, Rachael, Michael A. Cowley, and Stephanie E. Simonds. "Does activation of TRPM8 with menthol or icilin reduce blood glucose and body weight?" Obesity Research & Clinical Practice 13, no. 3 (May 2019): 297–98. http://dx.doi.org/10.1016/j.orcp.2018.11.176.

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14

Ewanchuk, Benjamin W., Euan R. O. Allan, Amy L. Warren, Rithwik Ramachandran, and Robin M. Yates. "The cooling compound icilin attenuates autoimmune neuroinflammation through modulation of the T‐cell response." FASEB Journal 32, no. 3 (January 3, 2018): 1236–49. http://dx.doi.org/10.1096/fj.201700552r.

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15

Selescu, Tudor, Alexandru C. Ciobanu, Cristian Dobre, Gordon Reid, and Alexandru Babes. "Camphor Activates and Sensitizes Transient Receptor Potential Melastatin 8 (TRPM8) to Cooling and Icilin." Chemical Senses 38, no. 7 (July 4, 2013): 563–75. http://dx.doi.org/10.1093/chemse/bjt027.

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16

Ito, Satoru, Hiroaki Kume, Akira Shiraki, Masashi Kondo, Yasushi Makino, Kaichiro Kamiya, and Yoshinori Hasegawa. "Inhibition by the cold receptor agonists menthol and icilin of airway smooth muscle contraction." Pulmonary Pharmacology & Therapeutics 21, no. 5 (October 2008): 812–17. http://dx.doi.org/10.1016/j.pupt.2008.07.001.

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17

Hyun, Eric, Rithwik Ramachandran, and Morley D. Hollenberg. "Icilin, an Agonist Cold Activated Transient Receptor Potential (TRP) Channels Protects Mice Against Colitis." Gastroenterology 140, no. 5 (May 2011): S—840. http://dx.doi.org/10.1016/s0016-5085(11)63485-9.

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18

Kühn, Frank J. P., Cornelia Kühn, and Andreas Lückhoff. "Inhibition of TRPM8 by Icilin Distinct from Desensitization Induced by Menthol and Menthol Derivatives." Journal of Biological Chemistry 284, no. 7 (December 18, 2008): 4102–11. http://dx.doi.org/10.1074/jbc.m806651200.

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19

Werkheiser, Jennifer L., Scott M. Rawls, and Alan Cowan. "Mu and kappa opioid receptor agonists antagonize icilin-induced wet-dog shaking in rats." European Journal of Pharmacology 547, no. 1-3 (October 2006): 101–5. http://dx.doi.org/10.1016/j.ejphar.2006.07.026.

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20

González-Muñiz, Rosario, M. Angeles Bonache, Cristina Martín-Escura, and Isabel Gómez-Monterrey. "Recent Progress in TRPM8 Modulation: An Update." International Journal of Molecular Sciences 20, no. 11 (May 28, 2019): 2618. http://dx.doi.org/10.3390/ijms20112618.

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The transient receptor potential melastatin subtype 8 (TRPM8) is a nonselective, multimodal ion channel, activated by low temperatures (<28 °C), pressure, and cooling compounds (menthol, icilin). Experimental evidences indicated a role of TRPM8 in cold thermal transduction, different life-threatening tumors, and other pathologies, including migraine, urinary tract dysfunction, dry eye disease, and obesity. Hence, the modulation of the TRPM8 channel could be essential in order to understand its implications in these pathologies and for therapeutic intervention. This short review will cover recent progress on the TRPM8 agonists and antagonists, describing newly reported chemotypes, and their application in the pharmacological characterization of TRPM8 in health and disease. The recently described structures of the TRPM8 channel alone or complexed with known agonists and PIP2 are also discussed.

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21

Rossi, Heather L., Charles J. Vierck, Robert M. Caudle, Robert P. Yezierski, and John K. Neubert. "Dose-Dependent Effects of Icilin on Thermal Preference in the Hindpaw and Face of Rats." Journal of Pain 10, no. 6 (June 2009): 646–53. http://dx.doi.org/10.1016/j.jpain.2009.01.002.

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22

Kim, Su-Hwa, Sung-Young Kim, Eun-Jung Park, Joon Kim, Hyun Ho Park, Insuk So, Seon Jeong Kim, and Ju-Hong Jeon. "Icilin induces G1 arrest through activating JNK and p38 kinase in a TRPM8-independent manner." Biochemical and Biophysical Research Communications 406, no. 1 (March 2011): 30–35. http://dx.doi.org/10.1016/j.bbrc.2011.01.094.

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23

Ma, Shuangtao. "Letter to the editor: “Is menthol- or icilin-induced vasodilation mediated by the activation of TRPM8?”." American Journal of Physiology-Heart and Circulatory Physiology 297, no. 2 (August 2009): H887. http://dx.doi.org/10.1152/ajpheart.00460.2009.

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24

Werkheiser, J. L., S. M. Rawls, and A. Cowan. "Icilin evokes a dose- and time-dependent increase in glutamate within the dorsal striatum of rats." Amino Acids 30, no. 3 (April 20, 2006): 307–9. http://dx.doi.org/10.1007/s00726-005-0306-6.

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25

Yeon, K. Y., G. Chung, M. S. Shin, S. J. Jung, J. S. Kim, and S. B. Oh. "Adult Rat Odontoblasts Lack Noxious Thermal Sensitivity." Journal of Dental Research 88, no. 4 (April 2009): 328–32. http://dx.doi.org/10.1177/0022034509334100.

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Dentin hypersensitivity is a common symptom treated in the dental clinic, yet the underlying cellular and molecular mechanisms are not clear. We hypothesized that odontoblasts detect noxious thermal stimuli by expressing temperature-sensing molecules, and investigated whether temperature-activated TRP channels (thermo-TRP channels), which are known to initiate temperature signaling, mediate temperature sensing in odontoblasts. mRNA expression of dentin sialophosphoprotein and collagenase type 1, odontoblast-specific proteins, was shown in acutely isolated adult rat odontoblasts by single-cell RT-PCR, while TRPV1, TRPV2, TRPM8, and TRPA1 were not detected. Application of noxious temperatures of 42°C and 12°C, as well as capsaicin, menthol, and icilin, agonists of thermo-TRP channels, failed to increase intracellular calcium concentration. Immunohistochemical study also revealed no expression of TRPV1. Thus, it is unlikely that odontoblasts serve as thermal sensors in teeth via thermo-TRP channels.

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26

Yin, Ying, Son C. Le, Allen L. Hsu, Mario J. Borgnia, Huanghe Yang, and Seok-Yong Lee. "Structural basis of cooling agent and lipid sensing by the cold-activated TRPM8 channel." Science 363, no. 6430 (February 7, 2019): eaav9334. http://dx.doi.org/10.1126/science.aav9334.

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Transient receptor potential melastatin member 8 (TRPM8) is a calcium ion (Ca2+)–permeable cation channel that serves as the primary cold and menthol sensor in humans. Activation of TRPM8 by cooling compounds relies on allosteric actions of agonist and membrane lipid phosphatidylinositol 4,5-bisphosphate (PIP2), but lack of structural information has thus far precluded a mechanistic understanding of ligand and lipid sensing by TRPM8. Using cryo–electron microscopy, we determined the structures of TRPM8 in complex with the synthetic cooling compound icilin, PIP2, and Ca2+, as well as in complex with the menthol analog WS-12 and PIP2. Our structures reveal the binding sites for cooling agonists and PIP2in TRPM8. Notably, PIP2binds to TRPM8 in two different modes, which illustrate the mechanism of allosteric coupling between PIP2and agonists. This study provides a platform for understanding the molecular mechanism of TRPM8 activation by cooling agents.

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27

Chuang, Huai-hu, Werner M. Neuhausser, and David Julius. "The Super-Cooling Agent Icilin Reveals a Mechanism of Coincidence Detection by a Temperature-Sensitive TRP Channel." Neuron 43, no. 6 (September 2004): 859–69. http://dx.doi.org/10.1016/j.neuron.2004.08.038.

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28

Werkheiser, Jennifer, Alan Cowan, Teresa Gomez, Craig Henry, Shreya Parekh, Sony Chau, David A. Baron, and Scott M. Rawls. "Icilin-induced wet-dog shakes in rats are dependent on NMDA receptor activation and nitric oxide production." Pharmacology Biochemistry and Behavior 92, no. 3 (May 2009): 543–48. http://dx.doi.org/10.1016/j.pbb.2009.02.005.

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29

Ding, Zhe, Teresa Gomez, Jennifer L. Werkheiser, Alan Cowan, and Scott M. Rawls. "Icilin induces a hyperthermia in rats that is dependent on nitric oxide production and NMDA receptor activation." European Journal of Pharmacology 578, no. 2-3 (January 2008): 201–8. http://dx.doi.org/10.1016/j.ejphar.2007.09.030.

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30

Sherkheli, Muhammad Azhar, Angela K. Vogt-Eisele, Daniel Bura, Leopoldo R. Beltrán Márques, Günter Gisselmann, and Hanns Hatt. "Characterization Of Selective TRPM8 Ligands And Their Structure Activity Response (S.A.R) Relationship." Journal of Pharmacy & Pharmaceutical Sciences 13, no. 2 (July 27, 2010): 242. http://dx.doi.org/10.18433/j3n88n.

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PURPOSE: Transient receptor potential melastatin-8 (TRPM8) is an ion channel expressed extensively in sensory nerves, human prostate and overexpressed in a variety of cancers including prostate, breast, lung, colon and skin melanomas. It is activated by innoxious cooling and chemical stimuli. TRPM8 activation by cooling or chemical agonists is reported to induce profound analgesia in neuropathic pain conditions. Known TRPM8 agonists like menthol and icilin cross-activate other thermo-TRP channels like TRPV3 and TRPA1 and mutually inhibit TRPM8. This limits the usefulness of menthol and icilin as TRPM8 ligands. Consequently, the identification of selective and potent ligands for TRPM8 is of high relevance both in basic research and for therapeutic applications. In the present investigation, a group of menthol derivates was characterized. These ligands are selective and potent agonists of TRPM8. Interestingly they do not activate other thermo-TRPs like TRPA1, TRPV1, TRPV2, TRPV3 and TRPV4. These ion channels are also nociceptors and target of many inflammatory mediators. METHODS: Investigations were performed in a recombinant system: Xenopus oocytes microinjected with cRNA of gene of interest were superfused with the test substances after initial responses of known standard agonists. Evoked currents were measured by two-electrode voltage clamp technique. RESULTS: The newly characterized ligands possess an up to six-fold higher potency (EC50 in low µM) and an up to two-fold increase in efficacy compared to the parent compound menthol. In addition, it is found that chemical derivatives of menthol like CPS-368, CPS-369, CPS-125, WS-5 and WS-12 are the most selective ligands for TRPM8. The enhanced activity and selectivity seems to be conferred by hexacyclic ring structure present in all ligands as substances like WS-23 which lack this functional group activate TRPM8 with much lower potency (EC50 in mM) and those with pentacyclcic ring structure (furanone compounds) are totally inactive. CONCLUSION: The new substances activate TRPM8 with a higher potency, efficacy and specificity than menthol and will thus be of importance for the development of pharmacological agents suitable for treatment and diagnosis of certain cancers and as analgesics. STATEMENT OF NOVELTY: The new compounds have an unmatched specificity for TRPM8 ion channels with additional display of high potency and efficacy. Thus these substances are better pharmacological tools for TRPM8 characterization then known compounds and it is suggested that these menthol-derivates may serve as model substances for the development of TRPM8 ligands.

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31

Johnson, Christopher, and Alexander Zholos. "Reply to “Letter to the editor: ‘Is menthol- or icilin-induced vasodilation mediated by the activation of TRPM8?'”." American Journal of Physiology-Heart and Circulatory Physiology 297, no. 2 (August 2009): H888. http://dx.doi.org/10.1152/ajpheart.00506.2009.

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32

Wu, Sheng-Nan, Pei-Yu Wu, and Mei-Ling Tsai. "Characterization of TRPM8-Like Channels Activated by the Cooling Agent Icilin in the Macrophage Cell Line RAW 264.7." Journal of Membrane Biology 241, no. 1 (March 29, 2011): 11–20. http://dx.doi.org/10.1007/s00232-011-9358-6.

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33

Izquierdo, Carolina, Mercedes Martín-Martínez, Isabel Gómez-Monterrey, and Rosario González-Muñiz. "TRPM8 Channels: Advances in Structural Studies and Pharmacological Modulation." International Journal of Molecular Sciences 22, no. 16 (August 7, 2021): 8502. http://dx.doi.org/10.3390/ijms22168502.

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The transient receptor potential melastatin subtype 8 (TRPM8) is a cold sensor in humans, activated by low temperatures (>10, <28 °C), but also a polymodal ion channel, stimulated by voltage, pressure, cooling compounds (menthol, icilin), and hyperosmolarity. An increased number of experimental results indicate the implication of TRPM8 channels in cold thermal transduction and pain detection, transmission, and maintenance in different tissues and organs. These channels also have a repercussion on different kinds of life-threatening tumors and other pathologies, which include urinary and respiratory tract dysfunctions, dry eye disease, and obesity. This compendium firstly covers newly described papers on the expression of TRPM8 channels and their correlation with pathological states. An overview on the structural knowledge, after cryo-electron microscopy success in solving different TRPM8 structures, as well as some insights obtained from mutagenesis studies, will follow. Most recently described families of TRPM8 modulators are also covered, along with a section of molecules that have reached clinical trials. To finalize, authors provide an outline of the potential prospects in the TRPM8 field.

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34

Hagenacker, T., M. Lampe, and M. Schäfers. "Icilin reduces voltage-gated calcium channel currents in naïve and injured DRG neurons in the rat spinal nerve ligation model." Brain Research 1557 (April 2014): 171–79. http://dx.doi.org/10.1016/j.brainres.2014.02.022.

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35

KAYANO, Tomohiko, Naoki KITAMURA, Taiki MORIYA, Atsushi TSUTSUMI, Yui OZAKI, Govindan DAYANITHI, and Izumi SHIBUYA. "Chronic Treatment with NGF Induces Spontaneous Fluctuations of Intracellular Ca2+ in Icilin-Sensitive Dorsal Root Ganglion Neurons of the Rat." Journal of Veterinary Medical Science 72, no. 12 (2010): 1531–38. http://dx.doi.org/10.1292/jvms.10-0196.

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36

LOWRY, J. K., and L. E. HUGHES. "Iciliidae." Zootaxa 2260, no. 1 (October 8, 2009): 453–57. http://dx.doi.org/10.11646/zootaxa.2260.1.25.

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One species of iciliid amphipod, Icilius caledoniana Watson, Lowry & Steinberg, 2004, is reported from the northern Great Barrier Reef, Queensland, Australia, living on the calcareous green alga, Halimeda sp.

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37

Werkheiser, Jennifer L., Scott M. Rawls, and Alan Cowan. "Nalfurafine, the kappa opioid agonist, inhibits icilin-induced wet-dog shakes in rats and antagonizes glutamate release in the dorsal striatum." Neuropharmacology 52, no. 3 (March 2007): 925–30. http://dx.doi.org/10.1016/j.neuropharm.2006.10.010.

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38

Wang, Chao, Chunfang Liu, Hongye Wan, Danhua Wang, Danni Sun, Tengfei Xu, Yue Yang, et al. "Wu-Tou Decoction Inhibits Chronic Inflammatory Pain in Mice: Participation of TRPV1 and TRPA1 Ion Channels." BioMed Research International 2015 (2015): 1–12. http://dx.doi.org/10.1155/2015/328707.

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Wu-tou decoction (WTD) is a classic traditional Chinese medicine formula and has been used effectively to treat joint diseases clinically. Previous reports indicated that WTD possesses anti-inflammatory activity; however, its actions on pain have not been clarified. Here, we investigated the antinociceptive activity of WTD in CFA-induced mice, and its possible mechanism of the action associated with transient receptor potential (TRP) ion channels was also explored. Our results showed that 1.58, 3.15, and 6.30 g/kg WTD significantly attenuated mechanical, cold, and heat hypersensitivities. Moreover, WTD effectively inhibited spontaneous nociceptive responses to intraplantar injections of capsaicin and cinnamaldehyde, respectively. WTD also effectively suppressed jumping and wet-dog-shake behaviors to intraperitoneal injection of icilin. Additionally, WTD significantly reduced protein expression of TRPV1 and TRPA1 in dorsal root ganglia and skins of injured paw. Collectively, our data demonstrate firstly that WTD exerts antinociceptive activity in inflammatory conditions by attenuating mechanical, cold, and heat hypersensitivities. This antinociceptive effect may result in part from inhibiting the activities of TRPV1, TRPA1, and TRPM8, and the suppression of TRPV1 and TRPA1 protein by WTD was also highly effective. These findings suggest that WTD might be an attractive and suitable therapeutic agent for the management of chronic inflammatory pain.

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39

Plevkova, J., M. Kollarik, I. Poliacek, M. Brozmanova, L. Surdenikova, M. Tatar, N. Mori, and B. J. Canning. "The role of trigeminal nasal TRPM8-expressing afferent neurons in the antitussive effects of menthol." Journal of Applied Physiology 115, no. 2 (July 15, 2013): 268–74. http://dx.doi.org/10.1152/japplphysiol.01144.2012.

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The cold-sensitive cation channel TRPM8 is a target for menthol, which is used routinely as a cough suppressant and as an additive to tobacco and food products. Given that cold temperatures and menthol activate neurons through gating of TRPM8, it is unclear how menthol actively suppresses cough. In this study we describe the antitussive effects of (−)-menthol in conscious and anesthetized guinea pigs. In anesthetized guinea pigs, cough evoked by citric acid applied topically to the tracheal mucosa was suppressed by menthol only when it was selectively administered as vapors to the upper airways. Menthol applied topically to the tracheal mucosa prior to and during citric acid application or administered continuously as vapors or as an aerosol to the lower airways was without effect on cough. These actions of upper airway menthol treatment were mimicked by cold air delivered to the upper airways but not by (+)-menthol, the inactive isomer of menthol, or by the TRPM8/TRPA1 agonist icilin administered directly to the trachea. Subsequent molecular analyses confirmed the expression of TRPM8 in a subset of nasal trigeminal afferent neurons that do not coincidently express TRPA1 or TRPV1. We conclude that menthol suppresses cough evoked in the lower airways primarily through a reflex initiated from the nose.

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Zhang, Lei, Sarahlouise Jones, Kate Brody, Marcello Costa, and Simon J. H. Brookes. "Thermosensitive transient receptor potential channels in vagal afferent neurons of the mouse." American Journal of Physiology-Gastrointestinal and Liver Physiology 286, no. 6 (June 2004): G983—G991. http://dx.doi.org/10.1152/ajpgi.00441.2003.

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A number of transient receptor potential (TRP) channels has recently been shown to mediate cutaneous thermosensitivity. Sensitivity to warm and cool stimuli has been demonstrated in both human and animal gastrointestinal tract; however, the molecular mechanisms that underlie this have not been determined. Vagal afferent neurons with cell bodies in the nodose ganglion are known to mediate nonnociceptive sensation from the upper gut. In this study, isolated cultured nodose ganglion from the mouse neurons showed changes in cytoplasmic-free Ca2+concentrations over a range of temperatures, as well as to icilin (a TRPM8 and TRPN1 agonist) and capsaicin (a TRPV1 agonist). RT-PCR was used to show the presence of six temperature-sensitive TRP channel transcripts (TRPV1–4, TRPN1, and TRPM8) in whole nodose ganglia. In addition, RT-PCR of single nodose cell bodies, which had been retrogradely labeled from the upper gut, detected transcripts for TRPV1, TRPV2, TRPV4, TRPN1, and TRPM8 in a proportion of cells. Immunohistochemical labeling detected TRPV1 and TRPV2 proteins in nodose ganglia. The presence of TRP channel transcripts and proteins was also detected in cells within several regions of the gastrointestinal tract. Our results reveal that TRP channels are present in subsets of vagal afferent neurons that project to the stomach and may confer temperature sensitivity on these cells.

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Brignell, Jennifer L., Victoria Chapman, and David A. Kendall. "Comparison of icilin- and cold-evoked responses of spinal neurones, and their modulation of mechanical activity, in a model of neuropathic pain." Brain Research 1215 (June 2008): 87–96. http://dx.doi.org/10.1016/j.brainres.2008.03.072.

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Vladymyrova, IA, IB Filippov, IeM Kuliieva, A. Iurkevych, R. Skryma, N. Prevarskaia, and IaM Shuba. "Comparative effects of menthol and icilin on the induced contraction of the smooth muscles of the vas deferens of normal and castrated rats." Fiziolohichnyĭ zhurnal 57, no. 4 (September 29, 2011): 21–33. http://dx.doi.org/10.15407/fz57.04.021.

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Kochukov, Mikhail Y., Terry A. McNearney, Yibing Fu, and Karin N. Westlund. "Thermosensitive TRP ion channels mediate cytosolic calcium response in human synoviocytes." American Journal of Physiology-Cell Physiology 291, no. 3 (September 2006): C424—C432. http://dx.doi.org/10.1152/ajpcell.00553.2005.

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The transient receptor potential (TRP) channels are important membrane sensors, responding to thermal, chemical, osmotic, or mechanical stimuli by activation of calcium and sodium fluxes. In this study, three distinct TRP channels were detected and their role established in mediating cytosolic free calcium concentration ([Ca2+]cyt) response in tumor-derived SW982 synoviocytes and primary cultures of human synovial cells from patients with inflammatory arthropathies. As shown by fura-2 ratio measurements while cells were incubated in a temperature-regulated chamber, significant [Ca2+]cyt elevation was elicited by rapid changes in bath temperature, application of TRPV1 receptor agonists capsaicin and resiniferatoxin, or a cold receptor stimulator, icilin. Temperature thresholds for calcium response were determined to be 12 ± 1°C for cold and 28 ± 2°C for heat activation. Temperature increases or decreases beyond these thresholds resulted in a significant rise in the magnitude of [Ca2+]cyt spikes. Observed changes in [Ca2+]cyt were completely abolished in calcium-free medium and thus resulted from direct calcium entry through TRP channels rather then by activation of voltage-dependent calcium channels. Two heat sensitive channels, TRPV1 and TRPV4, and a cold-sensitive channel, TRPA1, were detected by RT-PCR. Minimal mRNA for TRPV3 or TRPM8 was amplified. The RT-PCR results support the data obtained with the [Ca2+]cyt measurements. We propose that the TRP channels are functionally expressed in human synoviocytes and may play a critical role in adaptive or pathological changes in articular surfaces during arthritic inflammation.

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Lashinger, Erin S. R., Matthew S. Steiginga, J. Paul Hieble, Lisa A. Leon, Scott D. Gardner, Rakesh Nagilla, Elizabeth A. Davenport, Bryan E. Hoffman, Nicholas J. Laping, and Xin Su. "AMTB, a TRPM8 channel blocker: evidence in rats for activity in overactive bladder and painful bladder syndrome." American Journal of Physiology-Renal Physiology 295, no. 3 (September 2008): F803—F810. http://dx.doi.org/10.1152/ajprenal.90269.2008.

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The activation of the TRPM8 channel, a member of the large class of TRP ion channels, has been reported to be involved in overactive bladder and painful bladder syndrome, although an endogenous activator has not been identified. In this study, N-(3-aminopropyl)-2-{[(3-methylphenyl) methyl]oxy}- N-(2-thienylmethyl)benzamide hydrochloride salt (AMTB) was evaluated as a TRPM8 channel blocker and used as a tool to evaluate the effects of this class of ion channel blocker on volume-induced bladder contraction and nociceptive reflex responses to noxious bladder distension in the rat. AMTB inhibits icilin-induced TRPM8 channel activation as measured in a Ca2+ influx assay, with a pIC50 of 6.23. In the anesthetized rat, intravenous administration of AMTB (3 mg/kg) decreased the frequency of volume-induced bladder contractions, without reducing the amplitude of contraction. The nociceptive response was measured by analyzing both visceromotor reflex (VMR) and cardiovascular (pressor) responses to urinary bladder distension (UBD) under 1% isoflurane. AMTB (10 mg/kg) significantly attenuated reflex responses to noxious UBD to 5.42 and 56.51% of the maximal VMR response and pressor response, respectively. The ID50 value on VMR response was 2.42 ± 0.46 mg/kg. These results demonstrate that TRPM8 channel blocker can act on the bladder afferent pathway to attenuate the bladder micturition reflex and nociceptive reflex responses in the rat. Targeting TRPM8 channel may provide a new therapeutic opportunity for overactive bladder and painful bladder syndrome.

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Poulson, Sandra J., Ahmed Aldarraji, Iqra I. Arain, Natalia Dziekonski, Keza Motlana, Rachel Riley, Melissa M. Holmes, and Loren J. Martin. "Naked mole-rats lack cold sensitivity before and after nerve injury." Molecular Pain 16 (January 2020): 174480692095510. http://dx.doi.org/10.1177/1744806920955103.

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Neuropathic pain is a chronic disease state resulting from injury to the nervous system. This type of pain often responds poorly to standard treatments and occasionally may get worse instead of better over time. Patients who experience neuropathic pain report sensitivity to cold and mechanical stimuli. Since the nociceptive system of African naked mole-rats contains unique adaptations that result in insensitivity to some pain types, we investigated whether naked mole-rats may be resilient to sensitivity following nerve injury. Using the spared nerve injury model of neuropathic pain, we showed that sensitivity to mechanical stimuli developed similarly in mice and naked mole-rats. However, naked mole-rats lacked sensitivity to mild cold stimulation after nerve injury, while mice developed robust cold sensitivity. We pursued this response deficit by testing behavior to activators of transient receptor potential (TRP) receptors involved in detecting cold in naïve animals. Following mustard oil, a TRPA1 activator, naked mole-rats responded similarly to mice. Conversely, icilin, a TRPM8 agonist, did not evoke pain behavior in naked mole-rats when compared with mice. Finally, we used RNAscope to probe for TRPA1 and TRPM8 messenger RNA expression in dorsal root ganglia of both species. We found increased TRPA1 messenger RNA, but decreased TRPM8 punctae in naked mole-rats when compared with mice. Our findings likely reflect species differences due to evolutionary environmental responses that are not easily explained by differences in receptor expression between the species.

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Kullmann, F. Aura, M. A. Shah, L. A. Birder, and W. C. de Groat. "Functional TRP and ASIC-like channels in cultured urothelial cells from the rat." American Journal of Physiology-Renal Physiology 296, no. 4 (April 2009): F892—F901. http://dx.doi.org/10.1152/ajprenal.90718.2008.

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Transient receptor potential (TRP) and acid-sensing ion channels (ASIC) are molecular detectors of chemical, mechanical, thermal, and nociceptive stimuli in sensory neurons. They have been identified in the urothelium, a tissue considered part of bladder sensory pathways, where they might play a role in bladder function. This study investigated functional properties of TRP and ASIC channels in cultured urothelial cells from the rat using patch-clamp and fura 2 Ca2+ imaging techniques. The TRPV4 agonist 4α-phorbol-12,13 didecanoate (4α-PDD; 1–5 μM) and the TRPA1/TRPM8 agonist icilin (50–100 μM) elicited transient currents in a high percentage of cells (>70%). 4α-PDD responses were suppressed by the TRPV4 antagonist HC-010961 (10 μM). The TRPV1 agonist capsaicin (1–100 μM) and the TRPA1/TRPM8 agonist menthol (5–200 μM) elicited transient currents in a moderate percentage of cells (∼25%). All of these agonists increased intracellular calcium concentration ([Ca2+]i). Most cells responded to more than one TRP agonist (e.g., capsaicin and 4α-PDD), indicating coexpression of different TRP channels. In the presence of the TRPV1 antagonist capsazepine (10 μM), changes in pH induced by HCl elicited ionic currents (pH 5.5) and increased [Ca2+]i (pH 6.5) in ∼50% of cells. Changes in pH using acetic acid (pH 5.5) elicited biphasic-like currents. Responses induced by acid were sensitive to amiloride (10 μM). In summary, urothelial cells express multiple TRP and ASIC channels, whose activation elicits ionic currents and Ca2+ influx. These “neuron-like” properties might be involved in transmitter release, such as ATP, that can act on afferent nerves or smooth muscle to modulate their responses to different stimuli.

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Zimmer, Bastian, Osefame Ewaleifoh, Oliver Harschnitz, Yoon-Seung Lee, Camille Peneau, Jessica L. McAlpine, Becky Liu, et al. "Human iPSC-derived trigeminal neurons lack constitutive TLR3-dependent immunity that protects cortical neurons from HSV-1 infection." Proceedings of the National Academy of Sciences 115, no. 37 (August 28, 2018): E8775—E8782. http://dx.doi.org/10.1073/pnas.1809853115.

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Herpes simplex virus type 1 (HSV-1) encephalitis (HSE) is the most common sporadic viral encephalitis in Western countries. Some HSE children carry inborn errors of the Toll-like receptor 3 (TLR3)-dependent IFN-α/β– and -λ–inducing pathway. Induced pluripotent stem cell (iPSC)-derived cortical neurons with TLR3 pathway mutations are highly susceptible to HSV-1, due to impairment of cell-intrinsic TLR3-IFN immunity. In contrast, the contribution of cell-intrinsic immunity of human trigeminal ganglion (TG) neurons remains unclear. Here, we describe efficient in vitro derivation and purification of TG neurons from human iPSCs via a cranial placode intermediate. The resulting TG neurons are of sensory identity and exhibit robust responses to heat (capsaicin), cold (icilin), and inflammatory pain (ATP). Unlike control cortical neurons, both control and TLR3-deficient TG neurons were highly susceptible to HSV-1. However, pretreatment of control TG neurons with poly(I:C) induced the cells into an anti–HSV-1 state. Moreover, both control and TLR3-deficient TG neurons developed resistance to HSV-1 following pretreatment with IFN-β but not IFN-λ. These data indicate that TG neurons are vulnerable to HSV-1 because they require preemptive stimulation of the TLR3 or IFN-α/β receptors to induce antiviral immunity, whereas cortical neurons possess a TLR3-dependent constitutive resistance that is sufficient to block incoming HSV-1 in the absence of prior antiviral signals. The lack of constitutive resistance in TG neurons in vitro is consistent with their exploitation as a latent virus reservoir in vivo. Our results incriminate deficiencies in the constitutive TLR3-dependent response of cortical neurons in the pathogenesis of HSE.

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Fernández, José A., Roman Skryma, Gabriel Bidaux, Karl L. Magleby, C. Norman Scholfield, J. Graham McGeown, Natalia Prevarskaya, and Alexander V. Zholos. "Voltage- and cold-dependent gating of single TRPM8 ion channels." Journal of General Physiology 137, no. 2 (January 31, 2011): 173–95. http://dx.doi.org/10.1085/jgp.201010498.

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Transient receptor potential (TRP) channels play critical roles in cell signaling by coupling various environmental factors to changes in membrane potential that modulate calcium influx. TRP channels are typically activated in a polymodal manner, thus integrating multiple stimuli. Although much progress has been made, the underlying mechanisms of TRP channel activation are largely unknown. The TRPM8 cation channel has been extensively investigated as a major neuronal cold sensor but is also activated by voltage, calcium store depletion, and some lipids as well as by compounds that produce cooling sensations, such as menthol or icilin. Several models of TRPM8 activation have been proposed to explain the interaction between these diverse stimuli. However, a kinetic scheme is not yet available that can describe the detailed single-channel kinetics to gain further insight into the underlying gating mechanism. To work toward this goal, we investigated voltage-dependent single-channel gating in cell-attached patches at two different temperatures (20 and 30°C) using HEK293 cells stably expressing TRPM8. Both membrane depolarization and cooling increased channel open probability (Po) mainly by decreasing the duration of closed intervals, with a smaller increase in the duration of open intervals. Maximum likelihood analysis of dwell times at both temperatures indicated gating in a minimum of five closed and two open states, and global fitting over a wide range of voltages identified a seven-state model that described the voltage dependence of Po, the single-channel kinetics, and the response of whole-cell currents to voltage ramps and steps. The major action of depolarization and cooling was to accelerate forward transitions between the same two sets of adjacent closed states. The seven-state model provides a general mechanism to account for TRPM8 activation by membrane depolarization at two temperatures and can serve as a starting point for further investigations of multimodal TRP activation.

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Ulrich, Myriam, Ulrich Wissenbach, and Gerald Thiel. "The super-cooling compound icilin stimulates c-Fos and Egr-1 expression and activity involving TRPM8 channel activation, Ca2+ ion influx and activation of the ternary complex factor Elk-1." Biochemical Pharmacology 177 (July 2020): 113936. http://dx.doi.org/10.1016/j.bcp.2020.113936.

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Johnson, Christopher D., Donal Melanaphy, Andrew Purse, Susan A. Stokesberry, Paula Dickson, and Alexander V. Zholos. "Transient receptor potential melastatin 8 channel involvement in the regulation of vascular tone." American Journal of Physiology-Heart and Circulatory Physiology 296, no. 6 (June 2009): H1868—H1877. http://dx.doi.org/10.1152/ajpheart.01112.2008.

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The transient receptor potential melastatin 8 (TRPM8) channel has been characterized as a cold and menthol receptor expressed in a subpopulation of sensory neurons but was recently identified in other tissues, including the respiratory tract, urinary system, and vasculature. Thus TRPM8 may play multiple functional roles, likely to be in a tissue- and activation state-dependent manner. We examined the TRPM8 channel presence in large arteries from rats and the functional consequences of their activation. We also aimed to examine whether these channels contribute to control of conscious human skin blood flow. TRPM8 mRNA and protein were detected in rat tail, femoral and mesenteric arteries, and thoracic aorta. This was confirmed in single isolated vascular myocytes by immunocytochemistry. Isometric contraction studies on endothelium-denuded relaxed rat vessels found small contractions on application of the TRPM8-specific agonist menthol (300 μM). However, both menthol and another agonist icilin (50 μM) caused relaxation of vessels precontracted with KCl (60 mM) or the α-adrenoceptor agonist phenylephrine (2 μM) and a reduction in sympathetic nerve-mediated contraction. These effects were antagonized by bromoenol lactone treatment, suggesting the involvement of Ca2+-independent phospholipase A2 activation in TRPM8-mediated vasodilatation. In thoracic aorta with intact endothelium, menthol-induced inhibition of KCl-induced contraction was enhanced. This was unaltered by preincubation with either Nω-nitro-l-arginine methyl ester (l-NAME; 100 nM), a nitric oxide synthase inhibitor, or the ACh receptor antagonist atropine (1 μM). Application of menthol (3% solution, topical application) to skin caused increased blood flow in conscious humans, as measured by laser Doppler fluximetry. Vasodilatation was markedly reduced or abolished by prior application of l-NAME (passive application, 10 mM) or atropine (iontophoretic application, 100 nM, 30 s at 70 μA). We conclude that TRPM8 channels are present in rat artery vascular smooth muscle and on activation cause vasoconstriction or vasodilatation, dependent on previous vasomotor tone. TRPM8 channels may also contribute to human cutaneous vasculature control, likely with the involvement of additional neuronal mechanisms.

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