Relevant bibliographies by topics / HCN neuropathic pain

Academic literature on the topic 'HCN neuropathic pain'

Author: Grafiati
Published: 10 March 2023

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Journal articles on the topic "HCN neuropathic pain"

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Tanabe, Mitsuo, Keiko Takasu, and Hideki Ono. "Spinal HCN channels contribute to neuropathic pain." Neuroscience Research 58 (January 2007): S126. http://dx.doi.org/10.1016/j.neures.2007.06.1305.

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Jiang, Yu-Qiu, Qian Sun, Hui-Yin Tu, and You Wan. "Characteristics of HCN Channels and Their Participation in Neuropathic Pain." Neurochemical Research 33, no. 10 (May 7, 2008): 1979–89. http://dx.doi.org/10.1007/s11064-008-9717-6.

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Yang, Lujia, Xiaoyan Liu, Kai Yao, Yan sun, Fan Jiang, Haitao Yan, Peng Mao, et al. "HCN channel antagonist ZD7288 ameliorates neuropathic pain and associated depression." Brain Research 1717 (August 2019): 204–13. http://dx.doi.org/10.1016/j.brainres.2019.03.036.

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He, Jin-Ting, Xiao-Yan Li, Xin Zhao, and Xiaoliang Liu. "Hyperpolarization-activated and cyclic nucleotide-gated channel proteins as emerging new targets in neuropathic pain." Reviews in the Neurosciences 30, no. 6 (July 26, 2019): 639–49. http://dx.doi.org/10.1515/revneuro-2018-0094.

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Abstract Hyperpolarization-activated and cyclic nucleotide-gated (HCN) channels are activated during hyperpolarization, and there is an inward flow of current, which is termed as hyperpolarization-activated current, Ih. Initially, these channels were identified on the pacemaker cells of the heart. Nowadays, these are identified on different regions of the nervous system, including peripheral nerves, dorsal root ganglia, dorsal horns, and different parts of the brain. There are four different types of HCN channels (HCN1–HCN4); however, HCN1 and HCN2 are more prominent. A large number of studies have shown that peripheral nerve injury increases the amplitude of Ih current in the neurons of the spinal cord and the brain. Moreover, there is an increase in the expression of HCN1 and HCN2 protein channels in peripheral axons and the spinal cord and brain regions in experimental models of nerve injury. Studies have also documented the pain-attenuating actions of selective HCN inhibitors, such as ivabradine and ZD7288. Moreover, certain drugs with additional HCN-blocking activities have also shown pain-attenuating actions in different pain models. There have been few studies documenting the relationship of HCN channels with other mediators of pain. Nevertheless, it may be proposed that the HCN channel activity is modulated by endogenous opioids and cyclo-oxygenase-2, whereas the activation of these channels may modulate the actions of substance P and the expression of spinal N-methyl-D-aspartate receptor subunit 2B to modulate pain. The present review describes the role and mechanisms of HCN ion channels in the development of neuropathic pain.
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Du, Lu, Shao-Jun Wang, Jian Cui, Wen-Juan He, and Huai-Zhen Ruan. "The role of HCN channels within the periaqueductal gray in neuropathic pain." Brain Research 1500 (March 2013): 36–44. http://dx.doi.org/10.1016/j.brainres.2013.01.035.

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Du, Lu, Shao-Jun Wang, Jian Cui, Wen-Juan He, and Huai-Zhen Ruan. "Inhibition of HCN channels within the periaqueductal gray attenuates neuropathic pain in rats." Behavioral Neuroscience 127, no. 2 (April 2013): 325–29. http://dx.doi.org/10.1037/a0031893.

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Ding, Weihua, Zerong You, Shiqian Shen, Jinsheng Yang, Grewo Lim, Jason T. Doheny, Shengmei Zhu, Yi Zhang, Lucy Chen, and Jianren Mao. "Increased HCN Channel Activity in the Gasserian Ganglion Contributes to Trigeminal Neuropathic Pain." Journal of Pain 19, no. 6 (June 2018): 626–34. http://dx.doi.org/10.1016/j.jpain.2018.01.003.

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Tsantoulas, Christoforos, Elizabeth R. Mooney, and Peter A. McNaughton. "HCN2 ion channels: basic science opens up possibilities for therapeutic intervention in neuropathic pain." Biochemical Journal 473, no. 18 (September 12, 2016): 2717–36. http://dx.doi.org/10.1042/bcj20160287.

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Nociception — the ability to detect painful stimuli — is an invaluable sense that warns against present or imminent damage. In patients with chronic pain, however, this warning signal persists in the absence of any genuine threat and affects all aspects of everyday life. Neuropathic pain, a form of chronic pain caused by damage to sensory nerves themselves, is dishearteningly refractory to drugs that may work in other types of pain and is a major unmet medical need begging for novel analgesics. Hyperpolarisation-activated cyclic nucleotide (HCN)-modulated ion channels are best known for their fundamental pacemaker role in the heart; here, we review data demonstrating that the HCN2 isoform acts in an analogous way as a ‘pacemaker for pain’, in that its activity in nociceptive neurons is critical for the maintenance of electrical activity and for the sensation of chronic pain in pathological pain states. Pharmacological block or genetic deletion of HCN2 in sensory neurons provides robust pain relief in a variety of animal models of inflammatory and neuropathic pain, without any effect on normal sensation of acute pain. We discuss the implications of these findings for our understanding of neuropathic pain pathogenesis, and we outline possible future opportunities for the development of efficacious and safe pharmacotherapies in a range of chronic pain syndromes.
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Yang, Liuyue, Weihua Ding, Zerong You, Jinsheng Yang, Shiqian Shen, Jason T. Doheny, Lucy Chen, Ruhui Li, and Jianren Mao. "Alleviation of trigeminal neuropathic pain by electroacupuncture: the role of hyperpolarization-activated cyclic nucleotide-gated channel protein expression in the Gasserian ganglion." Acupuncture in Medicine 37, no. 3 (April 12, 2019): 192–98. http://dx.doi.org/10.1177/0964528419841614.

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Introduction: The aim of this study was to examine the effect of electroacupuncture (EA) on trigeminal neuropathic pain in rats and explore the potential mechanism underlying the putative therapeutic effect of EA. Methods: Trigeminal neuropathic pain behavior was induced in rats by unilateral chronic constriction injury of the distal infraorbital nerve (dIoN-CCI). EA was administered at ST2 ( Sibai) and Jiachengjiang. A total of 60 Sprague Dawley rats were divided into the following four groups ( n = 15 per group) to examine the behavioral outcomes after surgery and/or EA treatment: sham (no ligation); dIoN-CCI (received isoflurane only, without EA treatment); dIoN-CCI+EA-7d (received EA treatment for 7 days); and dIoN-CCI+EA-14d (received EA treatment for 14 days). Both evoked and spontaneous nociceptive behaviors were measured. Of these, 12 rats ( n = 4 from sham, dIoN-CCI, and dIoN-CCI+EA-14d groups, respectively) were used to analyze protein expression of hyperpolarization-activated cyclic nucleotide-gated (HCN) channel in the Gasserian ganglion (GG) by immunohistochemistry. Results: dIoN-CCI rats exhibited mechanical allodynia and increased face-grooming activity that lasted at least 35 days. EA treatment reduced mechanical allodynia and face-grooming in dIoN-CCI rats. Overall, 14 days of EA treatment produced a prolonged anti-nociceptive effect as compared to 7-day EA treatment. The counts of HCN1 and HCN2 immunopositive puncta were increased in the ipsilateral GG in dIoN-CCI rats and were reduced by 14 days of EA treatment. Discussion: EA treatment relieved trigeminal neuropathic pain in dIoN-CCI rats, and this effect was dependent on the duration of EA treatment. The downregulation of HCN expression may contribute to the anti-nociceptive effect of EA in this rat model of trigeminal neuropathic pain.
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Santoro, Bina, and Mala M. Shah. "Hyperpolarization-Activated Cyclic Nucleotide-Gated Channels as Drug Targets for Neurological Disorders." Annual Review of Pharmacology and Toxicology 60, no. 1 (January 6, 2020): 109–31. http://dx.doi.org/10.1146/annurev-pharmtox-010919-023356.

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The hyperpolarization-activated cyclic nucleotide-gated (HCN) channels are voltage-gated ion channels that critically modulate neuronal activity. Four HCN subunits ( HCN1–4) have been cloned, each having a unique expression profile and distinctive effects on neuronal excitability within the brain. Consistent with this, the expression and function of these subunits are altered in diverse ways in neurological disorders. Here, we review current knowledge on the structure and distribution of the individual HCN channel isoforms, their effects on neuronal activity under physiological conditions, and how their expression and function are altered in neurological disorders, particularly epilepsy, neuropathic pain, and affective disorders. We discuss the suitability of HCN channels as therapeutic targets and how drugs might be strategically designed to specifically act on particular isoforms. We conclude that medicines that target individual HCN isoforms and/or their auxiliary subunit, TRIP8b, may provide valuable means of treating distinct neurological conditions.
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Dissertations / Theses on the topic "HCN neuropathic pain"

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RESTA, FRANCESCO. "Hyperpolarization-activated Cyclic Nucleotide gated (HCN) channels as promising new target for neuropathic pain treatment." Doctoral thesis, 2016. http://hdl.handle.net/2158/1049658.

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Doheny, Jason. "Trigeminal neuropathic pain in rats: a role for thalamic hyperpolarization-activated cyclic nucleotide-gated channel activity." Thesis, 2020. https://hdl.handle.net/2144/41212.

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Trigeminal neuropathic pain (TNP) is a condition that occurs when one or more branches of the trigeminal nerve are insulted. Trigeminal neuropathic pain has been shown to be refractory to treatment. Hyperpolarization-activated cyclic nucleotide-gated (HCN) channels regulate neuronal excitability in both the peripheral and central nerve systems. Emerging evidence indicates that HCN channels are involved in the development and maintenance of chronic pain, however, the impact of thalamic HCN channel activity on TNP has yet to be elucidated. In this report, we used a chronic constriction of the distal infraorbital nerve (dIoN-CCI) to induce TNP in rats. By infusing HCN channel blockers into the ventral posteromedial (VPM) nucleus of the thalamus in dIoN-CCI rats, we demonstrated that inhibition of HCN channel activity ameliorated TNP. We found that the HCN blocker ZD7288 and the clinical drug ivabradine dose-dependently attenuated both evoked and none-evoked nociceptive behaviors in dIoN-CCI rats. Electrophysiological measurements showed the expression of HCN current (Ih) in the thalamocortical neurons in the VPM was sensitive to the HCN channel modulator cyclic adenosine monophosphate (cAMP), suggesting a contribution of the HCN2 subunit in thalamic HCN current. In the thalamus, surface expression of the HCN2 subunit was increased in dIoN-CCI rats. Taken together, we propose that an increase in HCN channel activity in the thalamus in the ascending nociceptive pathway contributed to trigeminal neuropathic pain.
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Books on the topic "HCN neuropathic pain"

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Caballero-Manrique, Esther, and Carlos A. Pino. Head and Neck Cancer Pain. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190271787.003.0026.

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In the United States, there are 48,000 new cases of head and neck cancer (HNC) annually. Although HNC used to be associated mainly with smoking and drinking, it is now found in many nonsmokers and nondrinkers in their 50s due to the spread of HPV. Pain is typically present at the time of diagnosis. Treatment usually includes radiation, chemotherapy, and/or surgery, which address the mass effect and pain. Yet, patients continue to experience pain during and after treatment, because the treatment modalities can cause significant inflammation and neuropathy and can lead to central sensitization. Painful mucositis is a complication of chemotherapy and radiation treatment; it can become severe, impacting patients’ ability to speak and eat, and sometimes limiting treatment. Pain treatment for HNC is multimodal, and includes preemptive approaches to prevent neuropathy and central sensitization with antiepileptics, such as gabapentin and pregabalin. Mucositis pain is treated using a stepwise protocol.
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Langendonk, Janneke G., and Timothy M. Cox. Porphyrias. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0043.

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The porphyrias are disorders caused by overproduction of metabolites involved in heme biosynthesis. The four acute porphyrias— acute intermittent porphyria (AIP), variegate porphyria (VP), hereditary coproporphyria (HCP), and Doss Porphyria—present with severe abdominal pain, often accompanied by agitation, hypertension, and tachycardia associated with neuropathy and sometimes paralysis. Painful and disabling neurovisceral attacks are due to excess production of the heme precursor ALA (delta-aminolevulinic acid).While 90% of individuals with an inherited defect in heme biosynthesis will never develop symptoms, acute attacks in those affected are provoked by drugs, fasting, and alcohol; in women of reproductive age, they usually occur in the progestagenic phase of the menstrual cycle. All other porphyrias are considered cutaneous porphyrias. They present with blisters or pain on light exposed areas, toxic porphyrins accumulate and give rise to skin symptoms. The cutaneous porphyrias (PCT, EPP, XLEPP, and HEP) do not present with acute neurovisceral attacks (e.g., abdominal pain). However, severe systemic complications can occur.
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Conference papers on the topic "HCN neuropathic pain"

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Dalenogare, Diéssica Padilha, Diulle Spat Peres, Maria Fernanda Pessano Fialho, and Gabriela Trevisan dos Santos. "Periorbital nociception in a progressive multiple sclerosis mouse model is dependent on TRPA1 channel activation." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.610.

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Background: Headache is one of the main painful symptoms described by multiple sclerosis patients. Previously, it was described that neuropathic pain-like behaviors were dependent on transient receptor potential ankyrin 1 (TRPA1) activation in a progressive multiple sclerosis model induced by experimental autoimmune encephalomyelitis (PMS- EAE) in mice. Objective: Here, we aimed to investigate if periorbital mechanical allodynia induced by PMS-EAE was also related to TRPA1 activation. Design and setting: Federal University of Santa Maria, Santa Maria, RS, Brazil. Methods: To induce a PMS-EAE we used female C57BL/6 wild-type and TRPA1- deficient (Trpa1-/-) mice. By the von Frey test, periorbital mechanical allodynia development was observed, and the nociception peak occurred 14 days after induction. At nociception peak day, the mice were treated with sumatriptan, TRPA1 antagonists (HC-030031, A-967079, metamizole, and propyphenazone. Results: The development of mechanical allodynia was showed as well as the antinociceptive effects for all treatments in induced mice. A significant reduction of TRPA1 expression was detected. Conclusion: Thus, these results suggest that headache-like symptoms induced by the PMS-EAE mouse model might occurring by TRPA1 activation.
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