TET1 Participates in Complete Freund’s Adjuvant-induced Trigeminal Inflammatory Pain by Regulating Kv7.2 in a Mouse Model

Zhan, Dengcheng; Zhang, Jingjing; Su, Songxue; Ren, Xiuhua; Zhao, Sen; Zang, Weidong; Cao, Jing

doi:10.1007/s12264-023-01139-1

Cited by 2 publications

(1 citation statement)

References 47 publications

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“…Calcium-activated potassium channel expression has been found to be decreased following infraorbital nerve ligation, and an agonist of the channel results in increased pain threshold (i.e., mechanical allodynia) [ 17 ]. A preclinical model of orofacial pain has found that nerve injury downregulates the voltage-gated potassium channel, Kv7.2 [ 18 ], and that downregulation results in increased excitability of the trigeminal ganglia neurons and induced trigeminal neuralgia-like behavior [ 19 ].…”

Section: Ion Channelsmentioning

confidence: 99%

Post-Traumatic Trigeminal Neuropathy: Neurobiology and Pathophysiology

Eliav,

Benoliel,

Korczeniewska

2024

Biology

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Painful traumatic trigeminal neuropathy (PTTN) is a chronic neuropathic pain that may develop following injury to the trigeminal nerve. Etiologies include cranio-orofacial trauma that may result from dental, surgical, or anesthetic procedures or physical trauma, such as a motor vehicle accident. Following nerve injury, there are various mechanisms, including peripheral and central, as well as phenotypic changes and genetic predispositions that may contribute to the development of neuropathic pain. In this article, we review current literature pertaining to the cellular processes that occur following traumatic damage to the trigeminal nerve, also called cranial nerve V, that results in chronic neuropathic pain. We examine the neurobiology and pathophysiology based mostly on pre-clinical animal models of neuropathic/trigeminal pain.

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Section: Ion Channelsmentioning

confidence: 99%

Post-Traumatic Trigeminal Neuropathy: Neurobiology and Pathophysiology

Eliav,

Benoliel,

Korczeniewska

2024

Biology

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Advances in the pathological mechanisms and clinical treatments of chronic visceral pain

Li,

Zhang,

et al. 2024

Mol Pain

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Chronic visceral pain stems from internal organs and is frequently associated with functional gastrointestinal disorders, like irritable bowel syndrome (IBS). Since the underlying mechanisms of visceral pain remain largely unclear, clinical management is often limited and ineffective. Comprehensive research into the pathogenesis of visceral pain, along with the development of personalized therapeutic strategies, is crucial for advancing treatment options. Studies suggest that imbalances in purinergic receptors and neural circuit function are closely linked to the onset of visceral pain. In this review, we will explore the etiology and pathological mechanisms underlying visceral pain, with a focus on ion channels, epigenetic factors, and neural circuits, using functional gastrointestinal disorders as case studies. Finally, we will summarize and evaluate emerging treatments and potential initiatives aimed at managing visceral pain.

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TET1 Participates in Complete Freund’s Adjuvant-induced Trigeminal Inflammatory Pain by Regulating Kv7.2 in a Mouse Model

Cited by 2 publications

References 47 publications

Post-Traumatic Trigeminal Neuropathy: Neurobiology and Pathophysiology

Post-Traumatic Trigeminal Neuropathy: Neurobiology and Pathophysiology

Advances in the pathological mechanisms and clinical treatments of chronic visceral pain

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