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Suk Yun Kang

Researcher at Seoul National University

Publications -  34
Citations -  784

Suk Yun Kang is an academic researcher from Seoul National University. The author has contributed to research in topics: Neuropathic pain & Nociception. The author has an hindex of 18, co-authored 30 publications receiving 674 citations.

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Chemical stimulation of the ST36 acupoint reduces both formalin-induced nociceptive behaviors and spinal astrocyte activation via spinal alpha-2 adrenoceptors.

TL;DR: DBV stimulation of the ST36 acupoint inhibits the formalin-induced activation of spinal astrocytes and nociceptive behaviors in this inflammatory pain model and this inhibition is associated with theactivation of spinal alpha-2 adrenoceptors.
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Peripheral Acid-Sensing Ion Channels and P2X Receptors Contribute to Mechanical Allodynia in a Rodent Thrombus- Induced Ischemic Pain Model

TL;DR: The results of the current study demonstrate that peripheral administration of an ASICs blocker or P2X antagonist significantly suppress TIIP, and implicate peripheral ASICs and P2x receptors in the maintenance of thrombus-induced ischemic pain.
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Acidic pH facilitates peripheral αβmeATP-mediated nociception in rats: differential roles of P2X, P2Y, ASIC and TRPV1 receptors in ATP-induced mechanical allodynia and thermal hyperalgesia.

TL;DR: It is demonstrated that low tissue pH facilitates ATP-mediated MA via the activation of P2X receptors and ASICs, whereas TH induced by ATP under low pH conditions is mediated by the P2Y1 receptor and TRPV1, but not ASIC.
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The differential effect of intrathecal Nav1.8 blockers on the induction and maintenance of capsaicin- and peripheral ischemia-induced mechanical allodynia and thermal hyperalgesia.

TL;DR: It is demonstrated that spinal activation of Nav1.8 mediates the early induction of MA, but not the maintenance ofMA, and both the induction and maintenance of TH are modulated by the intrathecal injection of Nav 1.8 blockers.
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Astrocyte D-serine modulates the activation of neuronal NOS leading to the development of mechanical allodynia in peripheral neuropathy.

TL;DR: It is shown that spinal D-serine modulates nNOS activity and concomitant NO production leading to increases in PKC-dependent pGluN1 and ultimately contributing to the induction of mechanical allodynia following peripheral nerve injury.