Jooyoung Jung
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Research Interests
Jooyoung Jung has a total of 5 co-authors. Here are the top co-authors by number of shared publications:
- Byeongjun Lee
Sensory Research Center, CRI, College of Pharmacy, Seoul National University, Gwanak, Daehak-Ro 1, Seoul 151-742, Republic of Korea
1 shared publication - Dong-Jin Yang
Sensory Research Center, CRI, College of Pharmacy, Seoul National University, Gwanak, Daehak-Ro 1, Seoul 151-742, Republic of Korea
1 shared publication - Hawon Cho
Sensory Research Center, CRI, College of Pharmacy, Seoul National University, Gwanak, Daehak-Ro 1, Seoul 151-742, Republic of Korea
1 shared publication - Uhtaek Oh
Seoul National University
1 shared publication - Young Duk Yang
Department of pharmacy, College of Pharmacy, CHA University, Gyeonggi-do, Republic of Korea
1 shared publication
Latest Publications
- Open Access
- 1 January 2014
- Published by SAGE Publications in Molecular Pain
- Vol. 10, 5
Anoctamin 1 Contributes to Inflammatory and Nerve-Injury Induced Hypersensitivity
Background: Various pathological conditions such as inflammation or injury can evoke pain hypersensitivity. That represents the response to innocuous stimuli or exaggerated response to noxious stimuli. The molecular mechanism based on the pain hypersensitivity is associated with changes in many of ion channels in dorsal-root ganglion (DRG) neurons. Anoctamin 1 (ANO1/TMEM16A), a Ca 2+ activated chloride channel is highly visible in small DRG neurons and responds to heat. Mice with an abolished function of ANO1 in DRG neurons demonstrated attenuated pain-like behaviors when exposed to noxious heat, suggesting a role in acute thermal nociception. In this study, we further examined the function of ANO1 in mediating inflammation- or injury-induced hyperalgesia or allodynia. Results: Using Advillin/Ano1 fl/fl ( Adv/Ano1 fl/fl ) mice that have a functional ablation of Ano1 mainly in DRG neurons, we were able to determine its role in mediating thermal hyperalgesia and mechanical allodynia induced by inflammation or nerve injury. The thermal hyperalgesia and mechanical allodynia induced by carrageenan injection and spared-nerve injury were significantly reduced in Adv/Ano1 fl/fl mice. In addition, flinching or licking behavior after bradykinin or formalin injection was also significantly reduced in Adv/Ano1 fl/fl mice. Since pathological conditions augment nociceptive behaviors, we expected ANO1's contribution to the excitability of DRG neurons. Indeed, the application of inflammatory mediators reduced the threshold for action potential (rheobase) or time for induction of the first action potential in DRG neurons isolated from control ( Ano1 fl/fl ) mice. These parameters for neuronal excitability induced by inflammatory mediators were not changed in Adv/Ano1 fl/fl mice, suggesting an active contribution of ANO1 in augmenting the neuronal excitability. Conclusions: In addition to ANO1's role in mediating acute thermal pain as a heat sensor, ANO1 is also capable of augmenting the excitability of DRG neurons under inflammatory or neuropathic conditions and thereby aggravates inflammation- or tissue injury-induced pathological pain.
- 1 January 2014
- Published by SAGE Publications in Molecular Pain
- Vol. 10, 5
Open AccessAnoctamin 1 Contributes to Inflammatory and Nerve-Injury Induced Hypersensitivity
Background: Various pathological conditions such as inflammation or injury can evoke pain hypersensitivity. That represents the response to innocuous stimuli or exaggerated response to noxious stimuli. The molecular mechanism based on the pain hypersensitivity is associated with changes in many of ion channels in dorsal-root ganglion (DRG) neurons. Anoctamin 1 (ANO1/TMEM16A), a Ca 2+ activated chloride channel is highly visible in small DRG neurons and responds to heat. Mice with an abolished function of ANO1 in DRG neurons demonstrated attenuated pain-like behaviors when exposed to noxious heat, suggesting a role in acute thermal nociception. In this study, we further examined the function of ANO1 in mediating inflammation- or injury-induced hyperalgesia or allodynia. Results: Using Advillin/Ano1 fl/fl ( Adv/Ano1 fl/fl ) mice that have a functional ablation of Ano1 mainly in DRG neurons, we were able to determine its role in mediating thermal hyperalgesia and mechanical allodynia induced by inflammation or nerve injury. The thermal hyperalgesia and mechanical allodynia induced by carrageenan injection and spared-nerve injury were significantly reduced in Adv/Ano1 fl/fl mice. In addition, flinching or licking behavior after bradykinin or formalin injection was also significantly reduced in Adv/Ano1 fl/fl mice. Since pathological conditions augment nociceptive behaviors, we expected ANO1's contribution to the excitability of DRG neurons. Indeed, the application of inflammatory mediators reduced the threshold for action potential (rheobase) or time for induction of the first action potential in DRG neurons isolated from control ( Ano1 fl/fl ) mice. These parameters for neuronal excitability induced by inflammatory mediators were not changed in Adv/Ano1 fl/fl mice, suggesting an active contribution of ANO1 in augmenting the neuronal excitability. Conclusions: In addition to ANO1's role in mediating acute thermal pain as a heat sensor, ANO1 is also capable of augmenting the excitability of DRG neurons under inflammatory or neuropathic conditions and thereby aggravates inflammation- or tissue injury-induced pathological pain.