안동국 교수(치과대학 치의학과)

o (1988) DDS, School of Dentistry, Kyungpook National University, Daegu, Korea
o (1991) Master of Dentistry (major in oral physiology), Graduate School, Kyungpook National University, Daegu, Korea
o (1994) Ph. D. in Dentistry (major in oral physiology), Graduate School, Kyungpook National University, Daegu, Korea

o (1988~1993) Teaching Assistant; Department of Oral Physiology, School of Dentistry, Kyungpook National University, Daegu
o (1993~1996) Military Service as a captain in Army
o (1996~1998) Full-time Instructor, Department of Oral Physiology, School of Dentistry, Kyungpook National University, Daegu
o (1997~1998) Visiting Professor, Department of Physiology, Meharry Medical School, Nashville, TN, USA
o (1998~2000) Visiting Professor, Dental Research Center, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA
o (1998~2002) Assistant Professor, Department of Oral Physiology, School of Dentistry, Kyungpook National University, Daegu
o (2002~2003) Visiting Professor, Department of Cell & Molecular Physiology, School of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA
o (2002~2007) Associate Professor, Department of Oral Physiology, School of Dentistry, Kyungpook National University, Daegu
o (2007~present) Professor, Chairman, Department of Oral Physiology, School of Dentistry, Kyungpook National University, Daegu

Neuroscience, Oral Physiology, Pain, Orofacial pain, Neuropathic pain, Trigeminal neuralgia, Trigeminal nucleus, Tooth Pain, Cytokines, Glial cells, Inflammasome, Botulinum toxin

o Astroglial RIPK1, activated by the TNF-α pathway, is a central driver of neuropathic pain and that the TNF-α mediated RIPK1 pathway is a potential therapeutic target for reducing neuropathic pain following nerve injury.
o The antinociceptive properties of BTX-A in a rat model of trigeminal neuralgia are mediated through the regulation of the HIF-1α associated cytokine pathway in the trigeminal ganglion. BTX-A is therefore a potentially effective treatment strategy for trigeminal neuralgia.
o Central Ang II-induced nociception is differentially regulated by AT1R and AT2R. Thus, distinct therapeutic targets must be regulated to overcome pain symptom caused by multiple underlying mechanisms.
o The central VEGF-A pathway plays a key role in the development of trigeminal neuropathic pain following nerve injury through two separate pathways: VEGF-A R1 and VEGF-A R2. Hence, a blockade of the central VEGF-A pathway provides a new therapeutic avenue for the treatment of trigeminal neuropathic pain.
o Antinociceptive effects of BoNT-A are mediated by an inhibition of up-regulated Nav isoform 1.7 expression in the trigeminal ganglion. BoNT-A is therefore a potential new therapeutic agent for chronic pain control including neuropathic pain.
o Prolonged nociceptive behavior following compression of the trigeminal nerve root may mimic trigeminal neuralgia in this animal model and that the activation of p38 MAPK in the microglia contributes to pain hypersensitivity in rats that have undergone compression of the trigeminal nerve root.