Chihiro Nozaki

Official Title

Associate Professor (without tenure)
Faculty of Science and Engineering
(Global Center for Science and Engineering)

Research Fields

Pain, Neuroimmunology, Neuropharmacology

Research

Increase of obese people together with increase of chronic inflammatory/metabolic disease patients are current world-wide problem. These disease often display chronic pain and neuroinflammation, however interaction between obesity, inflammation and pain still remain unknown. As endocannabinoids (eCBs) can modulate all these three phenomena, our major aim is to clarify if eCB deficiency can explain the interaction between obesity, chronic inflammation and pain. Also as eCB is known to have sexual dimorphism, we are studying the effect of eCB-mediated endocrine system modulation to the sexual dimorphism of known chronic painful disease such as migraine.

Selected publications

1.Nent E, Nozaki C, Schmöle A, Otte D, Zimmer A. (2019) CB2 receptor deletion on myeloid cells enhanced mechanical allodynia in a mouse model of neuropathic pain. pain. Scientific Reports, 9:7468.

2.Nozaki C, Nent E, Bilkei-Gorzo A, Zimmer A. (2018) Involvement of leptin signalling in the development of cannabinoid CB2 receptor-dependent mirror image pain. Scientific Reports, 8:10827.

3.Nozaki C*, Markert A, Zimmer A. (2015) Inhibition of FAAH reduces nitroglycerin-induced migraine-like pain and trigeminal neuronal hyperactivity in mice. Eur. Neuropshychopharm., 25(8):1388-96. *Corresponding author

4.Nozaki C*, Nagase H, Nemoto T, Matifas A, Kieffer BL, Gaveriaux-Ruff C. (2014) In vivo properties of KNT-127, a novel delta opioid agonist: receptor internalisation, antihyperalgesia and antidepressant effects in mice. Br. J. Pharmacol., 171: 5376-5386. *Corresponding author

5.Nozaki C*, Vergnano AM*, Filliol D, Ouagazzal AM, Le Goff A, Carvalho S, Reiss D, Gaveriaux-Ruff C, Neyton J, Paoletti P, Kieffer BL. (2011) Zinc alleviates pain through high-affinity binding to the NMDA receptor NR2A subunit. Nat. Neurosci., 14: 1017-22. *equal contribution