• A Vania Apkarian, Amelia A Mutso, Maria V Centeno, Lixin Kan, Melody Wu, Marjorie Levinstein, Ghazal Banisadr, Kevin T Gobeske, Richard J Miller, Jelena Radulovic, René Hen, and John A Kessler.
• Departments of Physiology and Neurology, Feinberg School of Medicine, Northwestern University, Chicago, IL, USA Department of Pharmacology, Columbia University, New York Psychiatric Institute, New York, NY, USA Departments of Molecular Pharmacology and Biological Chemistry and Psychiatry and Behavioral Sciences, Feinberg School of Medicine, Northwestern University, Chicago, IL, USA.
• Pain. 2016 Feb 1; 157 (2): 418-428.

AbstractThe full role of adult hippocampal neurogenesis (AHN) remains to be determined, yet it is implicated in learning and emotional functions, and is disrupted in negative mood disorders. Recent evidence indicates that AHN is decreased in persistent pain consistent with the idea that chronic pain is a major stressor, associated with negative moods and abnormal memories. Yet, the role of AHN in development of persistent pain has remained unexplored. In this study, we test the influence of AHN in postinjury inflammatory and neuropathic persistent pain-like behaviors by manipulating neurogenesis: pharmacologically through intracerebroventricular infusion of the antimitotic AraC; ablation of AHN by x-irradiation; and using transgenic mice with increased or decreased AHN. Downregulating neurogenesis reversibly diminished or blocked persistent pain; oppositely, upregulating neurogenesis led to prolonged persistent pain. Moreover, we could dissociate negative mood from persistent pain. These results suggest that AHN-mediated hippocampal learning mechanisms are involved in the emergence of persistent pain.

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