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Chronic pain and adult hippocampal neurogenesis: translational implications from preclinical studies

Authors Grilli M

Received 14 July 2017

Accepted for publication 25 August 2017

Published 21 September 2017 Volume 2017:10 Pages 2281—2286


Checked for plagiarism Yes

Review by Single anonymous peer review

Peer reviewer comments 3

Editor who approved publication: Dr Michael Schatman

Mariagrazia Grilli

Laboratory of Neuroplasticity, Department of Pharmaceutical Sciences, University of Piemonte Orientale, Novara, Italy

Abstract: Adult hippocampal neurogenesis (ahNG) occurs in the human brain. Adult generated neurons have been proposed to functionally contribute to relevant hippocampal functions such as learning and memory, mood regulation, and stress response. Learning, environmental enrichment, and physical exercise exert positive effects on ahNG. In parallel, these proneurogenic stimuli have been shown to ameliorate cognitive performance and/or depressive-like behavior in animal models. Conversely, aging, social isolation, and chronic stress exert negative effects on ahNG. Interestingly, reduction of hippocampal neurogenesis is suggested to potentially contribute to cognitive decline and mood alterations associated with aging and several neuropsychiatric disorders. Clinical observation demonstrates that patients affected by chronic pain often exhibit increased anxiety and depression, impaired cognitive flexibility, and memory capacities. As of today, our understanding of the molecular and cellular events that may underlie the comorbidity of chronic pain, depression, and cognitive impairment is limited. Herein we review recent preclinical data suggesting that chronic pain may induce profound changes in hippocampal plasticity, including reduced ahNG. We discuss the possibility that deregulated hippocampal neurogenesis in chronic pain may, at least in part, contribute to cognitive and mood alterations. Based on this hypothesis, the mechanisms underlying chronic pain-associated changes in hippocampal neurogenesis and related functions need to be addressed experimentally. One interesting feature of ahNG is its susceptibility to pharmacological modulation. Again, based on preclinical data we discuss the possibility that, at least in principle, distinct analgesic drugs commonly used in chronic pain states (typical and atypical opiates, a2δ ligands, and acetyl-L-carnitine) may differentially impact ahNG and that this aspect could be taken into account to reduce and/or prevent the potential risk of cognitive and emotional side effects in the clinical setting.

Keywords: chronic pain, adult neurogenesis, depression, cognition, opiates, tapentadol, pregabalin

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