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Utilization of a rodent model to examine the neurological effects of early life adversity on adolescent pain sensitivity
Authors:Sabrina Salberg  Melanie Noel  Nikita N. Burke  Jillian Vinall  Richelle Mychasiuk
Affiliation:1. Department of Psychology, University of Calgary, Calgary, AB, Canada

Alberta Children’s Hospital Research Institute, University of Calgary, Calgary, AB, Canada

Hotchkiss Brain Institute, University of Calgary, Calgary, AB, Canada;2. Hotchkiss Brain Institute, University of Calgary, Calgary, AB, Canada

Comparative Biology & Experimental Medicine, and Physiology & Pharmacology, University of Calgary, Calgary, AB, Canada;3. Department of Anesthesia, University of Calgary, Calgary, AB, Canada;4. Department of Psychology, University of Calgary, Calgary, AB, Canada

Abstract:All children experience pain, and although many recover quickly, some go on to develop chronic pain. Adolescent chronic pain is a growing epidemic. It is unknown why some adolescents recover without incident and others experience persistent pain. Although unexplored, early life adversity may contribute to the development and maintenance of chronic pain. This study investigated the effects and underlying neurobiological mechanisms of an early life stressor on nociceptive (pain) sensitivity and emotional function in male and female Sprague-Dawley rats. Using maternal separation (MS) as an established model of early life stress, we addressed two aims: investigation of the effects of MS on behavior (anxiety and pain sensitivity), and investigation of the effects of MS on mRNA and pathophysiological changes associated with an acutely painful stimulus. Our results indicate that MS increased anxiety-like behavior and altered nociceptive responsivity in adolescent rats, with decreased mechanical withdrawal thresholds indicative of heightened and prolonged pain-related behavior. The MS groups also demonstrated increased expression of genes involved in regulating the stress and fight-or-flight response, mood, and neuroplasticity; as well as increased levels of inflammatory markers. We conclude that nociception, both at the behavioral and molecular level, is altered in response to the MS stressor.
Keywords:adolescence  amygdala  chronic pain  hippocampus  mRNA  prefrontal cortex  telomere length
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