Abstract
Stress increases stimulus evoked pain after peripheral nerve injury but the mechanisms are unknown. Therefore to develop novel therapeutics to treat the pathophysiology of stress/pain, the molecular events that lead from stress to enhanced pain after injury need to be identified. Due to the ubiquitous nature of how stress can affect global physiology (e.g. stress elevates glucocorticoids (GCs), circulating steroid hormones involved in energy homeostasis, inflammation, and stress responses), identifying these molecular events is challenging.
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