BC Environmental and Occupational Health Research Network

Chronic pain and drug addiction are linked at every level of analysis; from the molecular to the molar levels. These associations are likely more than correlative. Chronic pain and drug addiction rely to some degree on shared neurobiological substrates and mechanisms. This helps explain why so many drugs of abuse have analgesic properties (e.g. heroin, nicotine, cannabinoids) and so many analgesics have abuse potential (e.g. opioids). However, there has not been a systematic effort to identify these mechanisms, and to elucidate how they interact. It is envisioned that a better understanding of these shared CNS mechanisms will lead to the development of improved analgesics without abuse potential, and improved treatments for addiction. The study of pain- and drug-induced brain changes can be examined at the morphological, molecular, cellular, or circuit level of analysis using appropriate state-of-the art techniques and methodologies. Also responsive to this FOA are studies of the environmental and genetic antecedents which may affect brain changes associated with chronic pain and drug abuse. Research conducted using animal models of pain and addiction or those employing human volunteers are responsive to this FOA. All responsive applications must include pain as a variable of study, and relate the CNS changes associated with pain to drug abuse/addiction.