Beggs, S., Currie, G., Salter, M. W., Fitzgerald, M., & Walker, S. M. (2012). Priming of adult pain responses by neonatal pain experience: maintenance by central neuroimmune activity. Brain: a journal of neurology, 135(2):404-17 Details
Customer study highlights
Sensory experience in the first 5–6 months of life has powerful and lasting effects on development of sensory circuits in the brain. While effects of sensory deprivation on visual and auditory pathways are well-established, how early experiences of pain affect development of nociceptive pathways are less well understood.
This is particularly pertinent for preterm infants who are often subjected to surgery and intensive care procedures. Previous studies have found that children who experienced early neonatal surgeries show alterations in pain-related behaviours, likely due to plasticity or ‘memory formation’ in nociceptive pathways in early development.
The present study sought to investigate the effects of neonatal injury using a rodent model. First, the authors established that ‘priming’ (performing a hindpaw incision on anesthetized 3 day-old rats) leads to subsequent hyperalgesia, evidenced by a decrease in pain tolerance in rats exposed to a repeat paw incision injury at 28 days. Hind limb flexion EMG activity, recorded using a PowerLab, was significantly greater in primed animals, indicating overactive spinal pain pathways.
Next, the authors sought to delineate the effects of neonatal injury on spinal nociceptive pathways. Results showed that priming doubled the number of activated microglial cells in the dorsal spinal cord. This neuroimmune response to priming is the likely cause for overactive pain reflexes because treatment with minocycline – a microglial inhibitor – prevented the development of hyperalgesia in primed rats.
Hence, by modulating these neuroimmune responses during early experiences of pain, we may be able to avoid enhanced future pain responses (hyperalgesia) altogether.