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groups of spinal projection neurons became sensitized. Other spinal neurons, with no direct projection to the brain and with no neurokinin 1 receptors for substance P but which were also involved in processing pain-related information were, in contrast, not affected. This suggests that enhanced pain sensitivity (hyperalgesia) is processed by a different population of spinal neurons as compared to normal, physiological pain.

Jennifer Laird, PhD, of the pharmaceutical company AstraZeneca in Montreal explains the mechanisms underlying pain evoked by tactile input after peripheral inflammation. She notes that we all have experienced the sensation of pain - injury or damage to body tissue produces an ongoing sensation so that the area hurts in the absence of any external stimulus.

Think of the last time you had a bad sunburn. Sunburnt skin usually hurts even more when you touch it! This is because damaged areas are also hypersensitive to external stimuli. So even light touch or pressure that feels fine when applied to normal skin is painful and unpleasant in the damaged area. This is the body's way of making you slow down and protect the injured area so that it has a chance to heal. Both the ongoing pain sensation and the hypersensitivity usually fade and disappear as the injury heals, but can last days or weeks and in patients with chronic pain, for years.

So how does the nervous system responsible for keeping the brain informed about touch or painful stimuli applied to that part of the body "remember" that the injury occurred? Laird has found that neurons in the central nervous system, in the spinal cord - where sensory information from the body is first processed - do "remember" a peripheral injury even when isolated and maintained in vitro.

The spinal cord was isolated from control rats and rats with an experimental inflammation of one paw. The spinal cord was maintained in vitro and the responses of the nociceptive circuitry analyzed
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Contact: Dawn McCoy
dawn@sfn.org
202-462-6688
Society for Neuroscience
10-Nov-2003

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