Rodent Models Of Pain Plasticity

In humans, tissue injury results in persistently increased pain sensation to mildly noxious stimuli (hyperalgesia) and pain perception to normally non-noxious stimuli (allodynia). These two forms of sensitization clearly fit within the definition of learning developed in the first chapter—persisting behavioral modification in response to an environmental signal. However, in this case, one mechanism contributing to the altered behavior is persisting production of chemical signals locally at the site of damage, which is in a sense not a memory event but a persisting "environmental" signal. However, it is clear that there are also pain-associated central plastic changes that occur in the CNS that alter perception of constant environmental signals.

Rodent model systems have allowed the delineation of two main mechanisms underlying persistent pain sensitization after tissue injury. First, primary sensory afferents known as AS and C fibers conveying peripheral pain signals to the central nervous system become sensitized. Physiologically, this sensitization manifests as a lower stimulus intensity threshold for firing and possibly increased transmitter release in the primary sensory neurons. Second, the CNS changes its processing of signals received from the periphery such that mildly noxious stimuli are coded more intensely and non-noxious stimuli are coded as noxious.

Rodents behaviorally exhibit the sequelae of peripheral and central sensitization in a manner analogous to human behavior. Simple reflexive behavior, such as paw withdrawal, allows experimenters to quantify and study responsiveness to stimuli in rodents. Analogous to human sensations, rodents with tissue injury withdraw their paws when given non-noxious stimuli such as warm heat or a light brush. Therefore, rodents provide a model system to dissect out the molecular mechanisms of sensitization through biochemistry and physiology in correlation with simple behavioral assays.

One of the main loci for central sensitiza-tion is the spinal cord dorsal horn, the first relay station for pain signals arriving from the periphery. This sensitization involves

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