Over the last 20 years, researchers have discovered that a variety of neural systems exist which can modulate our experience of pain. If we knew how these antinociceptive systems attenuate pain, and the circumstances under which they are engaged, we could devise better pharmacological, surgical and behavioral methods to treat pain in the clinical setting. Past work has revealed that supraspinal systems can modulate pain by controlling the flow of afferent nociceptive information at the level of the spinal cord. One of the most important determinants of whether these antinociceptive systems are engaged is the organism's conditioning history. For example, pairing a neutral stimulus with an aversive event like shock, endows the stimulus with the capacity to elicit a decrease in pain reactivity (""""""""conditioned antinociception""""""""). Similarly, both the magnitude and the form of the antinociception elicited by an aversive event depend on whether the organism has control over the event. It has been generally assumed that forebrain systems play an essential role in mediating the impact of learning and memory on the activation of spinal antinociceptive systems. However, we recently discovered that supraspinal systems are not always necessary; neurons within the spinal cord can support conditioned antinociception. In these studies, conditioned antinociception was demonstrated by pairing stimulation to one hind paw with tailshock in spinalized rats. After this training, stimulation of the conditioned hind paw produced a decrease in reactivity to radiant heat applied to the tail. The experiments proposed in the present grant would explore: 1) whether conditioned antinociception at the level of the spinal cord plays a functional role in intact subjects; 2) the neurochemical systems which mediate this effect; and 3) whether instituting a contingency between a response and the termination of shock influences the activation of antinociceptive systems in spinalized rats.
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