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.

Agency
National Institute of Health (NIH)
Institute
National Institute of Mental Health (NIMH)
Type
Research Project (R01)
Project #
5R01MH048994-03
Application #
2248551
Study Section
Psychobiology and Behavior Review Committee (PYB)
Project Start
1992-09-01
Project End
1996-04-30
Budget Start
1994-05-01
Budget End
1996-04-30
Support Year
3
Fiscal Year
1994
Total Cost
Indirect Cost
Name
Texas A&M University
Department
Psychology
Type
Schools of Arts and Sciences
DUNS #
City
College Station
State
TX
Country
United States
Zip Code
77845
Joynes, Robin L; Janjua, Kamran; Grau, James W (2004) Instrumental learning within the spinal cord: VI. The NMDA receptor antagonist, AP5, disrupts the acquisition and maintenance of an acquired flexion response. Behav Brain Res 154:431-8
Grau, J W; Barstow, D G; Joynes, R L (1998) Instrumental learning within the spinal cord: I. Behavioral properties. Behav Neurosci 112:1366-86
Joynes, R L; Illich, P A; Grau, J W (1997) Evidence for spinal conditioning in intact rats. Neurobiol Learn Mem 67:64-8
King, T E; Joynes, R L; Grau, J W (1997) Tail-flick test: II. The role of supraspinal systems and avoidance learning. Behav Neurosci 111:754-67
Prentice, T W; Joynes, R L; Meagher, M W et al. (1996) Impact of shock on pain reactivity: III. The magnitude of hypoalgesia observed depends on test location. Behav Neurosci 110:528-41
King, T E; Joynes, R L; Meagher, M W et al. (1996) Impact of shock on pain reactivity: II. Evidence for enhanced pain. J Exp Psychol Anim Behav Process 22:265-78
Joynes, R L; Grau, J W (1996) Mechanisms of Pavlovian conditioning: role of protection from habituation in spinal conditioning. Behav Neurosci 110:1375-87
Kallina, C F; Grau, J W (1995) Tail-flick test. I: Impact of a suprathreshold exposure to radiant heat on pain reactivity in rats. Physiol Behav 58:161-8
Illich, P A; King, T A; Grau, J W (1995) Impact of shock on pain reactivity: I. Whether hypo- or hyperalgesia is observed depends on how pain reactivity is tested. J Exp Psychol Anim Behav Process 21:331-47
Illich, P A; Salinas, J A; Grau, J W (1994) Latent inhibition, overshadowing, and blocking of a conditioned antinociceptive response in spinalized rats. Behav Neural Biol 62:140-50

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