Vertebrate learning is one of the major problems of neurobiology. Progress depends on models in which the plasticity underlying simple learning occurs in defined and accessible regions. Studies from this laboratory have demonstrated operant conditioning of the simplest behavior of vertebrate CNS, the H-reflex, which is the electrical analog of the spinal stretch reflex. The responsible plasticity is in the spinal cord, and H-reflex conditioning is a good model for studying the process underlying a learned change in behavior. In addition, it is the basis for anew therapeutic approach to spasticity and other forms of abnormal reflex function. Work up to the present has focused on defining the spinal cord plasticity underlying operably conditioned H-reflex change. The goal of this proposal is to learn which descending pathways from supraspinal areas are responsible for the development and long-term maintenance of the plasticity. The hypotheses, based on preliminary data, are: 1) that the corticospinal tract is essential for the development of apparently conditioned H-reflex increase or decrease; 2) that the corticospinal tract is also essential for the maintenance of conditioned increase or decrease once it has developed; and 3) that the rubrospinal, vestibulospinal, reticulospinal, and other major tracts are not essential for the development or maintenance or H-reflex conditioning. These hypotheses will be tested by studying the effects of well-defined lesions of thoracic spinal cord on operant conditioning of the soleus H-reflex in the Sprague-Dawley rat. The first set of experiments will determine whether transection of the corticospinal tract and/or transection of other major tracts prevent H-reflex conditioning. The second set of experiments will determine whether such lesions affect H-reflex conditioning after it has occurred. Lesion effects on both operantly conditioned H-reflex increase and decrease will be defined, and data from lesioned rats will be compared with control data from normal rats. We expect that corticospinal tract transection prior to conditioning will prevent conditioning, that transection of this tract after conditioning will lead to gradual loss of the conditioned change in H-reflex amplitude, and that transection of other tracts will not have these effects. The ultimate objective is to determine how supraspinal influence modifies the spinal cord. This work should lead to new understanding of the processes that underlie vertebrate learning. It may also lead to new therapy for the disabilities associated with spinal cord injury and other long-term disruptions of supraspinal control.
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