Vertebrate learning is one of the major problems of neurobiology. Progress depends on experimental 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 the vertebrate CNS, the H- reflex, which is the electrical analog of the spinal stretch reflex. Once an animal has been conditioned, the reflex change persists even if all supraspinal input is removed. Thus, the responsible plasticity is in the spinal cord, and H-reflex conditioning is a powerful model for studying the neuronal and synaptic substrates that underlie a learned change in behavior. In addition, it is the basis for a promising new therapeutic approach to spasticity and other forms of abnormal reflex function. The goal of this project is to define the changes in the spinal cord that are responsible for operantly conditioned change in the H-reflex. The central hypotheses, based on the results of the past grant period, are : 1) that H- reflex decrease is due to a positive shift in motoneuron firing threshold combined with a decrease in the Ia afferent EPSPs of fast motoneurons, and 2) that H-reflex increase is due to a change in short-latency polysynaptic input to the motoneuron. To test these hypotheses, rats in which the triceps surae H-reflex has been increased or decreased by operant conditioning will be studied. Intracellular recordings from motoneurons will define their intrinsic properties, motor unit type, and monosynaptic and polysynaptic responses to afferent inputs. Comparison of data from conditioned and naive rats will reveal the plasticity produced by H-reflex conditioning, and further analysis will examine the relationships between this plasticity and behavioral change. The ultimate objective is to define fully the adaptive plasticity produced by H-reflex conditioning and the translation of that plasticity into behavior. The project should lead to new understanding of the plasticity that underlies learning in vertebrates.
| Eftekhar, Amir; Norton, James J S; McDonough, Christine M et al. (2018) Retraining Reflexes: Clinical Translation of Spinal Reflex Operant Conditioning. Neurotherapeutics : |
| Norton, James J S; Wolpaw, Jonathan R (2018) Acquisition, Maintenance, and Therapeutic Use of a Simple Motor Skill. Curr Opin Behav Sci 20:138-144 |
| LaPallo, Brandon K; Wolpaw, Jonathan R; Yang Chen, Xiang et al. (2017) Spinal Transection Alters External Urethral Sphincter Activity during Spontaneous Voiding in Freely Moving Rats. J Neurotrauma 34:3012-3026 |
| Chen, Yi; Chen, Lu; Wang, Yu et al. (2017) Why New Spinal Cord Plasticity Does Not Disrupt Old Motor Behaviors. J Neurosci 37:8198-8206 |
| Chen, Xiang Yang; Wang, Yu; Chen, Yi et al. (2016) Ablation of the inferior olive prevents H-reflex down-conditioning in rats. J Neurophysiol 115:1630-6 |
| LaPallo, Brandon K; Wolpaw, Jonathan R; Chen, Xiang Yang et al. (2016) Contribution of the external urethral sphincter to urinary void size in unanesthetized unrestrained rats. Neurourol Urodyn 35:696-702 |
| Thompson, Aiko K; Wolpaw, Jonathan R (2015) Targeted neuroplasticity for rehabilitation. Prog Brain Res 218:157-72 |
| Boulay, Chadwick B; Chen, Xiang Yang; Wolpaw, Jonathan R (2015) Electrocorticographic activity over sensorimotor cortex and motor function in awake behaving rats. J Neurophysiol 113:2232-41 |
| Thompson, Aiko K; Wolpaw, Jonathan R (2015) Restoring walking after spinal cord injury: operant conditioning of spinal reflexes can help. Neuroscientist 21:203-15 |
| LaPallo, Brandon K; Wolpaw, Jonathan R; Chen, Xiang Yang et al. (2014) Long-term recording of external urethral sphincter EMG activity in unanesthetized, unrestrained rats. Am J Physiol Renal Physiol 307:F485-97 |
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