Influences of Peripheral, Cortical, and Intrinsic Inhibitory Inputs on Rapid Plasticity in the Brainstem Dorsal Column Nuclei

 
 
 
 

Influences of Peripheral, Cortical, and Intrinsic Inhibitory Inputs on Rapid Plasticity in the Brainstem Dorsal Column Nuclei

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Title: Influences of Peripheral, Cortical, and Intrinsic Inhibitory Inputs on Rapid Plasticity in the Brainstem Dorsal Column Nuclei
Author: Wang, Xin
Description: Each of us has a constantly ongoing image of our body, which includes feelings from the skin, that is constructed within the brains somatosensory system. Emerging from traditional views that the adult somatosensory system cannot change, research over the past 2 decades has shown that the functional organization of this system changes with the experiences of the body. Following experiences that disrupt peripheral inputs from the body, these changes can be rapid, i.e., within minutes/hours. The mechanisms for this rapid plasticity, and where mechanisms operate in the somatosensory system, remain unclear. In an attempt to understand the mechanisms and locations of rapid somatosensory changes, the present work tested the thesis that rapid plasticity in somatosensory functional organization after disruptions of peripheral inputs may be caused, in part, by mechanisms that operate at subcortical somatosensory synapses in the brainstem dorsal column nuclei (DCN). To study potential rapid DCN functional plasticity, the experiments tested how sizes of DCN tactile receptive fields (RFs) on the skin are affected by disruptions of major inputs to the DCN, i.e., ascending peripheral inputs, intrinsic inhibitory inputs, and descending cortical inputs. The underlying thinking was that balances of excitatory and inhibitory activity of these inputs likely contribute to DCN RF sizes on a moment-moment basis, and that experimental manipulation of these inputs might provide insight into potential rapid DCN functional plasticity. The results show how acute disruptions of these inputs, individually and in combination with each other, affect DCN RF size. Taken together, the findings support a proposal that disruptions of peripheral inputs from the body cause rapid RF enlargements that emerge within minutes. It is further proposed that these RF enlargements are initiated, in part, by decreases in DCN inhibition mechanisms. Supplementing these DCN mechanisms that initiate RF enlargements, cortical feedback mechanisms appear to act to constrain the magnitudes of these enlargements. The results provide a testable proposal for how intrinsic DCN and cortical feedback mechanisms contribute to rapid somatosensory plasticity after disruptions of peripheral inputs.
Permanent Link: http://rave.ohiolink.edu/etdc/view?acc_num=mco1147302973
http://hdl.handle.net/2374.OX/18063
Date: 2005

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