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  • About
  • The Global ETD Search service is a free service for researchers to find electronic theses and dissertations. This service is provided by the Networked Digital Library of Theses and Dissertations.
    Our metadata is collected from universities around the world. If you manage a university/consortium/country archive and want to be added, details can be found on the NDLTD website.
1

The Nucleus of the Solitary Tract is Necessary for Apnea-induced Respiratory Plasticity

Torontali, Zoltan 23 July 2012 (has links)
The respiratory system is attentive, adaptive, learns and has memory. The respiratory system remembers repeated respiratory challenges to fine tune its motor activity by modulating neuronal synaptic strength. This phenomenon, respiratory long term facilitation (LTF), functions to strengthen the ability of respiratory motor neurons to enhance contraction of breathing muscles. LTF could serve as a protective mechanism against obstructive sleep apnea, a disease characterized by the collapse of upper airways, by restoring upper airway patency. LTF can be induced through modulation of vagal afferent feedback via repeated apneas. Here, we used reverse microdialysis, electrophysiology, neuropharmacology, and histology to determine if the nucleus of the solitary tract (NTS), a brain region exclusively receiving vagal afferents, is the origin of the neural circuit responsible for apnea-induced plasticity. My work shows bilateral injection of 5% lidocaine into the NTS prevented LTF. We conclude the NTS is required for triggering apnea-induced LTF.
2

The Nucleus of the Solitary Tract is Necessary for Apnea-induced Respiratory Plasticity

Torontali, Zoltan 23 July 2012 (has links)
The respiratory system is attentive, adaptive, learns and has memory. The respiratory system remembers repeated respiratory challenges to fine tune its motor activity by modulating neuronal synaptic strength. This phenomenon, respiratory long term facilitation (LTF), functions to strengthen the ability of respiratory motor neurons to enhance contraction of breathing muscles. LTF could serve as a protective mechanism against obstructive sleep apnea, a disease characterized by the collapse of upper airways, by restoring upper airway patency. LTF can be induced through modulation of vagal afferent feedback via repeated apneas. Here, we used reverse microdialysis, electrophysiology, neuropharmacology, and histology to determine if the nucleus of the solitary tract (NTS), a brain region exclusively receiving vagal afferents, is the origin of the neural circuit responsible for apnea-induced plasticity. My work shows bilateral injection of 5% lidocaine into the NTS prevented LTF. We conclude the NTS is required for triggering apnea-induced LTF.

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