Biophysical Model of Retraction Motor Neurons and Their Modification by Operant Conditioning

<p>Operant conditioning (OC) is a form of associative learning in which an animal modifies its behavior based on the consequences that follow that behavior. Despite its ubiquity, the underlying mechanisms of OC are poorly understood. Insights into the mechanisms of OC can be obtained by studying <em>Aplysia </em>feeding behavior as it can be modified by OC. This behavior is mediated by a central pattern generator (CPG) network in the buccal ganglia that contains a relatively small number of neurons. This CPG generates rhythmic motor patterns (BMPs) that move food into the gut by closing a tongue-like structure (i.e., radula) during the retraction phase of the BMP (Susswein and Byrne, 1988). Recent studies show that OC leads to increased intrinsic excitability in the major retraction motor neurons B6 and B9, while no significant changes were observed in B3 neurons. Using conductance-based modeling, this study examined OC-induced biophysical changes in B6 and B9. Neuron B4 makes an inhibitory chemical synaptic connection and is electrically coupled to B3, B6, and B9 retraction motor neurons. B4 excitability is reduced following OC. Neuron B51 is electrically coupled to B3, B6, and B9. The excitability of B51 is increased following OC. I hypothesized that presynaptic inputs from B4 and B51 premotor neurons are sufficient to account for the firing activity of B3, B6, and B9 during a BMP, and also that changes in excitability of B6 and B9 produced by OC are responsible for changes in B6 and B9 activity during BMPs. Therefore, I developed biophysical models of B3, B6, and B9 by incorporating ionic currents including <em>I</em>_Na, <em>I</em>_Kd, <em>I</em>_A, <em>I</em>_Kca, and <em>I</em>_leak. I incorporated these conductance-based models, and synaptic connections from B4 and B51, into the existing computational model of the CPG circuit and examined neuronal activity during simulated buccal motor programs (BMPs) and OC. However, simulations revealed that these synaptic connections did not drive firing in B3, B6, and B9. This finding indicates there must be other, not yet identified, neurons that drive B3, B6, and, B9. Therefore, I included an artificial synapse to help drive firing in these neurons. Simulations including this synapse suggested that alterations in motor neuron activity post-OC are produced by the changes in excitability of B6 and B9. This study provides important extensions to the existing model of the CPG and elucidates principles of the relationship between neuron circuitry and motor output, advancing our understanding of the neural mechanisms underlying operant conditioning and their impact on motor neuron function.</p>

Name thesis:degree_name

Masters of Science (MS)

Level thesis:degree_level

Thesis (MS)

Year dc:date.available

2024

Authors dc:creator

• Rasheed, Maria
• <p><a href="https://orcid.org/0009-0009-1934-3218?lang=en" target="_blank">0009-0009-1934-3218</a></p>

Contributors dc:contributor

• John Byrne
• Valentin Dragoi
• Ruth Heidelberger

• computational
• neuroscience
• motor neurons
• Aplysia
• operant conditioning
• buccal ganglia
• CPG
• Feeding behaviors
• radula
• protraction
• retraction
• bmps
• ingestion
• rejection
• Behavioral Neurobiology
• Biology
• Cognitive Neuroscience
• Computational Neuroscience
• Developmental Neuroscience
• Integrative Biology
• Molecular and Cellular Neuroscience
• Nanoscience and Nanotechnology
• Other Cell and Developmental Biology
• Other Neuroscience and Neurobiology
• Systems Neuroscience

Repository record dc:identifier

https://digitalcommons.library.tmc.edu/utgsbs_dissertations/1366

OAI identifier oai:identifier

oai:digitalcommons.library.tmc.edu:utgsbs_dissertations-2423