Neuronal plasticity is an important mechanism for growth, learning and memory however many diseases arise from its dysfunction leading to degradation. Calcium is known to be a contributing factor to the formation and breaking of neural networks the effect of extended neurotransmitter induced calcium release is not fully understood. Here we outline how extended Gαq stimulation mediated by changes in membrane tension lead to retraction of neurites in PC12 cells and disruption of axons in C. elegans. To understand retraction, we systematically broke down and mathematically modeled the components of the Gαq/PLCβ /PI(4,5)P2 and found that the driving force of retraction was led by calcium mediate changes in membrane tension followed by cytoskeletal dynamics. Our model of calcium mediated tension driven retraction translated into C. elegans where retraction that we saw in cultured cell surfaced as morphological changes in neuronal processes. We found under extended stress two hallmark aging morphologies, beading and waving, occurred in higher concentrations compared to normal aging and show a connection between beading and mitochondrial stress with age.

Creator

• Pearce, Katherine

Colaboradores

• Olsen, Carissa Lynn
• Srinivasan, Jagan
• Rangamani, Padmini
• Scarlata, Suzanne Frances

Degree

• PhD

Unit

• Chemistry & Biochemistry

Publisher

• Worcester Polytechnic Institute

Identifier

• etd-27681

Advisor

• Scarlata, Suzanne Frances

Committee

• Olsen, Carissa
• Srinivasan, Jagan
• Rangamani, Padmini

Defense date

• 2021-08-13

Year

• 2021

Date created

• 2021-08-19

Resource type

• Dissertation

Rights statement

• In Copyright

Última modificación

• 2023-10-09