An organism's ability to detect and respond to environmental stimuli is critical for its survival. It is particularly important for animals to incorporate contextual information, such as internal state or external cues, in order to modify behavioral responses and maximize fitness. This behavioral plasticity has largely been studied in the context of learning or adaptation. However, how environmental cues modulate the valence of innate responses to nave stimuli remains poorly understood. Behavioral plasticity can stem from genetic, molecular, and circuit level changes in neural function, ultimately leading to an organism's ability to thrive in a dynamic environment. The overall goal of my thesis is to investigate the molecular and neuronal mechanisms underlying olfactory plasticity in C. elegans. Preliminarily, I have found that while C. elegans grown under sparse culture conditions avoid high concentrations of the volatile chemical 1-hexanol, animals grown at high population density are instead robustly attracted to this odorant. My results indicate that this plasticity in olfactoy responses is mediated by pheromones, which may serve as a population density cue. I will exploit the experimental amenability of C. elegans to identify the genes, neurons and circuits that underlie the responses to 1-hexanol, and investigate how these responses are modified by contextual cues and experience. To do so, I will utilize a novel quantitative approach and high-resolution data analysis algorithms. Insights from this research will shed light on conserved molecular and neuronal pathways involved in sensory plasticity. Many neurological disorders-from developmental disorders such as autism to neurodegenerative diseases such as Alzheimer's and Parkinson's-stem from underlying deficits in neuroplasticity. Therefore, in addition to understanding the mechanisms of plasticity in a healthy context, this work has important implications for understanding the mechanisms underlying disease states.

Public Health Relevance

This project will identify and characterize the genes and neurons required for olfactory plasticity; specifically, it will ask how animals such as the nematode, C. elegans, alters its responses to a chemical based on prior experience or current context. Many diseases and disorders such as schizophrenia and autism are in part, characterized by defects in plasticity leading to pathological changes at the synaptic, circuit, an behavioral levels. Given the conserved nature of molecular and neuronal mechanisms in C. elegans, findings from this work will lead to an increased understanding of plasticity pathways, and may identify potential therapeutic targets.

Agency
National Institute of Health (NIH)
Institute
National Institute on Deafness and Other Communication Disorders (NIDCD)
Type
Predoctoral Individual National Research Service Award (F31)
Project #
5F31DC015186-02
Application #
9173414
Study Section
Special Emphasis Panel (ZDC1)
Program Officer
Rivera-Rentas, Alberto L
Project Start
2015-09-16
Project End
2017-09-15
Budget Start
2016-09-16
Budget End
2017-09-15
Support Year
2
Fiscal Year
2016
Total Cost
Indirect Cost
Name
Brandeis University
Department
Biology
Type
Schools of Arts and Sciences
DUNS #
616845814
City
Waltham
State
MA
Country
United States
Zip Code