Faculty Advisor

Adams, David S.

Abstract

In this project, the locomotion of C. elegans was artificially modulated by inducing dopamine release and inhibiting backward locomotion. Using optogenetics, worms were observed yielding the following results: halorhodopsin inhibits backward locomotion; dopamine slows the nematode's locomotory rate; despite lacking a dopamine transporter, worms do not paralyze in the presence of excess dopamine expression. Based on these results, the following conclusions were made: the AVA neuron plays a major role in C. elegans ability to move backwards, and when inhibited, backward motion nothing assumes its role to compensate; an acute expression of dopamine induces a decrease in C. elegans locomotory rate; and worms compensate for dat-1 deficiency by regulating dopamine through other mechanisms.

Publisher

Worcester Polytechnic Institute

Date Accepted

June 2011

Major

Biology and Biotechnology

Project Type

Major Qualifying Project

Accessibility

Unrestricted

Advisor Department

Biology and Biotechnology

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