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.

• This report represents the work of one or more WPI undergraduate students submitted to the faculty as evidence of completion of a degree requirement. WPI routinely publishes these reports on its website without editorial or peer review.

Creator

• Karki, Nitya

Publisher

• Worcester Polytechnic Institute

Identifier

• E-project-062011-114244

Advisor

• Adams, David S.

Year

• 2011

Sponsor

• Mark Alkema

Date created

• 2011-06-20

Resource type

• Major Qualifying Project

Major

• Biology & Biotechnology

Rights statement

• In Copyright