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The role of DOP-2 D2-like auto-receptor in modulating levels of dopamine at synapses in
C.elegans.
The neurotransmitter dopamine influences a variety of neural processes that range from reward,
cognition and locomotion both in vertebrate and invertebrate. Several neuropsychiatric disorders
including Parkinson's disease, schizophrenia, depression and bipolar disorders are caused by
dopamine imbalances. In mammals, two classes of dopamine receptors, D1-like and D2-like
receptors, are responsible for transmitting the dopamine signal. Dopamine receptors are Gprotein coupled receptors (GPCR) found at both somatodendritic and axonal sites where they
control the amount and the timing of dopamine release.
We are using the Caenorhabditis elegans model to characterize the D2-like receptor DOP-2 to
understand its role in shaping the dopamine signaling in the nematode. In C. elegans, as in
humans, dopamine receptors modulate dopamine neurotransmission in many behaviors such as
locomotion and learning and memory. Previously, we have shown that DOP-2, which is
expressed in all eight C.elegans dopaminergic neurons, physically interacts with GPA-14, an
inhibitory G-alpha subunit, and that both dop-2 and gpa-14 deletion mutants habituate at a
significantly faster rate as compared to wild-type worms. We are currently assessing our work
towards analyzing synaptic vesicles release in dop-2 mutants using FRAP (Fluorescence
Recovery After Photobleaching) to study the activity at specific synapses in live animals. In
parallel we are using the SWIP assay (Swimming Induced Paralysis), a phenotype used for the
identification of genes that have an impact on dopamine signaling in C. elegans, to test for the
functional contribution of DOP-2 on the modulatory mechanisms that control the release,
synthesis and uptake of dopamine.