2004 West Coast Worm Meeting abstract 122
These abstracts should not be cited in bibliographies. Material contained herein should be treated as personal communication and should be cited as such only with the consent of the author.
| 1 | Institute of Neuroscience, University of Oregon, Eugene, OR 97403 |
| 2 | mailion@uoneuro.uoregon.edu |
C. elegans has a rich repertoire of sensory behaviors. Many cells and molecules involved in transducing sensory signals have been identified by the methods of laser ablation and molecular genetic analysis of mutants. However, little is known about how the nervous system encodes and processes sensory information. To begin to study this problem, we plan to directly characterize electrical responses to sensory stimuli by the techniques of electrophysiology and calcium imaging. We are particularly interested in the sensory neurons and interneurons that respond to chemical and thermal stimuli. Once we identify cells that respond electrically to the stimuli, we can investigate how the response is altered in mutants with behavioral defects to the stimuli and how the response is altered by sensory experience.
As a complementary approach, we are generating animals in which the electrical activity of certain neurons can be manipulated in predictable ways. We are expressing the capsaicin receptor TRPV1/VR1 in individual sensory neurons. Application of capsaicin leads to depolarization of the cell and we can then score the effect on worm behavior, as well as recording the electrical responses of downstream interneurons. We are also generating animals expressing the caspase ICE to kill cells or an activated EGL-2 K+ channel to hyperpolarize cells. In each case, we can measure behavioral responses as well as the electrical responses of other neurons in the circuit.
Signal transduction of several sensory stimuli involves the second messenger cGMP. To better understand how sensory information is encoded electrically, we are studying several mutants involved in cGMP signaling, particularly regarding chemotaxis to water soluble attractants. Non-null mutants of the cGMP-gated channel mutants tax-4 and tax-2 are sometimes stronger than null mutants, suggesting that they may affect electrical activity in interesting ways. Furthermore, there is evidence that the tax-2 beta subunit may partner with alpha subunits other than tax-4 and that some of the unusual phenotypes may be due to effects on subunit interactions. We are addressing these issues in three ways. First, we are performing a detailed phenotypic analysis of these mutants and others involved in cGMP signaling. Second, we are analyzing cGMP channel activity in cultured cells by electrophysiology to see how the different mutants affect electrical activity. Third, we are examining expression patterns of other alpha subunits to identify other subunits present in the sensory neurons.