| Description |
Behavior is a complex and poorly understood result of nervous system function. How do molecules, cell, and circuits function in response to sensory input to achieve a behavioral response? This remains a fundamental question in the field of neurobiology. My thesis work addressed this question by undertaking a functional, genetic and electrophysiological analysis of a defined neuronal circuit in the nematode <italic>Caenorhabditis elegans</italic>. The <italic>C. elegans</italic> nervous system functions to allow animals to sense and navigate a wide variety of gradients. Worms use thermotactic behavior to maintain a favorable internal temperature, a fundamental component of worm behavior and survival. Chemotactic behavior is used to sense or avoid various stimuli. We describe the role of glutamate receptors in these circuits and provide insight into the molecular control of circuit function and behavior. The thermotaxis circuit is a well-defined circuit that directs worm movement in response to previous temperature experiences. One neuronal pair, RIA, functions as the major integrating and decision-making neuron within the circuit. Specific chemotactic behavior shares common circuitry with the thermotaxis circuit; including RIA. Understanding how RIA functions at the molecular level up to the level of circuit communication is vital to determining how these circuits control behavior. We show the characterization of two classes of glutamate receptors, kainate and AMPA, within RIA and the fundamental differences found at the levels of localization, channel kinetics and behavior during gradient taxis behaviors. Within RIA, the AMPA receptor GLR-1 is expressed at high levels and mediates the majority of glutamate-gated current. Alternatively, kainate receptors; composed of GLR-3 and GLR-6 subunits are expressed exclusively in RIA, show limited expression, and contribute a fraction of the glutamate-gated current. However despite these differences, glr-1 mutants show only subtle thermotaxis and chemotactic defects while <italic>glr-3, glr-6</italic> mutants are severely impaired. AMPA and kainate receptors also localize to independent synapses in RIA. We show input from upstream neurons common to both circuits signal primarily through kainate receptors at specific synaptic inputs. We took advantage of this unique opportunity to study a highly conserved family of receptors within a single neuron and the behaviors that they regulate. |
