Work in the Kaplan lab is focused on understanding how signals in the brain lead to particular patterns of behavior. We utilize a combination of behavioral, genetic, biochemical, imaging, and electrophysiological techniques to study signaling in the brain of a worm, C. elegans. Current projects include:

Cellular and circuit defects caused by mutations linked to autism. Current data suggest that mutations in 500 genes confer risk for Autism spectrum disorders (ASD). These results highlight two important questions. Do ASD mutations alter circuit development or function and (if so) do these cellular defects contribute to the cognitive and developmental defects in ASD? Do these mutations cause ASD by shared or by many distinct mechanisms? We address these questions, using C. elegans as a genetic model system. Thus far, our results suggest that ASD mutations alter: 1) the strength of inhibitory synapses; 2) the ability of target (i.e. post-syaptic) cells to adjust the strength of their incoming (pre-synaptic) inputs; and 3) changes in gene expression evoked by electrical activity.

Neuropeptide regulation of a sleep-like state.  During larval molts, worms undergo a period of profound behavioral quiescence, termed lethargus. We have identified neuropeptides that induce quiescence and arousal as part of this molting cycle. Current experiments aim to identify the circuit mechanisms leading to arousal and quiescence.