The studies reported here were designed to investigate the role of the mutation
eat-4 in the response to tap and in habituation in the nematode Caenorhabditis elegans. In C. elegans
eat-4 has been found to affect a number of glutamatergic pathways. It has been hypothesized to positively regulate glutaminase activity and therefore glutamatergic neurotransmission. In the
eat-4(
ky5) loss-of-function worms, there is presumably insufficient glutamate available for sustained transmission. In the experiments reported here
eat-4 worms showed no differences from wild-type in the magnitude of response to a single tap, indicating that the neural circuit underlying the response was intact and functional in the mutant worms. However, when
eat-4 worms were given repeated taps the resulting habituation was different from that seen in wild-type worms:
eat-4 worms habituate more rapidly and recover more slowly than wild-type worms at all interstimulus intervals tested. In addition,
eat-4 worms do not show dishabituation. The same transgene rescues pharyngeal activity defects and both the habituation and dishabituation deficits seen in the
eat-4 worms. Our results suggest that neurotransmitter regulation plays a role in habituation and may play a role in dishabituation.