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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. InC. 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, wheneat-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 theeat-4 worms. Our results suggest that neurotransmitter regulation plays a role in habituation and may play a role in dishabituation.

the journal of neuroscience/the journal of neuroscience

Mutations of the<i>Caenorhabditis elegans</i>Brain-Specific Inorganic Phosphate Transporter<i>eat-4</i>Affect Habituation of the Tap–Withdrawal Response without Affecting the Response Itself

Mutations of theCaenorhabditis elegansBrain-Specific Inorganic Phosphate Transportereat-4Affect Habituation of the Tap–Withdrawal Response without Affecting the Response Itself