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avr-14 selectively affects short-term and long-term habituation at short interstimulus intervals in Caenorhabditis elegans Steidl, Stephan

Abstract

The role of interstimulus interval (ISI) in habituation has been well documented in a large number of species. Habituation occurs at a faster rate when stimuli are presented at a high frequency with short I Sis and at a slower rate when stimuli are presented at a low frequency with long ISIs. Spontaneous recovery, a return of response amplitudes to prehabituation levels upon cessation of stimulation, is also affected by ISI, such that spontaneous recovery occurs more rapidly when trained with short ISIs and less rapidly when trained with long ISIs. This has led to the hypothesis that short-term habituation is mediated by a family of ISI-sensitive cellular mechanisms that somehow encode the ISI of training and set the rate of spontaneous recovery. If this is the case, then there should exist genetic mutations that selectively affect habituation at short ISIs, long ISIs, or more than one ISI. The gene avr-14 encodes for a glutamate-gated chloride channel expressed on the sensory neurons of the tapwithdrawal (TWR) circuit in Caenorhabditis elegans. Results show that mutations in avr-14 affect both short-term and long-term memory in an ISI-dependant manner. Short-term habituation at short ISIs (10s and 30s) was affected while short-term habituation at long ISIs (45s and 60s) was not. Long-term memory for distributed or massed training at a 60s ISI did not appear to be affected by mutations in avr-14. On the other hand, worms with mutations in avr-14, unlike wild-type worms, showed significant long-term memory for distributed training with a 10s ISI. This form of memory was shown to be dependent on protein synthesis. Results from the series of experiments in this paper support the hypothesis of multiple shortterm memory systems. The effect of mutations in avr-14 on long-term memory are very unique as there exists no other example in the literature of a gene whose presence blocks the formation of long-term memory.

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