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Kokan, N.

Publications and source records attributed to Kokan, N..

2 recordsLinked to original sources

Neuropeptides Involved in Elicited Reversal Speed Plasticity in C. elegans During Mechanosensory Habituation

Caenorhabditis elegans respond to mechanosensory taps with brief reversal responses. In past research, speed of the response was averaged over the entire reversal for each tap to analyze reversal speed habituation; however, with this measure, only a modest decrement in speed was observed. Using a more detailed breakdown of reversal speed, we found that speed is most plastic early in the reversal and stable later on. Using this analysis, we found that worms with mutations in neuropeptide genes show reduced speed plasticity during the first second of reversals, indicating peptidergic signaling may be involved in reversal speed plasticity.

animal behavior and cognition↗

Ethanol alters mechanosensory habituation in C. elegans by way of the BK potassium channel through a novel mechanism

In this research, we investigated how alcohol modulates the simplest form of learning, habituation, in Caenorhabditis elegans. We used our high throughput Multi-Worm Tracker to conduct a large scale study of more than 21,000 wild-type worms to assess the effects of different doses of alcohol on habituation of the well-characterized tap withdrawal response. We found that the effect of alcohol on habituation of the reversal response to repeated mechanosensory stimuli (taps) differed depending on the component of the reversal response assessed. Furthermore, we discovered that alcohol shifted the dominant response to tap from a backward reversal to a brief forward movement. Because the large conductance potassium (BK) channel has been shown to be important for alcohols effects on behaviour in a variety of organisms, including C. elegans, we investigated whether the C. elegans BK channel ortholog, SLO-1, mediated the effects of alcohol on habituation. We tested several different strains of worms with mutations in slo-1 along with wild-type controls; null mutations in slo-1 made animals resistant to alcohol induced changes in learning. However, a mutation in the putative ethanol binding site on SLO-1 did not disrupt ethanols impact on habituation. Finally, by degrading SLO-1 in different parts of the nervous system we found that SLO-1s function in ethanols impact on habituation is likely distributed throughout the neural circuit that responds to tap. Based on these results, our main conclusions are 1) ethanol is not a general facilitator or inhibitor of habituation but rather a complex modulator, 2) SLO-1 is required for ethanols effect on habituation, 3) ethanol is interacting (directly or indirectly) with SLO-1 through a novel unidentified mechanism to influence response plasticity.

neuroscience↗