In our previous work we have shown that partial inhibition of ACh-esterase by neostigmine protected C. elegans behavior against disturbances caused by extreme high temperature 36°C (Kalinnikova et al., 2013). These data show that extreme high temperature can inhibit ACh release from C. elegans neurons. For further analysis of this possibility we investigated the effect of extreme high temperature on toxicity of other ACh-esterase inhibitor aldicarb for organisms of two closely-related species of free-living soil nematodes C. elegans and C. briggsae. It is known that numerous mutations leading to decrease in ACh secretion cause C. elegans resistance to aldicarb. Therefore hyperthermia must have similar effect on aldicarb resistance if extreme high temperature inhibits ACh release.
Our experiments were carried out in liquid medium (NG buffer). In these experiments either temperature 36°C or aldicarb caused C. elegans paralysis (worms’ inability to swim, induced by mechanical stimulus), depending on exposure time to high temperature or toxicant. The temperature rise from 23 to 33°C didn’t cause worms’ paralysis but accelerated time course for paralysis induced by aldicarb. In contrast, aldicarb concentrations which are toxic at 33°C (50–200 μM) were nontoxic at 36°C. Moreover, these aldicarb concentrations protected C. elegans against paralysis induced by hyperthermia. These data can be explained by inhibition of ACh release by hyperthermia, because partial inhibition of ACh-esterase can compensate ACh deficiency. The additional evidence for this explanation was obtained from experiments with worms preadapted for 2 hours to moderate high temperature 30°C. Such adaptation in accordance with our previous data (Kalinnikova et al., 2013) caused the rise in C. elegans resistance to temperature 36°C but sensitized worms to toxic aldicarb effect at 23°C. Under these conditions extreme high temperature 36°C strongly protected C. elegans against toxic aldicarb effect while aldicarb protected C. elegans against extreme high temperature.
In order to reveal the possible role of inhibition of ACh release from C. elegans neurons in the organism’s resistance to hyperthermia we have compared the dependence of behavior sensitivity to aldicarb from rise of temperature in two closely-related species – C. elegans and C. briggsae. Since behavior thermotolerance of C. briggsae is significantly higher than such of C. elegans (Kalinnikova et al., 2011) one might propose that this difference in thermotolerance can correlate with thermostability of cholinergic synapses of these species. The dependence of aldicarb toxicity for C. briggsae in temperature range 23–33°C is similar with such for C. elegans. However at 36°C there was great difference in aldicarb action on organisms of C. elegans and C. briggsae. At this temperature aldicarb caused paralysis of C. briggsae, but protected C. elegans behavior against negative action of hyperthermia. It is known that C. briggsae resistance to temperature 36°C is strongly higher than such of C. elegans (Kalinnikova et al., 2011). These data indicate that exposure to temperature 36°C caused the inhibition of ACh release in C. elegans, but not in C. briggsae organism. Therefore it is evident that in C. briggsae organism the threshold both for thermal paralysis and inhibition of ACh release is higher than in C. elegans.
Therefore it is evident that cholinergic system is one of targets for high temperature effect on nematodes’ nervous system.
Kalinnikova TB, Shagidullin RR, Kolsanova RR, Osipova EB, Zakharov SV, and Gainutdinov MKh. (2013). Acetylcholine deficiency in Caenorhabditis elegans induced by hyperthermia can be compensated by ACh-esterase inhibition or activation of GAR-3 mAChRs. Environment and Natural Resources Research. 3, 98–113. PubMed
Kalinnikova TB, Timoshenko AKh, Tarasov OYu, Gainutdinov TM, and Gainutdinov MKh. (2011). Thermotolerance of soil nematodes Caenorhabditis briggsae AF16 and Caenorhabditis elegans N2 under experimental conditions. Russian Journal of Ecology. 42, 435–437. PubMed
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