Rymut, JA. 2018.Determining the effects of nitric oxide on Procambarus fallax forma virginalis. Poster given at the International Crustacean Congress IX, Washington DC, USA, 22-25 May 2018. http://www.birenheide.com/ICC2018/program/singlesession.php3?sessid=P, poster P.33.
Abstract
Ethanol (EtOH) effects inducible nitric oxide synthase (iNOS) activity by inhibiting the production of iNOS in cells. Acute doses increase the production of nitric oxide (NO) and endothelial NOS (eNOS). At higher dosages, ethanol impairs endothelial functions. NO has been found to suppress the feeding response in pond snails, Lymnaea stagnalis, induce synaptic depression in crayfish, and inhibit the swimming rhythm of Xeonpus laevis tadpoles. This in vivo study will be performed in order to determine if synaptic depression is caused by free radical NO and determine if overall movements are decreased in Procambarus forma fallax virginalis (P.f.f virginalis) in the presence of NO. It was hypothesized that there will be a depression in synaptic activity and less movement in crayfish exposed to free radical NO. A probe will be inserted near the cerebral ganglion to assess depression in synaptic inputs. Movement will be tested by placing crayfish into a partitioned tank and counting each movement across a partition as one movement. Movement will be tested on both an individual and group level to determine if group activity will be a variable factor. NO will be introduced through the usage of ethanol, an L-arginine supplement, and chlorhexidine in an approximate range of five to ten parts per million (5 mg/L and 10 mg/L).
Keywords: None provided.
Update, 30 May 2018: At the author’s request, here is the updated abstract from the poster as it was presented at the meeting (above).
Ethanol (Et-OH) effects inducible nitric oxide synthase (iNOS) activity by inhibiting the production of iNOS in cells. Acute doses increase the production of nitric oxide (NO) and endothelial NOS (eNOS). At higher dosages, ethanol impairs endothelial functions. NO has been found to suppress the feeding response in pond snails, Lymnaea stagnalis, induce synaptic depression in crayfish, and inhibit the swimming rhythm of Xenopus laevis tadpoles (Aonuma, et al. 2000). This in vivo study has been performed in order to determine if synaptic depression is caused by NO, and if overall movements are decreased in Procambarus forma fallax virginalis (P.f.f virginalis) and Procambarus blandingii, in the presence of NO. Movement was assessed in a labeled gridded tanks of water, denatured ethanol (3 ppm), L-arginine (Reagent grade, 1ppb) and chlorhexidine (99.95%, 1ppb). There was an evident trend over a time interval of 6 minutes ≤ t ≤ 8 minutes, where the control, ethanol and chlorhexidine all had a stark drop off in activity, whilst L-arginine had a stark increase. It is hypothesized that this could be due to a metabolic pathway of L-arginine is converted through nitric oxide synthase (NOS) to L-citrulline (Racke, et al. 2010); whereas ethanol has proven to inhibit iNOS, and due to the cytostatic characteristics of chlorhexidine, it can be assumed that the correlation of chlorhexidine to ethanol lies in this pathway as well. Synaptic depression is shown where L-arginine is present, over a time interval of 0 ms ≤ t ≤ 10ms (Aonuma et al. 2010); as found in the study, there is a correlation between L-arginine and chlorhexidine pre-wash, and it is hypothesized that this is from the terminal guanylyl group.
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