Nitric oxide synthase inhibitor L-NAME decreases long-term depression at the crayfish neuromuscular junction

Abstract

Nitric oxide (NO) is a gaseous neuromodulator in the central nervous system that acts as a retrograde messenger and has been found to both facilitate and depress synaptic transmission in various synapses. However, the role of NO remains unclear in the crayfish neuromuscular junction (NMJ). We investigated NOs effect on synaptic plasticity, the strengthening and weakening of synapses over time, in the crayfish NMJ using the nitric oxide synthase inhibitor L-NAME. First, we hypothesized that applying L-NAME exogenously would decrease percent change in excitatory postsynaptic potentials (EPSPs), and thus restrain long-term facilitation (LTF) or long-term depression (LTD) at the crayfish NMJ. Second, we hypothesized that increasing concentrations of L-NAME would amplify the decrease in percent change in EPSP and further restrain synaptic plasticity. We compared the percent change in EPSPs between the control (0 mM L-NAME), 0.075 mM L-NAME, and 0.15 mM L-NAME conditions. Our results showed a large percent change in EPSP and thus strong LTD in the control condition that was significantly different from the small percent change in EPSP and thus weak LTD in 0.15 mM L-NAME. However, we found no significant difference in percent change in EPSP between the 0.15mM and 0.075 L-NAME conditions, and therefore deduced that inhibition of nitric oxide synthase (NOS) restrains LTD at the crayfish NMJ but could not confirm that increased concentrations of L-NAME amplify resulting changes in plasticity.