Brain function relies profoundly on the intercommunication between neurons, a process facilitated by chemical and electrical synapses. Although both modalities of synaptic transmission coexist, significantly less is known about the regulatory factors and pathways underlying the development and function of gap junction (GJ)-mediated electrical synapses. To help fill this knowledge gap, our study focused on the intrinsic and extrinsic factors that regulate the GJ encoding gene innexin (Lst Inx 1) in the nervous system of the freshwater snail, Lymnaea stagnalis. We hypothesized that Lst Inx 1 expression is distinctly regulated by developmental stage, metabolic physiology, and environmental exposures. To test this hypothesis, we examined changes in Lst Inx 1 expression in the Lymnaea nervous system in response to developmental age, after starvation, and upon exposure to various environmental factors, including the GJ inhibitors niflumic acid (NFA) and meclofenamic acid (McFA), the neurotoxins rotenone and hydrogen peroxide, and the neuroprotective factor taurine. RNA extraction and qPCR experiments showed that Lst Inx 1 levels increased with age and after seven days of starvation. The GJ inhibitors NFA and McFA and the neurotoxins rotenone and hydrogen peroxide generally resulted in the upregulation of Lst Inx 1 expression while exposure to neuroprotective taurine downregulated Lst Inx 1 expression. These results advance our knowledge about the internal and environmental conditions which may alter the expression of Lst Inx 1 gene and, hence, the formation and function of electrical synapses during animal development and under physiological and environmental stresses.

Sonia Jolly would like to thank their faculty sponsor Fenglian Xu for their support of this project.