Requirement of gene transcription for experience-dependent long-term plasticity in the feeding neural circuit of an invertebrate model

Long-term memory formation is known to generally require gene transcription (Kandel 2001). Previous research within the marine mollusk Aplysia revealed that repeated exposure to aversive stimuli induces a lasting enhancement of defensive responses, known as long-term sensitization (LTS). LTS is mediated, at least in part, by long-term increased excitability (LTIE) of sensory neurons (SN), which is known to depend on gene transcription (Byrne and Hawkins 2015). Repeated exposure to aversive stimuli also induces long- term feeding suppression (LTFS) via a long-term decreased excitability (LTDE) of decision-making neuron B51 (Shields-Johnson et al. 2013). However, it is unknown whether B51 LTDE depends on transcription processes like those in the defensive circuits. Therefore, this study examines the molecular requirements for LTFS by determining whether B51 LTDE is transcription dependent. Actinomycin D (ACT-D) is being used to selectively inhibit gene transcription (Montarolo et al. 1986). This project utilizes a previously established in vitro preparation that includes the neural circuits responsible for LTS and LTFS. Electrical stimulation of afferent nerves from the body wall to mimic aversive training in vitro co-induces SN LTIE and B51 LTDE lasting 24 h (Weisz et al. 2017). Ongoing experiments utilize 4 groups: trained/vehicle, trained/ACT-D, untrained/vehicle, and untrained/ACT-D (Weisz et al. 2017). Statistical analysis is being conducted using the Kruskal-Wallis test (Farruggella et al. 2019). Current results indicate that ACT-D is effective in blocking the expression of SN LTIE, as previously shown (Montarolo et al. 1986). Regarding B51, although overall statistical significance across groups has not been reached yet, current findings show a trend that LTDE expressed in the trained/vehicle group is blocked in the trained/ACT-D group. If these results are confirmed statistically, they will demonstrate that ACT-D inhibits B51 LTDE, thus indicating that B51 LTDE requires transcription processes for long-term memory formation analogous to SN LTIE in the defensive circuits