Investigation of the role of Nitric Oxide in the synaptic facilitation that underlies long-term sensitization in the mollusk Aplysia




Chen, Ayleen
Wainwright, Marcy
Mozzachiodi, Riccardo


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Long-term memory (LTM) is the capability of an organism to store information for an extended period of time and is meditated by intrinsic plasticity (modulation of neuronal excitability) and synaptic plasticity (facilitation/depression of synaptic responses; Mozzachiodi and Byrne 2010). A simple form of LTM found in virtually all organisms is long-term sensitization (LTS), where the response of an organism to a noxious stimulus is strengthened. In the invertebrate organism, Aplysia sensitization manifests as the enhancement of defensive reflexes, for example the withdrawal of the siphon in response to an electrical stimulus applied to the tail (Byrne and Hawkins 2015). The two cellular mechanisms known to be responsible for LTS in Aplysia are long-term increased excitability (LTIE) of the tail sensory neurons (SN) and long-term synaptic facilitation (LTF) between SNs and motor neurons (MNs), expressed as enlarged excitatory post-synaptic potentials (EPSP) in MNs (Cleary et al. 1998). Recent research on Aplysia has identified the gaseous neurotransmitter nitric oxide (NO) as an important co-modulator for long-term sensitization by utilizing L-NAME, a compound responsible for blocking NO synthesis (Farruggella et al. 2019). The application of L-NAME prevented LTS in vivo, which implied that NO was necessary for LTS. However, long-term increased SN excitability persisted at the cellular and molecular levels. This project investigates the discrepancy between the absence of LTS and the persisting SN excitability by analyzing the MN EPSPs following L-NAME application.


Department of Life Sciences, College of Science



This project is funded by Grant 15NS118408 from the National Institute of Neurological Disorders and Stroke awarded to Riccardo Mozzachiodi and by the McNair Scholars Program to Ayleen Chen.