(full paper is archived in the Miller Library)
Title: Nitric oxide signaling in Aplysia californica
Student Author(s): Davis, Rachel
Faculty Advisor(s): Thompson, Stuart
Location: Final Papers Biology 176H
Date: June 2001
Abstract: Nitric oxide (NO) is an unconventional neurotransmitter. It is not stored in vesicles and released by exocytosis. Rather, it is produced from arginine by the activation of a calcium/calmodulin-dependent enzyme, nitric oxide synthase (NOS). NO acts as an orthograde neurotransmitter in the central nervous system, which means that it is released by pre-synaptic cells and affects post-synaptic cells. This unusual molecule stimulates soluble guanylyl cylcase and increases intracellular levels of cGMP in the post-synaptic cell. I wondered if an exogenous NO donor like sodium nitroprusside would result in post-synaptic membrane depolarization and increased input resistance in cells thought to receive this type of input. Using microelectrode techniques, I measured resting potentials and action potentials in the MCC (metacerebral cell) in the cerebral ganglion of Aplysia californica. I found that sodium nitroprusside caused a subthreshold membrane depolarization and increase in input resistance. The literature suggests that these effects may be the result of NO donors acting on potassium channels in the post-synaptic membrane. These experiments support the idea that NO acts as a transmitter or as a neuromodulator to influence the excitability of post-synaptic neurons in Aplysia.