摘要：The long-term potentiation (LTP), an activity-induced increase in the efficacy of neurotransmission, has long been conceived to be a physiological correlate of learning and memory. Investigations of synaptic transmission suggest that the postsynaptic N-methyl-D-aspartate (NMDA) receptor is the upstream mediator of LTP, while nitric oxide (NO), a retrograde messenger from postsynaptic neurons to presynaptic neuron, is the downstream mediator of LTP. Our previous studies showed that microinjections of NMDA receptor antagonist D-AP5 to the goldfish telencephalon prior to trainings impaired learning of avoidance conditioning in goldfish. However, microinjections of D-AP5 to the goldfish telencephalon immediately following trainings did not impair memory of avoidance conditioning. Carboxy-PTIO is a NO scavenger that prevents NO from reaching the presynaptic neurons. The present study investigated the effects of microinjections of carboxy-PTIO to the goldfish telencephalon immediately following trainings on avoidance conditioning. The results showed that microinjections of carboxy-PTIO to the goldfish telencephalon immediately following trainings impaired memory of avoidance conditioning.
