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Lu, Y.-F., Kandel, E.R. and Kawkins, R.D. (1999) Nitric Oxide Signaling Contributes to Late-Phase LTP and CREB Phosphorylation in the Hippocampus. Journal of Neuroscience, 19, 10250-10261.

has been cited by the following article:

  • TITLE: Nitric Oxide Scavenger Carboxy-PTIO Impaired Memory of Avoidance Conditioning in Goldfish

    AUTHORS: X. Xu, K. Zmolek

    KEYWORDS: Avoidance Conditioning, Memory Consolidation, Nitric oxide, Goldfish

    JOURNAL NAME: Open Journal of Social Sciences, Vol.2 No.5, May 13, 2014

    ABSTRACT: 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.