ABSTRACT In the hippocampus, •NO participates in the mechanisms of synaptic plasticity, including long-term potentiation, but neurotoxic actions of •NO, such as the participation in excitotoxicity, have also been documented. Both phenomena involve the stimulation of ionotropic glutamate receptors, implying that the regulation of the glutamate receptor-nitric oxide synthase pathway is an important determinant of the physiological and pathological •NO actions in the hippocampus. Being a highly diffusible signaling molecule, overcoming storage and selective membrane receptor recognition, •NO produced by a neuron does not distinguish between the functionally coupled post-synaptic neuron versus adjacent cells not functionally linked to the generator neuron. This concept implies that the rate and pattern of •NO concentration change in hippocampus as determined, among other mechanisms, by ionotropic glutamate receptors, as well as its diffusion in biological tissue are critical determinants for the understanding of •NO diverse actions in hippocampus. Both tasks require the selective measurement of •NO with spatial-temporal resolution for which technology development is demanded. These notions are critically addressed in this review on basis of the molecular mechanisms involved.
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