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The Journal of Neuroscience, August 15, 1999, 19(16):6784-6794
Nitric Oxide Acts as a Postsynaptic Signaling Molecule in Calcium/Calmodulin-Induced Synaptic Potentiation in Hippocampal CA1 Pyramidal Neurons
Gladys Y. Ko and Paul T. Kelly Department of Neurobiology and Anatomy, University of Texas Medical School at Houston, Houston, Texas 77225
Postsynaptic injection of Ca2+/calmodulin (Ca2+/CaM) into hippocampal CA1 pyramidal neurons induces synaptic potentiation, which can occlude tetanus-induced potentiation (Wang and Kelly, 1995). Because Ca2+/CaM activates the major forms of nitric oxide synthase (NOS) to produce nitric oxide (NO), NO may play a role during Ca2+/CaM-induced potentiation. Here we show that extracellular application of the NOS inhibitor NG-nitro-L-arginine methyl ester (L-NAME) or postsynaptic co-injection of L-NAME with Ca2+/CaM blocked Ca2+/CaM-induced synaptic potentiation. Thus, NO is necessary for Ca2+/CaM-induced synaptic potentiation. In contrast, extracellular perfusion of membrane-impermeable NO scavengers N-methyl-D-glucamine dithiocarbamate/ferrous sulfate mixture (MGD-Fe) or 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (carboxy-PTIO) did not attenuate Ca2+/CaM-induced synaptic potentiation, even though MGD-Fe or carboxy-PTIO blocked tetanus-induced synaptic potentiation. This result indicates that NO is not a retrograde messenger in Ca2+/CaM-induced synaptic potentiation. However, postsynaptic co-injection of carboxy-PTIO with Ca2+/CaM blocked Ca2+/CaM-induced potentiation. Postsynaptic injection of carboxy-PTIO alone blocked tetanus-induced synaptic potentiation without affecting basal synaptic transmission. Our results suggest that NO works as a postsynaptic (intracellular) messenger during Ca2+/CaM-induced synaptic potentiation.
Key words: nitric oxide; calmodulin; hippocampus; synaptic plasticity; synaptic potentiation; nitric oxide scavengers; nitric oxide synthase inhibitors
Copyright © 1999 Society for Neuroscience 0270-6474/99/19166784-11$05.00/0
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