| 10436036 |
Ko GY, Kelly PT: Nitric oxide acts as a postsynaptic signaling molecule in calcium/calmodulin-induced synaptic potentiation in hippocampal CA1 pyramidal neurons. J Neurosci. 1999 Aug 15;19(16):6784-94.
Postsynaptic injection of Ca (2+)/calmodulin (Ca (2+)/CaM) into hippocampal CA1 pyramidal neurons induces synaptic potentiation, which can occlude tetanus-induced potentiation (Wang and Kelly, 1995). Because Ca (2+)/CaM activates the major forms of nitric oxide synthase (NOS) to produce nitric oxide (NO), NO may play a role during Ca (2+)/CaM-induced potentiation. Here we show that extracellular application of the NOS inhibitor N (G)-nitro-L-arginine methyl ester (L-NAME) or postsynaptic co-injection of L-NAME with Ca (2+)/CaM blocked Ca (2+)/CaM-induced synaptic potentiation. Thus, NO is necessary for Ca (2+)/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 Ca (2+)/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 Ca (2+)/CaM-induced synaptic potentiation. However, postsynaptic co-injection of carboxy-PTIO with Ca (2+)/CaM blocked Ca (2+)/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 Ca (2+)/CaM-induced synaptic potentiation. |
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