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Stimulation of the cAMP system by the nitric oxide-cGMP system underlying the formation of long-term memory in an insect
| Title: | Stimulation of the cAMP system by the nitric oxide-cGMP system underlying the formation of long-term memory in an insect |
| Authors: | Matsumoto, Yukihisa Browse this author | | Hatano, Ai Browse this author | | Unoki, Sae Browse this author | | Mizunami, Makoto Browse this author |
| Keywords: | Olfactory learning | | Memory | | Nitric oxide synthase | | Antagonist | | Cricket |
| Issue Date: | 25-Dec-2009 |
| Publisher: | Elsevier Ireland Ltd. |
| Journal Title: | Neuroscience Letters |
| Volume: | 467 |
| Issue: | 2 |
| Start Page: | 81 |
| End Page: | 85 |
| Publisher DOI: | 10.1016/j.neulet.2009.10.008 |
| PMID: | 19818830 |
| Abstract: | The nitric oxide (NO)-cGMP signaling system and CAMP system play critical roles in the formation of multiple-trial induced, protein synthesis-dependent long-term memory (LTM) in many vertebrates and invertebrates. The relationship between the NO-cGMP system and cAMP system, however, remains controversial. In honey bees, the two systems have been suggested to converge on protein kinase A (PKA), based on the finding in vitro that cGMP activates PKA when sub-optimal dose of cAMP is present. In crickets, however, we have suggested that NO-cGMP pathway operates on PKA via activation of adenylyl cyclase and production of cAMP for LTM formation. To resolve this issue, we compared the effect of multiple-trial conditioning against the effect of an externally applied cGMP analog for LTM formation in crickets, in the presence of sub-optimal dose of cAMP analog and in condition in which adenylyl cyclase was inhibited. The obtained results suggest that an externally applied cGMP analog activates PKA when sub-optimal dose of cAMP analog is present, as is suggested in honey bees, but cGMP produced by multiple-trial conditioning cannot activate PKA even when sub-optimal dose of cAMP analog is present, thus indicating that cGMP produced by multiple-trial conditioning is not accessible to PKA. We conclude that the NO-cGMP system stimulates the cAMP system for LTM formation. We propose that LTM is formed by an interplay of two classes of neurons, namely, NO-producing neurons regulating LTM formation and NO-receptive neurons that are more directly involved in the formation of long-term synaptic plasticity underlying LTM formation. |
| Type: | article (author version) |
| URI: | http://hdl.handle.net/2115/40042 |
| Appears in Collections: | 生命科学院・先端生命科学研究院 (Graduate School of Life Science / Faculty of Advanced Life Science) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)
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Submitter: 水波 誠
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