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Consolidation of long-term memory by insulin in Lymnaea is not brought about by changing the number of insulin receptors
The pond snail Lymnaea stagnalis learns taste aversion and consolidates it into long-term memory (LTM). This is referred to as conditioned taste aversion (CTA). The superfusion of molluscan insulin-related peptides (MIPs) over the isolated snail brain causes a long-term enhancement of synaptic input...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Landes Bioscience
2013
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3656023/ https://www.ncbi.nlm.nih.gov/pubmed/23710281 http://dx.doi.org/10.4161/cib.23955 |
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author | Hatakeyama, Dai Okuta, Akiko Otsuka, Emi Lukowiak, Ken Ito, Etsuro |
author_facet | Hatakeyama, Dai Okuta, Akiko Otsuka, Emi Lukowiak, Ken Ito, Etsuro |
author_sort | Hatakeyama, Dai |
collection | PubMed |
description | The pond snail Lymnaea stagnalis learns taste aversion and consolidates it into long-term memory (LTM). This is referred to as conditioned taste aversion (CTA). The superfusion of molluscan insulin-related peptides (MIPs) over the isolated snail brain causes a long-term enhancement of synaptic input between the cerebral giant cell and the B1 buccal motor neuron. This enhancement is hypothesized to underlie CTA. The synaptic enhancement caused by the superfusion of MIPs can be blocked by the application of human insulin receptor antibody, which recognizes the extracellular domain of human insulin receptor and acts as an antagonist even for MIP receptors. An injection of the human insulin receptor antibody into the abdominal cavity of trained snails blocks the consolidation process leading to LTM, even though the snails acquire taste aversion. Here, we examined whether or not taste-aversion training changes the mRNA expression level of MIP receptor in the snail brain and found that it does not. This result, taken together with previous findings, suggest that the MIPs’ effect on synaptic function in the snail brain is attributable to a change in the MIP concentration, and not to a change in the mRNA expression level of MIP receptor, which is thought to reflect the number of MIP receptors. |
format | Online Article Text |
id | pubmed-3656023 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2013 |
publisher | Landes Bioscience |
record_format | MEDLINE/PubMed |
spelling | pubmed-36560232013-05-24 Consolidation of long-term memory by insulin in Lymnaea is not brought about by changing the number of insulin receptors Hatakeyama, Dai Okuta, Akiko Otsuka, Emi Lukowiak, Ken Ito, Etsuro Commun Integr Biol Short Communication The pond snail Lymnaea stagnalis learns taste aversion and consolidates it into long-term memory (LTM). This is referred to as conditioned taste aversion (CTA). The superfusion of molluscan insulin-related peptides (MIPs) over the isolated snail brain causes a long-term enhancement of synaptic input between the cerebral giant cell and the B1 buccal motor neuron. This enhancement is hypothesized to underlie CTA. The synaptic enhancement caused by the superfusion of MIPs can be blocked by the application of human insulin receptor antibody, which recognizes the extracellular domain of human insulin receptor and acts as an antagonist even for MIP receptors. An injection of the human insulin receptor antibody into the abdominal cavity of trained snails blocks the consolidation process leading to LTM, even though the snails acquire taste aversion. Here, we examined whether or not taste-aversion training changes the mRNA expression level of MIP receptor in the snail brain and found that it does not. This result, taken together with previous findings, suggest that the MIPs’ effect on synaptic function in the snail brain is attributable to a change in the MIP concentration, and not to a change in the mRNA expression level of MIP receptor, which is thought to reflect the number of MIP receptors. Landes Bioscience 2013-05-01 2013-04-09 /pmc/articles/PMC3656023/ /pubmed/23710281 http://dx.doi.org/10.4161/cib.23955 Text en Copyright © 2013 Landes Bioscience http://creativecommons.org/licenses/by-nc/3.0/ This is an open-access article licensed under a Creative Commons Attribution-NonCommercial 3.0 Unported License. The article may be redistributed, reproduced, and reused for non-commercial purposes, provided the original source is properly cited. |
spellingShingle | Short Communication Hatakeyama, Dai Okuta, Akiko Otsuka, Emi Lukowiak, Ken Ito, Etsuro Consolidation of long-term memory by insulin in Lymnaea is not brought about by changing the number of insulin receptors |
title | Consolidation of long-term memory by insulin in Lymnaea is not brought about by changing the number of insulin receptors |
title_full | Consolidation of long-term memory by insulin in Lymnaea is not brought about by changing the number of insulin receptors |
title_fullStr | Consolidation of long-term memory by insulin in Lymnaea is not brought about by changing the number of insulin receptors |
title_full_unstemmed | Consolidation of long-term memory by insulin in Lymnaea is not brought about by changing the number of insulin receptors |
title_short | Consolidation of long-term memory by insulin in Lymnaea is not brought about by changing the number of insulin receptors |
title_sort | consolidation of long-term memory by insulin in lymnaea is not brought about by changing the number of insulin receptors |
topic | Short Communication |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3656023/ https://www.ncbi.nlm.nih.gov/pubmed/23710281 http://dx.doi.org/10.4161/cib.23955 |
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