α7-type nicotinic acetylcholine receptor and prodynorphin mRNA expression after administration of (-)-nicotine and U-50,488H in β-amyloid peptide (25-35)-treated mice

M. Hiramatsu, M. Watanabe, S. Baba, R. Kojima, Toshitaka Nabeshima

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Abstract

We previously reported that (-)-nicotine and κ-opioid receptor gonists lessened impairment of learning and/or memory in several animal models. Furthermore, these drugs prevented neurodegenerative damage induced by ischemia or β-amyloid peptide (25-35). In the present study, we tested whether (-)-nicotine and U-50,488H prevent delayed-memory impairment induced by β-amyloid peptide (25-35), and changes of expression of α7-type nicotinic acetylcholine receptor mRNA and prodynorphin mRNA. Seven days after treatment with β-amyloid peptide (25-35) (9 nmol/mouse, i.c.v.), memory impairment was observed in the Y-maze test. Memory impairment was prevented when (-)-nicotine (6.16 μmol/kg, s.c.) or U-50,488H (21 μmol/kg, s.c.) was administered 1 h before, but not 1 h after, β-amyloid peptide (25-35) treatment. There was no change in prodynorphin mRNA or α7-type nicotinic acetylcholine receptor mRNA expression in the hippocampus 10 days after β-amyloid peptide (25-35) treatment alone. Of interest, mRNA expression of not only prodynorphin, but also the α7-type nicotinic acetylcholine receptor, was significantly decreased when U-50,488H was administered 1 h before, but not 1 h after, treatment with β-amyloid peptide (25-35). However, these changes were not observed after the administration of (-)-nicetine. These results suggest that activation of the κ-opioid system, but not α7-type nicotinic receptors has a neuroprotective effect on β-amyloid peptide (25-35)-induced memory impairment, and may be involved in the long-lasting changes in the expression of these mRNAs.

Original languageEnglish
Pages (from-to)508-514
Number of pages7
JournalAnnals of the New York Academy of Sciences
Volume1025
DOIs
Publication statusPublished - 01-01-2004
Externally publishedYes

Fingerprint

(trans)-Isomer 3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cyclohexyl)-benzeneacetamide
Nicotinic Receptors
Nicotine
Amyloid
Messenger RNA
Peptides
Data storage equipment
Repression (Psychology)
Opioid Receptors
Neuroprotective Agents
preproenkephalin
Mouse
Impairment
Opioid Analgesics
Hippocampus
Animals
Ischemia
Animal Models
Chemical activation
Learning

All Science Journal Classification (ASJC) codes

  • Neuroscience(all)
  • Biochemistry, Genetics and Molecular Biology(all)
  • History and Philosophy of Science

Cite this

@article{186aeabba07445aca76c3e275d24c5ff,
title = "α7-type nicotinic acetylcholine receptor and prodynorphin mRNA expression after administration of (-)-nicotine and U-50,488H in β-amyloid peptide (25-35)-treated mice",
abstract = "We previously reported that (-)-nicotine and κ-opioid receptor gonists lessened impairment of learning and/or memory in several animal models. Furthermore, these drugs prevented neurodegenerative damage induced by ischemia or β-amyloid peptide (25-35). In the present study, we tested whether (-)-nicotine and U-50,488H prevent delayed-memory impairment induced by β-amyloid peptide (25-35), and changes of expression of α7-type nicotinic acetylcholine receptor mRNA and prodynorphin mRNA. Seven days after treatment with β-amyloid peptide (25-35) (9 nmol/mouse, i.c.v.), memory impairment was observed in the Y-maze test. Memory impairment was prevented when (-)-nicotine (6.16 μmol/kg, s.c.) or U-50,488H (21 μmol/kg, s.c.) was administered 1 h before, but not 1 h after, β-amyloid peptide (25-35) treatment. There was no change in prodynorphin mRNA or α7-type nicotinic acetylcholine receptor mRNA expression in the hippocampus 10 days after β-amyloid peptide (25-35) treatment alone. Of interest, mRNA expression of not only prodynorphin, but also the α7-type nicotinic acetylcholine receptor, was significantly decreased when U-50,488H was administered 1 h before, but not 1 h after, treatment with β-amyloid peptide (25-35). However, these changes were not observed after the administration of (-)-nicetine. These results suggest that activation of the κ-opioid system, but not α7-type nicotinic receptors has a neuroprotective effect on β-amyloid peptide (25-35)-induced memory impairment, and may be involved in the long-lasting changes in the expression of these mRNAs.",
author = "M. Hiramatsu and M. Watanabe and S. Baba and R. Kojima and Toshitaka Nabeshima",
year = "2004",
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T1 - α7-type nicotinic acetylcholine receptor and prodynorphin mRNA expression after administration of (-)-nicotine and U-50,488H in β-amyloid peptide (25-35)-treated mice

AU - Hiramatsu, M.

AU - Watanabe, M.

AU - Baba, S.

AU - Kojima, R.

AU - Nabeshima, Toshitaka

PY - 2004/1/1

Y1 - 2004/1/1

N2 - We previously reported that (-)-nicotine and κ-opioid receptor gonists lessened impairment of learning and/or memory in several animal models. Furthermore, these drugs prevented neurodegenerative damage induced by ischemia or β-amyloid peptide (25-35). In the present study, we tested whether (-)-nicotine and U-50,488H prevent delayed-memory impairment induced by β-amyloid peptide (25-35), and changes of expression of α7-type nicotinic acetylcholine receptor mRNA and prodynorphin mRNA. Seven days after treatment with β-amyloid peptide (25-35) (9 nmol/mouse, i.c.v.), memory impairment was observed in the Y-maze test. Memory impairment was prevented when (-)-nicotine (6.16 μmol/kg, s.c.) or U-50,488H (21 μmol/kg, s.c.) was administered 1 h before, but not 1 h after, β-amyloid peptide (25-35) treatment. There was no change in prodynorphin mRNA or α7-type nicotinic acetylcholine receptor mRNA expression in the hippocampus 10 days after β-amyloid peptide (25-35) treatment alone. Of interest, mRNA expression of not only prodynorphin, but also the α7-type nicotinic acetylcholine receptor, was significantly decreased when U-50,488H was administered 1 h before, but not 1 h after, treatment with β-amyloid peptide (25-35). However, these changes were not observed after the administration of (-)-nicetine. These results suggest that activation of the κ-opioid system, but not α7-type nicotinic receptors has a neuroprotective effect on β-amyloid peptide (25-35)-induced memory impairment, and may be involved in the long-lasting changes in the expression of these mRNAs.

AB - We previously reported that (-)-nicotine and κ-opioid receptor gonists lessened impairment of learning and/or memory in several animal models. Furthermore, these drugs prevented neurodegenerative damage induced by ischemia or β-amyloid peptide (25-35). In the present study, we tested whether (-)-nicotine and U-50,488H prevent delayed-memory impairment induced by β-amyloid peptide (25-35), and changes of expression of α7-type nicotinic acetylcholine receptor mRNA and prodynorphin mRNA. Seven days after treatment with β-amyloid peptide (25-35) (9 nmol/mouse, i.c.v.), memory impairment was observed in the Y-maze test. Memory impairment was prevented when (-)-nicotine (6.16 μmol/kg, s.c.) or U-50,488H (21 μmol/kg, s.c.) was administered 1 h before, but not 1 h after, β-amyloid peptide (25-35) treatment. There was no change in prodynorphin mRNA or α7-type nicotinic acetylcholine receptor mRNA expression in the hippocampus 10 days after β-amyloid peptide (25-35) treatment alone. Of interest, mRNA expression of not only prodynorphin, but also the α7-type nicotinic acetylcholine receptor, was significantly decreased when U-50,488H was administered 1 h before, but not 1 h after, treatment with β-amyloid peptide (25-35). However, these changes were not observed after the administration of (-)-nicetine. These results suggest that activation of the κ-opioid system, but not α7-type nicotinic receptors has a neuroprotective effect on β-amyloid peptide (25-35)-induced memory impairment, and may be involved in the long-lasting changes in the expression of these mRNAs.

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