Advertisement

Expression of Nicotinic Acetylcholine Receptor mRNA in the Rat Cerebral Cortex after Lesioning of the Nucleus Basalis Magnocellularis

  • Ichiro Miyai
  • Satoshi Ueno
  • Shiro Yorifuji
  • Harutoshi Fujimura
  • Seiichiro Tarui
Part of the Advances in Behavioral Biology book series (ABBI, volume 38A)

Summary

We investigated the effect of a unilateral lesion made in the nucleus basalis magnocellularis (nbm) on the expression of nicotinic acetylcholine receptors (nAChR’s) in the rat cerebral cortex. Cortical [3H]nicotine binding was not affected by the nbm lesion. Expression of nAChR mRNA in the cerebral cortex was determined by use of cDNA clones coding for nAChR subunits alpha-3, alpha-4, and beta-2. At 1 week after the lesioning, expression of alpha-4 and beta-2 was increased by 82% and 19%, respectively. By 4 weeks afterward, expression levels of these nAChR subunits on the ipsilateral side did not differ from those on the control side. Expression of alpha-3 was not altered. These results suggest that nAChR transcripts are regulated by cell-to-cell interactions and may represent supporting evidence for the occurrence of supersensitivity in deafferentated cholinergic neurons.

Keywords

Nicotinic Acetylcholine Receptor Control Side ChAT Activity Ibotenic Acid nAChR Subunit 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

Preview

Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.

References

  1. Arendash, G. W., Millard, W. J., Dunn, A. J., and Meyer, E. M., 1987, Longterm neuropatological and neurochemical effects of nucleus basalis lesions in the rat, Science, 238: 952.PubMedCrossRefGoogle Scholar
  2. Boulter, J., Evans, K., Goldman, D., Martin, G., Treco, D., Heinemann, S., and Patrick, J., 1986, Isolation of a cDNA clone coding for a possible neuronal acetylcholine receptor alpha-subunit, Nature (Lond.),319: 368.CrossRefGoogle Scholar
  3. Boulter, J., Connolly, J., Deneris, E., Goldman, D., Heinemann, S., and Patrick, J., 1987, Functional expression of two neuronal nicotinic acetylcholine receptors from cDNA clones identifies a gene family, Pro. Natl. Acad. Sci. U. S. A.,84: 7763.CrossRefGoogle Scholar
  4. Deneris E. S., Connolly, J., Boulter, J., Wada, E., Wada, K., Swanson, L. W., Patrick, J., and Heinemann, S., 1988, Primary structure and expression of beta2: a novel subunit of neuronal nicotinic acetylcholine receptors, Neuron, 1: 45.PubMedCrossRefGoogle Scholar
  5. Flicker C., Dean, R. L., Watkins, D. L., Fisher, S. K., and Bartus, R. T., 1983, Behavioral and neurochemical effects following neurotoxic lesions of a major cholinergic input to the cerebral cortex in the rat, Pharmacol. Biochem. Behay., 18: 973.CrossRefGoogle Scholar
  6. Flynn, D. D. and Mash, D. C., 1986, Characterization of L-[3H]nicotine binding in human cerebral cortex: comparison between Alzheimer’s disease and the normal, J. Neurochem., 47: 1948.PubMedCrossRefGoogle Scholar
  7. Fonnum, F., 1975, A rapid radiochemical method of the determination of choline acetyltransferase, J. Neurochem., 24: 407.PubMedCrossRefGoogle Scholar
  8. Goldman, D., Deneris, E., Luyten, W., Kochhar, A., Patrick, J., and Heinemann, S., 1987, Members of a nicotinic acetylcholine receptor gene family are expressed in different regions of the mammalian central nervous system, Cell, 48: 965.PubMedCrossRefGoogle Scholar
  9. Helper, D. J., Wenk, G. L., Cribbs, B. L., Olton, D. S., and Coyle, J. T., 1985, Memory impairments following basal forebrain lesions, Brain Res., 346: 8.CrossRefGoogle Scholar
  10. Lippiello, P. M. and Fernandes, K. G., 1986, The binding of L[3H]nicotine to a single class of high affinity sites in rat brain membranes, Molec. Pharmacol., 29: 448.Google Scholar
  11. LoConte, G., Bartolini, L., Casamenti, F., Marconcini-Pepeu, I., and Pepeu, G., 1982, Lesions of cholinergic forebrain nuclei: changes in avoidance behavior and scopolamine actions, Pharmacol. Biochem. Behay., 17: 933.CrossRefGoogle Scholar
  12. Nordberg, A. and Winbald, B., 1986, Reduced number of 3H-nicotine and H-acetylcholine binding sites in the frontal cortex of Alzheimer’s brains, Neurosci. Lett., 72: 115.PubMedCrossRefGoogle Scholar
  13. Salamone, J. D., Beart, P. M., Alpert, J. E., and Iversen, S. D., 1984, Impairment in T-maze reinforced alternation performance following nucleus basalis magnocellularis lesions in rats, Behay. Brain Res., 13: 63.CrossRefGoogle Scholar
  14. Whitehouse, P. J., Martino, A. M., Price, D. L., and Kellar, K. J., 1985, Reductions in nicotinic but not muscarinic cholinergic receptors in Alzheimer’s disease measured using [3H]acetylcholine, Ann. Neurol., 18: 145.Google Scholar
  15. Whitehouse, P. J., Marrtino, A. M., Antuono, P. G., Lowenstein, P. R., Coyle, J. T., Price, D. L., and Kellar K.J., 1986, Nicotinic acetylcholine sites in Alzheimer’s disease, Brain Res., 371: 146.PubMedCrossRefGoogle Scholar
  16. Whitehouse, P. J., Martino, A. M., Wagster, M. W., Price, D. L., Mayeux, R., Atack, J. R., and Kellar, K. J., 1988, Reductions in [3H]nicotinic acetylcholine binding in Alzheimer’s disease and Parkinson’s disease: an autoradiographic study, Neurology, 38: 720.PubMedCrossRefGoogle Scholar

Copyright information

© Plenum Press, New York 1990

Authors and Affiliations

  • Ichiro Miyai
    • 1
  • Satoshi Ueno
    • 1
  • Shiro Yorifuji
    • 1
  • Harutoshi Fujimura
    • 1
  • Seiichiro Tarui
    • 1
  1. 1.Department of NeurologyOsaka University Medical SchoolFukushima, Fukushima-ku, Osaka, 553Japan

Personalised recommendations