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Excitotoxin lesion of nucleus basalis causes a specific decrease in Go mRNA in cerebral cortex. Sensitivity to

H Wood1, J de Belleroche

  • 1Department of Biochemistry, Charing Cross and Westminster Medical School, London, UK.

FEBS Letters
|October 29, 1990
PubMed
Summary
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Nucleus basalis lesions selectively reduce cortical Go alpha mRNA levels, with recovery by 28 days. NMDA receptor blockade partially prevents this decrease, suggesting their involvement in cholinergic pathway regulation.

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Cellular Signaling

Background:

  • Ascending cholinergic pathway lesions impact cortical function.
  • Carbachol-stimulated polyphosphoinositide turnover is potentiated post-lesion.
  • G-protein alpha-subunit mRNAs are crucial for neuronal signaling.

Purpose of the Study:

  • Investigate the effect of nucleus basalis lesions on G-protein alpha-subunit mRNA levels.
  • Determine the selectivity of lesion effects on specific G-protein alpha subunits.
  • Explore the role of NMDA receptors in the observed changes.

Main Methods:

  • Excitotoxin lesion of the nucleus basalis in rodents.
  • Quantitative analysis of G-protein alpha-subunit mRNA levels (Go alpha, Gs alpha, Gi alpha) in the cerebral cortex.

Related Experiment Videos

  • Treatment with MK-801 to assess NMDA receptor involvement.

    • Main Results:

    • Selective reduction in Go alpha mRNA levels in the ipsilateral cerebral cortex post-lesion.
    • Maximal decrease of 40% in Go alpha mRNA at 3 days, returning to normal by 28 days.
    • Gs alpha and Gi alpha mRNA levels remained unaffected.
    • MK-801 treatment significantly attenuated the decrease in Go alpha mRNA.

    Conclusions:

    • Nucleus basalis lesions specifically downregulate cortical Go alpha mRNA.
    • The reduction in Go alpha mRNA is transient, with full recovery within 28 days.
    • NMDA receptor activation contributes to the decrease in Go alpha mRNA following cholinergic pathway lesions.