Skip to main content

A Metabotropic Hypothesis for Ethanol Sensitivity of GABAergic and Glutamatergic Central Synapses

  • Chapter

Abstract

This chapter will address the sensitivity of ligand-gated ion channels to ethanol and show that such ethanol sensitivity (or lack of sensitivity) is not invariable for any given neuron. In fact, bringing together several pieces of electrophysiological and pharmacological data leads us to put forward a hypothesis that the ethanol sensitivity of ligand- gated ion channels is regulated by ‘metabotropic’ systems defined in the generic sense: that is, by receptor-activated, G-protein-linked, non-ionotropic, energetic mechanisms. This hypothesis might provide an explanation for the variability of ethanol-transmitter interactions seen in various laboratories.

This is a preview of subscription content, log in via an institution.

Buying options

Chapter
USD   29.95
Price excludes VAT (USA)
  • Available as PDF
  • Read on any device
  • Instant download
  • Own it forever
eBook
USD   39.99
Price excludes VAT (USA)
  • Available as EPUB and PDF
  • Read on any device
  • Instant download
  • Own it forever
Softcover Book
USD   54.99
Price excludes VAT (USA)
  • Compact, lightweight edition
  • Dispatched in 3 to 5 business days
  • Free shipping worldwide - see info

Tax calculation will be finalised at checkout

Purchases are for personal use only

Learn about institutional subscriptions

Preview

Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.

References

  • Berton F, Francesconi W, Madamba SG, Zieglgänsberger W, Siggins GR (1998) Acamprosate enhances N-Methyl-D-Aspartate receptor-mediated neurotransmission but inhibits presynaptic GABAB receptors in nucleus accumbens neurons. Alcohol Clin Exp Res 22:183–191.

    Article  PubMed  CAS  Google Scholar 

  • Bloom FE, Siggins GR, Foote SL, Gruol D, Aston-Jones G, Rogers J, Pittman Q, Staunton D (1984) Noradrenergic involvement in the cellular actions of ethanol. In: Catecholamines, Neurology and Neurobiology, Volume 13. (Usdin E, ed.), pp. 159–168, New York: Alan R. Liss, Inc.

    Google Scholar 

  • Lovinger DM (1993) High ethanol sensitivity of recombinant AMPA-type glutamate receptors expressed in mammalian cells. Neurosci Lett 159:83–87.

    Article  PubMed  CAS  Google Scholar 

  • Madamba SG, Schweitzer P, Zieglgaensberger W, Siggins GR (1996) Acamprosate (calcium acetylhomotaurinate) enhances the NMDA component of excitatory neurotransmission in rat hippocampal CA1 neurons in vitro. Alcohol Clin Exp Res 20:651–658.

    Article  PubMed  CAS  Google Scholar 

  • Mancillas JR, Siggins GR, Bloom FE (1986) Ethanol selectively enhances responses to acetylcholine and somatostatin in the rat hippocampus. Science 231:161–163.

    Article  PubMed  CAS  Google Scholar 

  • Martin G, Nie Z, Siggins GR (1997) Mu-opioid receptors modulate NMDA receptor-mediated responses in nucleus accumbens neurons. J Neurosci 17:11–22.

    PubMed  CAS  Google Scholar 

  • Nie Z, Madamba SG, Siggins GR (1993a) Low ethanol concentrations reduce NMDA currents in rat nucleus accumbens neurons. Soc Neurosci Abst 19:377.

    Google Scholar 

  • Nie Z, Madamba SG, Siggins GR (1994) Ethanol inhibits glutamatergic neurotransmission in nucleus accumbens neurons by multiple mechanisms. J Pharmacol Exp Ther 271:1566–1573.

    PubMed  CAS  Google Scholar 

  • Nie Z, Yuan X, Madamba SG, Siggins GR (1993b) Ethanol decreases glutamatergic synaptic transmission in rat nucleus accumbens in vitro: naloxone reversal. J Pharmacol Exp Ther 266:1705–1712.

    PubMed  CAS  Google Scholar 

  • Nie Z, Steffensen SC, Criado JR, Henriksen SJ, Siggins GR (1996) Ethanol inhibition of NMDA responses involves presynaptic GABAB receptors. Soc Neurosci Abst 22:2074

    Google Scholar 

  • Siggins GR, Pittman Q, French E (1987) Effects of ethanol on CA1 and CA3 pyramidal cells in the hippocampal slice preparation: An intracellular study. Brain Res, 414:22–34.

    Article  PubMed  CAS  Google Scholar 

  • Stelzer A, Wong RK (1989) GABAA responses in hippocampal neurons are potentiated by glutamate. Nature 337:170–173.

    Article  PubMed  CAS  Google Scholar 

  • Wan FJ, Berton F, Madamba SG, Francesconi W, Siggins GR (1996) Low ethanol concentrations enhance GABAergic inhibitory postsynaptic potentials in hippocampal pyramidal neurons only after block of GABAB receptors. Proc Natl Acad Sci (USA) 93:5049–5054.

    Article  CAS  Google Scholar 

  • Weiner JL, Zhang L, Carlen PL (1994a) Guanosine phosphate analogs modulate ethanol potentiation of GABAA-mediated synaptic currents in hippocampal CA1 neurons. Brain Res 665:307–310.

    Article  PubMed  CAS  Google Scholar 

  • Weiner JL, Zhang L, Carlen PL (1994b) Potentiation of GABAA-mediated synaptic current by ethanol in hippocampal CA1 neurons: Possible role of protein kinase C. J Pharmacol Exp Ther 268:1388–1395.

    PubMed  CAS  Google Scholar 

  • Yuan X, Madamba SG, Siggins GR (1992) Opioid peptides reduce synaptic transmission in the nucleus accumbens. Neurosci Lett 134:223–228.

    Article  PubMed  CAS  Google Scholar 

Download references

Author information

Authors and Affiliations

Authors

Editor information

Editors and Affiliations

Rights and permissions

Reprints and permissions

Copyright information

© 1999 Springer Science+Business Media New York

About this chapter

Cite this chapter

Siggins, G.R., Nie, Z., Madamba, S.G. (1999). A Metabotropic Hypothesis for Ethanol Sensitivity of GABAergic and Glutamatergic Central Synapses. In: Liu, Y., Hunt, W.A. (eds) The “Drunken” Synapse. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-4739-6_10

Download citation

  • DOI: https://doi.org/10.1007/978-1-4615-4739-6_10

  • Publisher Name: Springer, Boston, MA

  • Print ISBN: 978-1-4613-7148-9

  • Online ISBN: 978-1-4615-4739-6

  • eBook Packages: Springer Book Archive

Publish with us

Policies and ethics