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Neuronal signaling systems and ethanol dependence

S C Pandey1

  • 1Department of Psychiatry, College of Medicine, University of Illinois at Chicago, USA.

Molecular Neurobiology
|January 15, 1999
PubMed
Summary

Ethanol dependence involves changes in neuronal cyclic adenosine 3

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Pharmacology

Background:

  • Ethanol dependence is linked to molecular and cellular alterations in neuronal signaling pathways.
  • The cyclic adenosine 3',5'-monophosphate (cAMP) and phosphoinositide (PI) signal-transduction pathways are key targets for ethanol's effects.
  • Understanding these pathways is crucial for elucidating the mechanisms of ethanol tolerance and dependence.

Purpose of the Study:

  • To review the molecular and cellular changes in neuronal second-messenger pathways during ethanol dependence.
  • To explore the roles of cAMP and PI signaling cascades in mediating ethanol's actions.
  • To identify potential molecular targets involved in the neuro-adaptational mechanisms of ethanol dependence.

Main Methods:

  • Review of existing literature on ethanol's effects on neuronal signaling pathways.
  • Analysis of studies investigating changes in adenylate cyclase activity, Gs protein, protein kinase A (PKA), and cAMP-responsive element binding protein (CREB) following ethanol exposure.
  • Examination of research on phospholipase C (PLC) activity, its isozymes (PLC-beta 1, PLC-delta 1, PLC-gamma 1), and protein kinase C (PKC) in response to ethanol.

Main Results:

  • Acute ethanol exposure increases, while chronic exposure decreases, agonist-stimulated adenylate cyclase activity.
  • Chronic ethanol modulates postreceptor events in the cAMP cascade, including Gs protein, PKA, and CREB.
  • Protracted ethanol exposure decreases phospholipase C (PLC) activity, potentially due to reduced PLC-beta 1 levels, and alters protein kinase C (PKC) activity.

Conclusions:

  • Neuronal signaling proteins are molecular targets for ethanol's action.
  • Alterations in cAMP and PI signaling cascades are critically involved in the development of ethanol dependence.
  • These pathways are implicated in the neuro-adaptational mechanisms underlying chronic ethanol exposure.

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