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Related Experiment Videos

Alpha-2 adrenoceptor agonists decrease cyclic guanosine 3',5'-monophosphate in the mouse brain

Y Vulliemoz1, H Shen, L Virag

  • 1Department of Anesthesiology, College of Physicians and Surgeons, Columbia University, New York, New York 10032, USA.

Anesthesiology
|September 1, 1996
PubMed
Summary
This summary is machine-generated.

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Alpha-2 adrenoceptor agonists like clonidine and dexmedetomidine decrease cyclic guanosine 3

Area of Science:

  • Neuroscience
  • Pharmacology

Background:

  • Central nervous system activity is modulated by neurotransmitters affecting cyclic guanosine 3',5'-monophosphate (cGMP) levels.
  • Nitric oxide (NO) mediates the effects of excitatory and sedative agents on cGMP.
  • Volatile anesthetics reduce cerebellar cGMP, correlating with anesthetic and anticonvulsant effects.

Purpose of the Study:

  • To investigate the role of the NO-cGMP pathway in the action of alpha-2 adrenoceptor agonists.
  • To determine if clonidine and dexmedetomidine utilize the NO-cGMP pathway for their anesthetic effects.

Main Methods:

  • Mice received intraperitoneal doses of clonidine, dexmedetomidine, or L-medetomidine.
  • Alpha-2 antagonists (yohimbine, atipamezole), an alpha-1 antagonist (prazosin), and NO synthase inhibitors were administered prior to agonists.

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  • cGMP levels were measured in brain extracts using radioimmunoassay.

    • Main Results:

    • Clonidine and dexmedetomidine dose-dependently decreased cerebellar cGMP, an effect blocked by alpha-2 antagonists but not prazosin.
    • L-medetomidine, lacking sedative effects, did not alter cGMP levels.
    • NO synthase inhibition abolished the cGMP response to the agonists in multiple brain regions.

    Conclusions:

    • The nitric oxide-cGMP pathway is an effector system linked to alpha-2 adrenoceptors.
    • This pathway mediates the sedative effects of alpha-2 adrenoceptor agonists.