Adenosine A1 Receptor Blockade Mimics Caffeine's Attenuation of Ethanol-Induced Motor Incoordination

Authors

  • Laura Connole,

    1. Department of Safety Pharmacology, H. Lundbeck A/S, Valby, Copenhagen, Denmark,
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  • Andrew Harkin,

    Corresponding author
    1. Department of Pharmacology and Therapeutics, School of Pharmacy, University College Cork, Ireland
      Author for correspondence: Andrew Harkin, Department of Pharmacology and Therapeutics, School of Pharmacy, University College Cork, Ireland (fax +353 21 4904616, e-mail a.harkin@ucc.ie).
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  • Mark Maginn

    1. Department of Safety Pharmacology, H. Lundbeck A/S, Valby, Copenhagen, Denmark,
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Author for correspondence: Andrew Harkin, Department of Pharmacology and Therapeutics, School of Pharmacy, University College Cork, Ireland (fax +353 21 4904616, e-mail a.harkin@ucc.ie).

Abstract

Abstract: The effects of co-administration of caffeine and ethanol were assessed on the motor coordination of rats on the accelerating rotarod (accelerod). Ethanol (2.5 g/kg, orally) decreased motor performance on the accelerod. Co-administration of caffeine (5 and 20 mg/kg, orally) dose-dependently attenuated this ethanol-induced deficit. Caffeine (20 mg/kg, orally) alone did not affect motor performance in the test. As caffeine is a non-selective adenosine receptor antagonist the ability of adenosine A1 and A2A receptor blockade to attenuate ethanol-induced motor incoordination was determined. Pre-treatment with the adenosine A1 receptor antagonist DPCPX (5 mg/kg, intraperitoneally) attenuated ethanol (2.5 g/kg, orally)-induced motor incoordination. By contrast, prior administration of the adenosine A2A selective antagonist SCH 58261 (10 mg/kg intraperitoneally) had no effect on the ethanol-induced motor deficit. These data demonstrate that adenosine A1 receptor blockade mimics the inhibitory action of caffeine on ethanol-induced motor incorordination, and may contribute to the ability of caffeine to offset the acute intoxicating actions of ethanol.

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