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GENERAL ARTICLES

The Involvement of Adenosine Neuromodulation in Pentobarbital-Induced Field Excitatory Postsynaptic Potentials Depression in Rat Hippocampal Slices

Department of Anesthesiology, Sapporo Medical University School of Medicine, South 1, West 16, Chuo-ku, Sapporo, Hokkaido 060-0061, Japan

Address correspondence and reprint requests to Yurie Tohdoh, MD, Department of Anesthesiology, Sapporo Medical University, School of Medicine, South 1, West 16, Sapporo, Hokkaido 060-0061, Japan. Address e-mail to yurie-toudou{at}ghs.hospital.hokkaido.east.ntt.co.jp

We investigated the contribution of adenosine neuromodulation to mechanisms of pentobarbital-induced depression of excitatory synaptic transmission in vitro. Transverse hippocampal slices were prepared from brains removed from isoflurane-anesthetized male Wistar rats. Field excitatory postsynaptic potentials (fEPSPs), elicited by orthodromic electrical stimulation of Schaffer collateral at 0.05 Hz, were recorded from the CA1 region in oxygenated artificial cerebrospinal fluid. Amplitude of fEPSP was analyzed for assessing drug effects. Pentobarbital (100 µM) transiently depressed fEPSPs (P < 0.01); i.e., fEPSP was initially depressed to approximately 60% of control and then recovered to approximately 80% of control. The fEPSP depression was partially suppressed by pretreatment with 50 µM aminophylline, a nonselective adenosine receptor antagonist, and 0.2 µM 3, 7-Dimethyl-1-propagylxanthine, an adenosine A₁ receptor antagonist (P < 0.01 each). However, the fEPSP depression was not affected by pretreatment with 10 µM 8-cyclopentyl-1, 3-dipropylxanthine, an A₂ receptor antagonist, or 10 µM bicuculline, a -aminobutyric acid (GABA) A receptor antagonist. The results indicate that adenosine neuromodulation through A₁ receptors and other undefined mechanisms, which are independent from GABAergic mechanisms, are involved in pentobarbital-induced depression of excitatory synaptic transmission.

Implications: Adenosine neuromodulation contributes to mechanisms of pentobarbital-induced excitatory postsynaptic potentials depression.

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