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흰쥐 해마에서 Acetylcholine 유리에 미치는 Adenosine 수용체의 역할

The Role of Adenosine Receptors on Acetylcholine Release in the Rat Hippocampus

As it has been reported that the depolarization induced acetylcholine(ACh) release is modulated by activation of presynaptic A<sub>1</sub>-adenosine heteroreceptor and various lines of evidence indicate the A<sub>2</sub>-receptor is present In hippocampus, this study was undertaken to delineate the role of adenosine receptors on hippocampal ACh release. Slices from the rat hippocampus were equilibrated with [<sup>3</sup>H]-choline and the release of the labelled product, [<sup>3</sup>H]-ACh, which evoked by electrical stimulation(3 Hz, 5 Vcm<sup>-1</sup>, 2 ms, rectangular pulses) was measured, and the influence of various agents on the evoked tritium outflow was Investigated. Adenosine(0.3 ~ 100μM) and CPA(0.1 ~ 30μM) decreased the [<sup>3</sup>H]-ACh release in a dose-dependent manner without changing the basal rate of release. DPCPX(1 ~ 10μM), a selective A<sub>1</sub>-receptor, antagonist, increased the [<sup>3</sup>H]-ACh release in a dose related fashion with slight increase of basal tritium release. And the effects of adenosine and CPA were significantly inhibited by DPCPX(2μM) treatment. CPCA, a specific A<sub>2</sub>-agonist, in concentration ranging from 0.3 to 30 μM, decreased the evoked tritium outflow, and these effects were also abolished by DPCPX(2μM) treatment. But the CPCA effects were not affected by DMPX(2μM), a specific Aa-antagonist, treatment. However, CGS 21680c, a recently introduced potent A<sub>2</sub>-agonist, in concentration ranging from 0.1 to 10μM, did not alter the evoked tritium outflow. These results indicate that the decrement of the evoked ACh release by adenosine is mediated by A<sub>1</sub>-heteroreceptor, but A<sub>2</sub>-adenosine receptor is not involved in ACh release in the rat hippocampus.

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