Tohdoh Y, Narimatsu E, Kawamata M, Namiki A
Department of Anesthesiology, Sapporo Medical University School of Medicine, South 1, West 16, Chuo-ku, Sapporo, Hokkaido 060-0061, Japan.
Anesth Analg. 2000 Dec;91(6):1537-41. doi: 10.1097/00000539-200012000-00044.
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 microM) 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 microM aminophylline, a nonselective adenosine receptor antagonist, and 0.2 microM 3, 7-Dimethyl-1-propagylxanthine, an adenosine A(1) receptor antagonist (P<0.01 each). However, the fEPSP depression was not affected by pretreatment with 10 microM 8-cyclopentyl-1, 3-dipropylxanthine, an A(2) receptor antagonist, or 10 microM bicuculline, a gamma-aminobutyric acid (GABA) A receptor antagonist. The results indicate that adenosine neuromodulation through A(1) receptors and other undefined mechanisms, which are independent from GABAergic mechanisms, are involved in pentobarbital-induced depression of excitatory synaptic transmission.
我们研究了腺苷神经调节在体外戊巴比妥诱导的兴奋性突触传递抑制机制中的作用。从异氟烷麻醉的雄性Wistar大鼠脑中制备横向海马切片。在含氧人工脑脊液中，从CA1区记录由0.05 Hz的Schaffer侧支的正向电刺激诱发的场兴奋性突触后电位（fEPSP）。分析fEPSP的幅度以评估药物作用。戊巴比妥（100 microM）短暂抑制fEPSP（P<0.01）；即，fEPSP最初被抑制至对照的约60%，然后恢复至对照的约80%。用50 microM氨茶碱（一种非选择性腺苷受体拮抗剂）和0.2 microM 3,7-二甲基-1-丙基黄嘌呤（一种腺苷A(1)受体拮抗剂）预处理可部分抑制fEPSP的抑制（各P<0.01）。然而，fEPSP的抑制不受10 microM 8-环戊基-1,3-二丙基黄嘌呤（一种A(2)受体拮抗剂）或10 microM荷包牡丹碱（一种γ-氨基丁酸（GABA）A受体拮抗剂）预处理的影响。结果表明，通过A(1)受体的腺苷神经调节以及其他与GABA能机制无关的未定义机制参与了戊巴比妥诱导的兴奋性突触传递抑制。
