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应用细胞外记录单位放电技术 ,在大鼠海马脑片上观察腺苷 (adenosine ,Ado)对CA1区神经元自发和谷氨酸所致癫痫样放电的影响。实验结果如下 :(1) 2 0个海马CA1神经元在给予Ado (0 0 1～ 0 1μmol/L)时自发放电频率降低 ,且呈明显的剂量依赖性 ;(2 )在 2 2个CA1单位 ,应用腺苷受体非选择性拮抗剂 8 苯茶碱 (8 phenyl theophylline,8 PT ,0 5mmol/L)和腺苷A1受体选择性拮抗剂 8 环戊 1,3 二丙基黄嘌呤 (8 cyclopentyl 1,3 dipropyl xanthine ,DPCPX ,5 0nmol/L)均可完全阻断腺苷的抑制效应 ;(3)在应用ATP敏感性钾通道抑制剂格列苯脲 (gliben clamide ,Gli,15mmol/L)的 10个单位 ,腺苷的上述抑制效应亦被阻断 ;(4 )在 15个单位 ,预先用谷氨酸 (glutamate ,Glu ,0 2mmol)灌流海马脑片 2min ,CA1神经元放电频率明显增加 ,表现为癫痫样放电 ,灌流Ado (10 μmol/L)后则可抑制其癫痫样放电 ;(5 ) 10个CA1单位 ,灌流 8 PT (2mmol/L)或DPCPX (2 0 0nmol/L)均可阻断腺苷对谷氨酸效应的抑制作用 ;对 5个CA1单位应用Gli (7mmol/L)亦可消除上述效应。结果提示 :Ado与海马神经元上的A1受体结合后 ,引起细胞膜上的ATP敏感性钾通道的开放 ,从而对海马神经元自发放电及Glu所致的癫痫样放电呈现抑制作用。
The effect of adenosine (Ado) on spontaneous glutamate-induced epileptiform discharges in CA1 neurons was observed in rat hippocampal slices by using extracellular recording unit discharge technique. The experimental results are as follows: (1) The frequency of spontaneous firing in 20 hippocampal CA1 neurons decreased with the dose of Ado (0 0 1 ~ 0 1μmol / L) in a dose-dependent manner; (2) , A selective antagonist of adenosine receptor 8 8 phenyl theophylline (8 PT, 0 5 mmol / L) and selective adenosine A1 receptor antagonist 8 cyclopentyl 1,3 dipropylxanthine ( 8 cyclopentyl 1,3 dipropyl xanthine, DPCPX, 5 0 nmol / L) could completely block the inhibitory effect of adenosine. (3) When glibenclamide (Gli, 15 mmol / L), the inhibitory effect of adenosine was also blocked. (4) In 15 units, preincubation of hippocampal slices with glutamate (Glu, 0.2 mmol) for 2 min, the firing rate of CA1 neurons (5 μmol / L), 10 PT1 (2 mmol / L), or DPCPX (200 nmol / L) were significantly increased in epileptiform discharges and epileptiform discharges. ) Can block the inhibitory effect of adenosine on the glutamate effect; the application of Gli (7mmol / L) to 5 CA1 units can also eliminate the above effect. The results suggest that the binding of Ado to the A1 receptor on hippocampal neurons causes the opening of ATP-sensitive potassium channels on the cell membrane, thus inhibiting the spontaneous discharge of hippocampal neurons and the epileptiform discharge induced by Glu.