[Adenosine inhibits spontaneous and glutamate induced discharges of hippocampal CA1 neurons].

Effects of adenosine (Ado) on spontaneous and glutamate induced discharges of neurons in CA1 area of hippocampal slices were examined using extracelluar recording technique. The results are as follows. (1) In response to the application of Ado (0.01 0.1 micromol/L, n=20) into the superfusate, spontaneous discharge rates (SDR) of 20 neurons decreased significantly in a dose dependent manner. (2) Both Ado non selective receptor antagonist 8 phenyltheophylline (8-PT, 0.5 mmol/L) and Ado selective A1 receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine (DPCPX, 50 nmol/L), completely blocked the inhibitory effects of Ado in 22 CA1 units. (3) In 10 units, ATP sensitive K(+) channel blocker glibenclamide (Gli, 15 mmol/L) also abolished the effect of Ado. (4) Application of glutamate (Glu, 0.2 mmol/L) into the superfusate for 2 min led to a marked increase in the discharge rate of 15 neurons in an epileptiform pattern; the epileptiform discharges induced by glutamate (Glu, 0.2 mmol/L) in 15 neurons were suppressed significantly by application of Ado (10 micromol/L) into the superfusate. (5) 8-PT (2 mmol/L), DPCPX (200 nmol/L) and Gli (7 mmol/L) were all capable of abolishing the inhibiting effect of Ado on the action of glutamate. Taken together, it is suggested that Ado can bind with adenosine A1-receptors on CA1 neurons, resulting in an activation of K(ATP) channels and inhibition of neuronal activity. The inhibitory effect of Ado on glutamate induced epileptiform activities in rat hippocampal neurons is also mediated by adenosine A1-receptor with involvement of ATP-sensitive potassium channels.