Abstract
Adenosine amine congener (ADAC), a selective A1 agonist, has been reported to protect hippocampal neurons against ischemia without producing harmful cardiovascular side effects. We examined effects of ADAC on the neuronal activity of CA1 neurons in rat hippocampal slice preparations using intracellular and whole-cell patch-clamp recording methods. Bath-application of ADAC (0.1-2μM) produced a hyperpolarizing response and outward current (IADAC) in a concentration-dependent manner. At a concentration of 1μM, ADAC produced a hyperpolarizing response (4.4±0.3mV, n=9) and IADAC (173.3±27.5pA, n=6) with an increased membrane conductance to 140％ of the control at –65mV. The IADAC reversed its polarity at near –90mV, that is close to the equilibrium potential for K+ in the ACSF. The IADAC was not blocked by TTX (1μM) but partially depressed by BaCl2(100μM). ADAC (2μM) depressed the amplitude of EPSC to 10％ of the control (n=4). ADAC did not affect the glutamate-induced inward currents. Furthermore, ADAC depressed the frequency of mEPSP without changing their amplitude. 8-CPT, a selective A1 antagonist, blocked the IADAC and the depression of the EPSC. These results suggest that ADAC depresses the release of glutamate via A1 receptors. [Jpn J Physiol 54 Suppl:S151 (2004)]
