Costenla A R, Lopes L V, de Mendonça A, Ribeiro J A
Laboratory of Neurosciences, Faculty of Medicine of Lisbon, Avenue Professor Egas Moniz, 1649-028, Lisbon, Portugal.
Neurosci Lett. 2001 Apr 13;302(1):53-7. doi: 10.1016/s0304-3940(01)01633-0.
Adenosine modulates hippocampal synaptic plasticity, namely long-term potentiation (LTP) and long-term depression (LTD), through activation of A1 and A2A receptors. We now report a novel role for the recently described adenosine A3 receptor in the regulation of synaptic plasticity in the CA1 area of hippocampal slices. Activation of adenosine A3 receptors by (1-[2-chloro-6-[[(3-iodophenyl)methyl]amino]-9H-purin-p-yl]-1-deoxy-N-methyl-beta-D-ribofuranuronamide (Cl-IBMECA) (100 nM) increased the magnitude of theta-burst induced LTP (from 1.2+/-0.6% in the control solution to 25.5+/-0.8% in the presence of Cl-IBMECA) and attenuated LTD (from 30.0+/-5.5% decrease in the control solution to 13.6+/-6.6% decrease in the presence of Cl-IBMECA). The selective adenosine A3 receptor antagonist, MRS 1191 (5-10 microM), prevented the effects of Cl-IBMECA. These findings indicate a functional role for adenosine A3 receptors in the modulation of synaptic plasticity.
腺苷通过激活A1和A2A受体来调节海马体突触可塑性，即长时程增强（LTP）和长时程抑制（LTD）。我们现在报告最近描述的腺苷A3受体在调节海马切片CA1区突触可塑性中的新作用。(1-[2-氯-6-[[(3-碘苯基)甲基]氨基]-9H-嘌呤-9-基]-1-脱氧-N-甲基-β-D-呋喃核糖酰胺（Cl-IBMECA）（100 nM）激活腺苷A3受体可增加θ波爆发诱导的LTP幅度（从对照溶液中的1.2±0.6%增加到存在Cl-IBMECA时的25.5±0.8%）并减弱LTD（从对照溶液中的30.0±5.5%降低到存在Cl-IBMECA时的13.6±6.6%降低）。选择性腺苷A3受体拮抗剂MRS 1191（5-10 microM）可阻止Cl-IBMECA的作用。这些发现表明腺苷A3受体在调节突触可塑性中具有功能作用。
