Although reductions in neurotransmission have been reported in response to agonist-mediated adenosine A1 receptor activation, the implications of A2 receptor activation on synaptic transmission have not been well explored. We examined the role adenosine A2 receptors play in the efficacy of neurotransmission between the Schaffer collateral-CA1 pathway in the rat transverse hippocampal slice. A2 receptor blockade in the presence of complete A1 receptor inhibition led to a reversible reduction of the field excitatory post-synaptic potential (EPSP) slope in response to low-frequency test pulses (0.033 Hz) indicating that A2 receptors can enhance synaptic transmission. A2 receptor blockade by the A2 antagonist, DMPX (3,7-dimethyl-1-propargylxanthine) prevented the induction of tetanus-induced long-term potentiation (LTP) of the EPSP. In contrast, no such effect on LTP induction was observed during A1 receptor blockade. We also examined the effects of DMPX on the induction of LTP during continued A1 receptor blockade with CPT. Under this condition, LTP was significantly reduced when compared to LTP induced in the presence of CPT alone. A similar result was found using the highly polar A2 antagonist 8-SPT (8-(p-sulfophenyl)theophylline) suggesting that the effects of DMPX on LTP were not due to a direct action on an intracellular intermediate. DMPX had no effect on LTP expression if applied 45 min following the tetanus indicating that A2 receptors play no significant role in the maintenance phase of LTP. Selective A2a receptor activation did not alter the field EPSP. Similarly, selective blockade of the A2a receptor did not interfere with tetanus-induced LTP. Increases in neuronal firing rates can result in elevations in the concentration of extracellular adenosine. Together, these results suggest that the A2 receptors may play an important role in the induction although not the maintenance of hippocampal LTP and that the effect is likely to be mediated by the A2b receptor.

译文

尽管据报道,由于激动剂介导的腺苷A1受体激活,神经传递减少,但A2受体激活对突触传递的影响尚未得到很好的探讨。我们检查了腺苷A2受体在大鼠横海马切片中Schaffer collateral-CA1途径之间的神经传递功效中的作用。在完全A1受体抑制的存在下,A2受体阻断导致场兴奋性突触后电位 (EPSP) 斜率响应于低频测试脉冲 (0.033Hz) 的可逆降低,表明A2受体可以增强突触传递。A2拮抗剂DMPX (3,7-二甲基-1-炔基黄嘌呤) 对A2受体的阻断阻止了破伤风诱导的EPSP长期增强 (LTP) 的诱导。相反,在A1受体阻滞期间未观察到对LTP诱导的这种作用。我们还研究了在CPT持续阻断A1受体期间DMPX对LTP诱导的影响。在这种情况下,与单独在CPT存在下诱导的LTP相比,LTP显着降低。使用高度极性的A2拮抗剂8-SPT (8-(对磺苯基) 茶碱) 发现了类似的结果,表明DMPX对LTP的作用不是由于对细胞内中间体的直接作用。如果在破伤风后45分钟使用DMPX,则表明A2受体对LTP表达没有影响在LTP的维持阶段没有重要作用。选择性A2a受体激活不会改变EPSP。同样,选择性阻断A2a受体不会干扰破伤风诱导的LTP。神经元放电速率的增加会导致细胞外腺苷浓度的升高。这些结果表明,A2受体可能在诱导中起重要作用,尽管不是维持海马LTP,并且该作用可能是由A2b受体介导的。

+1
+2
100研值 100研值 ¥99课程
检索文献一次
下载文献一次

去下载>

成功解锁2个技能,为你点赞

《SCI写作十大必备语法》
解决你的SCI语法难题!

技能熟练度+1

视频课《玩转文献检索》
让你成为检索达人!

恭喜完成新手挑战

手机微信扫一扫,添加好友领取

免费领《Endnote文献管理工具+教程》

微信扫码, 免费领取

手机登录

获取验证码
登录