Cho Jin-Hwa, Choi In-Sun, Jang Il-Sung
Department of Pharmacology, School of Dentistry, Kyungpook National University, Jung-gu, Daegu, Republic of Korea.
Neuroreport. 2010 Sep 15;21(13):865-70. doi: 10.1097/WNR.0b013e32833d9142.
We examined the effect of 2'-3'-O-(4-benzoylbenzoyl)-adenosine-5'-triphosphate (Bz-ATP), a P2X7 receptor agonist, on action potential-independent glutamate release from nerve terminals attached to mechanically isolated immature hilar neurons. Bz-ATP increased spontaneous excitatory postsynaptic current (sEPSC) frequency, and this effect was blocked by Brilliant blue G, a P2X7 receptor antagonist, suggesting that P2X7 receptors mediate the facilitatory action of Bz-ATP on sEPSCs. In most of hilar neurons tested, the Bz-ATP-induced increase in sEPSC frequency was blocked by tetrodotoxin or Cd, suggesting that the activation of P2X7 receptors leads to a presynaptic depolarization. The P2X7 receptor-mediated facilitation of glutamate release would modulate the excitability of hilar neurons, and eventually have a broad impact on the pathophysiological functions mediated by the hippocampus.
我们研究了P2X7受体激动剂2'-3'-O-(4-苯甲酰苯甲酰基)-腺苷-5'-三磷酸（Bz-ATP）对机械分离的未成熟海马门区神经元神经末梢非动作电位依赖性谷氨酸释放的影响。Bz-ATP增加了自发兴奋性突触后电流（sEPSC）频率，且这种效应被P2X7受体拮抗剂亮蓝G阻断，提示P2X7受体介导了Bz-ATP对sEPSC的促进作用。在大多数被检测的海马门区神经元中，Bz-ATP诱导的sEPSC频率增加被河豚毒素或镉阻断，提示P2X7受体的激活导致突触前膜去极化。P2X7受体介导的谷氨酸释放促进作用会调节海马门区神经元的兴奋性，并最终对海马介导的病理生理功能产生广泛影响。
