Identification of neurotransmitter receptors on Muller cells and their function.

我们以前获得的大量证据表明，AMPA/Kainater受体不仅在神经元中表达，而且在Muller细胞中也有表达。用Fura-2 AM荧光分光光度法检测激动剂作用于成年兔视网膜培养的Muller细胞后的胞浆钙瞬变。神经毒性海人藻酸盐暴露于对照细胞时，钙瞬变的发生更多，这表明AMPA/海人藻酸受体在病理状态下是新发展的。用上述方法检测钙瞬变，我们发现大约50%的新生大鼠视网膜培养的神经元在50um时对毒扁豆碱有反应，但在50%的培养Muller细胞中，50um是形成钙瞬变所必需的。阿托品可阻断毒鼠碱对钙瞬变的诱导作用。M1激动剂MCN-A-343在神经元和Muller细胞上都能引起最显著的钙瞬变。因此，穆勒细胞似乎拥有敏感度较低的M受体，至少包括M1。P_1-/P_2-嘌呤能受体激动剂A2和P_2y诱导培养的Muller细胞钙瞬变。因此，Muller细胞可能具有P_1-/P_2-嘌呤能受体。我们还研究了一种新的兴奋性毒性氨基酸Dysiherbaine，它诱导了Muller细胞的钙瞬变，但似乎不是由已知的AMPA/海人藻酸受体介导的，因为受体拮抗剂(CNQX和DNQX)是由kmown的AMPM/海人藻酸受体介导的，因为受体拮抗剂(CNQX和DNQX)不能阻断这种瞬变。

We obtained previously considerable evidence indicating the expression of AMPA/kainater receptors not only by neurons but also Muller cells. Cytosolic calcium transients following an agonist administration to Muller cells cultured from adult rabbit retinas were examined with spectrofluorometry using fura-2 AM.Calcium transients occurred more in number for neurotoxic kainate exposed that control cells, suggesting the AMPA/kainate receptors develop be novo in pathological state. Using the above methods to detect calcium transients, we found approximately 50% of neurons cultured from neonatal rat retinas responded to muscarine at 50 muM , but 50 muM was requisite for the formation of calcium transients in 50% of cultured Muller cells. The muscarine inducement of calcium transients was blocked by atropine. The agonist of M1, McN-A-343 eliciteed the most significant calcium transients both in neurons and Muller cells. Thus, Muller cells appeared to possess the less sensitive muscarinic receptor including at least M1. P_1-/P_2-purinergic receptor agonists including A2 and P2y induced calcium transients in cultured Muller cells. Muller cells are thus shown guite likely to possess the P_1-/P_2-purinergic receptors. A new excitotoxic amino acid, dysiherbaine is also studied and it induced calcium transients in Muller cells but appeared not to be mediated by known AMPA/Kainate receptors, since the receptor antagonists (CNQX and DNQX) to be mediated by kmown AMPM/Kainate receptors, since the receptor antagonists (CNQX and DNQX) could not block the transients.