中文摘要：

目的利用电生理方法，鉴定大鼠视网膜Muller细胞钙通道，进而研究慢性眼内压增高对Muller细胞钙通道电流的影响。方法在急性分离的大鼠Muller细胞上，利用全细胞膜片钳的电压钳技术记录钙通道电流。采用结扎巩膜上静脉的方法制备大鼠高眼压模型。结果当细胞外液中不含二价阳离子时，可以记录到电流幅度较大的钙通道介导的Na＋流。该电流可被L-型钙通道阻断剂nimodipine和T-钙通道阻断剂mibefradil可逆地压抑到加药前的（39．8±5．4）％（P〈0．001）和（46．7±8．7）％（P〈0．001）。与假手术组相比，高眼压术后1周、2周和4周的大鼠视网膜Mtiller细胞钙通道的电流幅度没有明显的变化。然而，电流成分分析发现，与对照组相比，高眼压大鼠Muller细胞的nimodipine敏感电流呈降低的趋势[1周：（70，9±13．3）％；2周：（70．5±21．9）％；4周：（69．2±23．9）％]，而mibefradil敏感的电流在高眼压术后1周和2周呈增高趋势[（157．5±21．2）％和（158．6±35．5）％]，4周时趋于正常（109．2±37．9）％。结论大鼠视网膜Mailer细胞功能性表达L-型和T-型钙通道。慢性眼内压增高导致L-型钙通道电流减小，T-型钙通道电流增大，从而增加胞内钙，共同参与Mtiller细胞的去极化和激活。

英文摘要：

Objective To identify the Ca2＋ channel types on rat retinal Mtiller cells by using electrophysiological techniques and to explore the changes of Ca 2＋ channel currents in retinal Muller cells in a rat chronic ocular hypertension （COH） model. Methods Ca2＋ channel currents were recorded by using whole-cell recording of patch-clamp techniques on acutely isolated rat Mailer cells. The COH rats were reproduced by blocking the episcleral veins. Results Na ~ currents through Ca2＋ channels could be recorded in a bath solution without divalent cation. The Ca2 ＋ channel currents were reversibly suppressed to 39.8% ± 5.4% （ P 〈 0. 001 ） and 46.7% ±8.7% of control （P 〈0.001 ） by nimodipine, an L-type Ca2＋ channel blocker, and mibefradil, a T-type Ca2＋ channel blocker, respectively. In Mtiller cells isolated from COH rats, although the total Ca2＋ current amplitudes did not show significant changes as compared with control, the nimodipine-sensitive current component showed a moderate decrease （ 1 week： 70.9% ±13.3% ; 2 weeks： 70.5% ± 21.9% ; 4 weeks： 69.2% ± 23.9% ）. Meanwhile, the mibefradil-sensitive current component was increased to 157.5% ±21.2% and 158.6% ±35.5% at 1 week and 2 weeks after the operation respectively, and then declined to control level at 4 weeks （ 109.2% ±37.9% ）. Conclusions L- and T-type calcium channels were functionally expressed on rat retinal Muller cells. Elevated intraoeular pressure in the COH rats increased the T-type Ca2＋ channel currents, which may contribute to Muller cell depolarization and gliosis.