Yun S H, Cheong M Y, Mook-Jung I, Huh K, Lee C, Jung M W
Neuroscience Laboratory, Institute for Medical Sciences, Ajou University School of Medicine, 442-721, Suwon, South Korea.
Neuroscience. 2000;97(4):671-6. doi: 10.1016/s0306-4522(00)00108-1.
Effects of cholinergic agents on synaptic transmission and plasticity were examined in entorhinal cortex and hippocampus. Bath application of carbachol (0.25-0.75 microM) induced transient depression of field potential responses in all cases tested (24/24 in layer III of medial entorhinal cortex slices and 24/24 in CA1 of hippocampal slices; 11.0+/-1.9% and 7.8+/-2.5%, respectively) and long-lasting potentiation in some cases (4/24 in entorhinal cortex and 12/24 in hippocampus; 33.7+/-3.7% and 32.1+/-9.9%, respectively, in successful cases). Carbachol (0.5 microM) induced transient depression, but not long-lasting potentiation, of N-methyl-D-aspartate receptor-mediated responses in entorhinal cortex. At 5 microM, carbachol induced transient depression only (55. 9+/-4.7% in entorhinal cortex and 41.4+/-2.9% in hippocampus), which was blocked by atropine. Paired-pulse facilitation was not altered during carbachol-induced potentiation but enhanced during carbachol-induced depression. These results suggest that the underlying mechanisms of carbachol-induced depression and potentiation are decreased transmitter release and selective enhancement of non-N-methyl-D-aspartate receptor-mediated responses, respectively. Long-term potentiation could be induced in the presence of 10 microM atropine by theta burst stimulation. The magnitude was significantly lower (15.2+/-5.2%, n=9) compared with control (37.2+/-6.1%, n=8) in entorhinal cortex, however. These results demonstrate similar, but not identical, cholinergic modulation of synaptic transmission and plasticity in entorhinal cortex and hippocampus.
研究了胆碱能药物对内嗅皮层和海马体突触传递及可塑性的影响。在所有测试案例中，浴用卡巴胆碱（0.25 - 0.75微摩尔）均诱发了场电位反应的短暂抑制（在内侧内嗅皮层切片的III层中为24/24，在海马体切片的CA1区中为24/24；分别为11.0±1.9%和7.8±2.5%），在某些案例中还诱发了长时程增强（在内嗅皮层中为4/24，在海马体中为12/24；成功案例中分别为33.7±3.7%和32.1±9.9%）。卡巴胆碱（0.5微摩尔）在内嗅皮层中诱发了N - 甲基 - D - 天冬氨酸受体介导反应的短暂抑制，但未诱发长时程增强。在5微摩尔时，卡巴胆碱仅诱发了短暂抑制（在内嗅皮层中为55.9±4.7%，在海马体中为41.4±2.9%），该抑制可被阿托品阻断。在卡巴胆碱诱发长时程增强期间，双脉冲易化未改变，但在卡巴胆碱诱发抑制期间增强。这些结果表明，卡巴胆碱诱发抑制和长时程增强的潜在机制分别是递质释放减少和非N - 甲基 - D - 天冬氨酸受体介导反应的选择性增强。在存在10微摩尔阿托品的情况下，通过theta爆发刺激可诱导长时程增强。然而，在内嗅皮层中，其幅度与对照组（37.2±6.1%，n = 8）相比显著更低（15.2±5.2%，n = 9）。这些结果表明，内嗅皮层和海马体中突触传递及可塑性的胆碱能调节相似但不完全相同。
