Surround inhibition of mammalian AII amacrine cells is generated in the proximal retina
Surround inhibition of mammalian AII amacrine cells is generated in the proximal retina
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DOI：
10.1111/j.1469-7793.2000.t01-1-00771.x
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发表时间：
2000-03-15
影响因子：
5.5
通讯作者：
Xin, DY
中科院分区：
文献类型：
--
作者：
Bloomfield, SA;Xin, DY
1. 在黑暗适应条件下，从兔视网膜-眼杯制备的神经元中获得细胞内记录。神经递质激动剂和拮抗剂外源性应用于通过超液解剖突触通路药理学，从而确定那些负责产生AII腺分泌细胞的中心/周围感受野的通路。应用代谢性谷氨酸受体激动剂，APE，可逆地阻断了AII细胞的中心和外环反应。这些数据与中心和周围介导的反应都来自突触前杆状双极细胞的输入的观点是一致的。然而，杆状双极细胞显示出类似于100 μ m宽的接受野，我们发现没有证据表明使用光刺激可以有效地引起AII无突细胞的离周围反应。这些结果表明，AII细胞的周围不是来自杆双极细胞输入。应用嗜离子性谷氨酸受体拮抗剂CNQX或DNQX增强了AII细胞的中心内应答，但减弱了周围外应答。这些数据表明，中心介导和周围介导的反应不可能都来自穿过杆状双极到aii细胞突触的信号。应用甘氨酸拮抗剂士的宁对AII细胞反应只有轻微和可变的影响。然而，GABA拮抗剂微旋毒素和双核碱增强了AII细胞的中心外反应，但减弱或完全阻断了AII细胞的周围外反应。GABA拮抗剂对水平细胞的反应没有影响，表明其对AII细胞反应的影响反映了视网膜内回路的作用，而不是外网状层的反馈回路。电压门控钠通道阻滞剂TTX的应用增强了AII细胞的中心内反应，但减弱或消除了它们的环外反应。综上所述，我们的结果表明，AII细胞的中心反应是由棒双极细胞的主要兴奋驱动引起的。然而，AII细胞的周围感受野似乎是由来自邻近gaba能的中心无突细胞的侧向抑制信号产生的。提出了一个模型，其中S1无突细胞产生AII无突细胞的周围感受野通过抑制，反馈电路到杆状双极细胞的轴突终端。
1. Intracellular recordings were obtained from neurons in the superfused retina-eyecup preparation of the rabbit under dark-adapted conditions. Neurotransmitter agonists and antagonists were applied exogenously via the superfusate to dissect the synaptic pathways pharmacologically and thereby determine those pathways responsible for the generation of the on-centre/off-surround receptive fields of AII amacrine cells.2. Application of the metabotropic glutamate receptor agonist, APE, reversibly blocked both the on-centre and off-surround responses of AII cells. These data were consistent with the idea that both the centre- and surround-mediated responses are derived from inputs from the presynaptic rod bipolar cells.3. Whereas rod bipolar cells showed on-receptive fields similar to 100 mu m across, we found no evidence for an antagonistic off-surround response using light stimuli which effectively elicited the off-surrounds of AII amacrine cells. These results indicated that the surrounds of AII cells are not derived from rod bipolar cell inputs.4. Application of the ionotropic glutamate receptor antagonists CNQX or DNQX enhanced the on-centre responses of AII cells but attenuated the off-surround responses. These data indicated that the centre- and surround-mediated responses could not both be derived from signals crossing the rod bipolar-to-AII cell synapse.5. Application of the glycine antagonist, strychnine, had only minor and variable effects on AII cell responses. However, the GABA antagonists picrotoxin and bicuculline enhanced the on-centre response but attenuated or completely blocked the off-surround response of AII cells. The GABA antagonists had no effect on the responses of horizontal cells indicating that their effects on AII cell responses reflected actions on inner retinal circuitry rather than feedback circuitry in the outer plexiform layer.6. Application of the voltage-gated sodium channel blocker TTX enhanced the on-centre responses of AII cells but attenuated or abolished their off-surround responses.7. Taken together, our results suggest that the on-centre responses of AII cells result from the major excitatory drive from rod bipolar cells. However, the surround receptive fields of AII cells appear to be generated by lateral, inhibitory signals derived from neighbouring GABAergic, on-centre amacrine cells. A model is presented whereby the S1 amacrine cells produce the surround receptive fields of AII amacrine cells via inhibitory, feedback circuitry to the axon terminals of rod bipolar cells.