McLean J, Palmer L A
Department of Neuroscience, University of Pennsylvania, Philadelphia 19104, USA.
Vis Neurosci. 1996 Nov-Dec;13(6):1069-87. doi: 10.1017/s0952523800007720.
We have employed two paradigms to investigate the mechanisms of contrast gain control in cat striate cortex. In the first paradigm, optimal drifting gratings were presented in three consecutive periods. The contrast was near threshold in the first and third periods and accompanied by iontophoretic pulses of glutamate or glutamate receptor (GluR) agonists. The contrast was set to evoke a higher firing rate in the second period. Although both visual and iontophoretic conditions were identical in the first and third periods, responses to glutamate, N-methyl-D-aspartic acid (NMDA), and (IS,3R)-1-Aminocyclopentane-1,3-dicarboxylic acid (ACPD) were reduced following the adapting interval. (S)-alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) responses were not reduced. Administration of ionotropic GluR antagonists did not affect adaptation to the high-contrast grating. The metabotropic GluR antagonist (+/-)-alpha-Methyl-4-carboxyphenylglycine (MCPG), which acts at presynaptic glutamate autoreceptors, decreased the degree of adaptation exhibited by striate cells. In a second paradigm, contrast response functions (CRFs) were obtained at various adapting contrasts and least-squares fits to a hyperbolic ratio equation generated for each adapting level. Similar to previous reports, DL-2-amino-5-phosphonovaleric acid (APV) reduced the slope of the CRF and increased the responsiveness of the cells but did not affect the semisaturation constant, sigma, or the exponent of the CRF, n. Only MCPG significantly altered the distribution of sigma and n for 19 cells. The effect on sigma suggests that this drug can interfere with the cell's ability to shift its operating point to match the adapting contrast. These results suggest the involvement of a presynaptic mechanism for contrast adaptation. The decrease in neuronal responsiveness immediately following the high-contrast period may reflect an additional, postsynaptic effect in which there is a decrease in the NMDA-mediated component of the visual response.
我们采用了两种范式来研究猫纹状皮层中对比度增益控制的机制。在第一种范式中，最佳漂移光栅在三个连续的时间段内呈现。在第一个和第三个时间段，对比度接近阈值，并伴有谷氨酸或谷氨酸受体（GluR）激动剂的离子电渗脉冲。在第二个时间段，对比度被设置为诱发更高的放电率。尽管在第一个和第三个时间段视觉和离子电渗条件相同，但在适应间隔后，对谷氨酸、N-甲基-D-天冬氨酸（NMDA）和（IS,3R）-1-氨基环戊烷-1,3-二羧酸（ACPD）的反应降低。（S）-α-氨基-3-羟基-5-甲基-4-异恶唑丙酸（AMPA）反应未降低。离子型GluR拮抗剂的给药不影响对高对比度光栅的适应。代谢型GluR拮抗剂（±）-α-甲基-4-羧基苯基甘氨酸（MCPG）作用于突触前谷氨酸自身受体，降低了纹状细胞表现出的适应程度。在第二种范式中，在各种适应对比度下获得对比度响应函数（CRF），并对每个适应水平生成的双曲线比率方程进行最小二乘拟合。与先前的报告相似，DL-2-氨基-5-磷酸缬氨酸（APV）降低了CRF的斜率并增加了细胞的反应性，但不影响半饱和常数σ或CRF的指数n。只有MCPG显著改变了19个细胞的σ和n的分布。对σ的影响表明，这种药物可以干扰细胞将其工作点转移以匹配适应对比度的能力。这些结果表明存在一种用于对比度适应的突触前机制。高对比度时间段后神经元反应性的立即降低可能反映了一种额外的突触后效应，即视觉反应中NMDA介导的成分减少。
