Non-Hebbian type of plasticity in the developing visual cortex.

出生后早期的单眼视觉剥夺（MD）导致皮质对被剥夺的眼睛的反应显著丧失，并导致为被剥夺的眼睛服务的神经皮质轴突缩回（眼优势可塑性）。另一方面，当MD与使用GABAA激动剂muscimol对视觉皮层进行药理学抑制时，皮质神经元会失去对睁开眼睛的反应。此外，服务于睁开眼睛的活跃的树杈有选择性地缩回，而来自被剥夺眼睛的树杈的分支大部分保持完整，这表明突触前输入和皮层神经元之间的不相关活动导致传入轴突的修剪。目的：阐明受抑制皮层眼优势可塑性的机制。我们测试了它是否具有类似于正常皮质可塑性的特征，比如年龄依赖性。成人视觉皮层的肌醇治疗并没有引起睁眼反应的丧失，这表明受抑制的皮层中更多的ce可塑性只在发育中的动物中运作，就像在正常的皮层中一样。进一步的研究表明，与正常皮质相比，眼优势可塑性的时间过程较慢。3 d MD未诱导抑制皮层的眼优势可塑性，而在正常皮层有饱和作用。双眼剥夺（BD）对皮层反应的影响比MD弱得多，并且不会引起传入轴突的收缩。因此，我们研究了在没有双眼失衡的情况下，是否可以诱导受抑制的皮质中基因皮质轴突的收缩。我们分析了药物抑制正常视力动物和双目失明动物的视觉皮层中基因皮质轴突的形态。在正常视力的动物中，被抑制皮层的轴突突表现出强劲的回缩。另一方面，双目失明的动物的树干基本完好无损。这些结果表明，在眼优势可塑性中发挥重要作用的可能是同突触联想机制，而不是输入间的异突触竞争机制。少

Monocular visual deprivation (MD) in the early postnatal life causes a significant loss of cortical responses to a deprived eye and a retraction of geniculocortical axons serving the deprived eye (ocular dominance plasticity). On the other hand, when MD is combined with a pharmacological inhibition of the visual cortex by administering a GABAA agonist, muscimol, cortical neurons lose their responses to an open eye. Furthermore, active arbors serving an open eye selectively retract, whereas the branches of arbors from a deprived eye remain mostly intact, suggesting that uncorrelated activity between presynaptic inputs and cortical neurons leads to the pruning of afferent axons. To clarify the mechanism of ocular dominance plasticity in the inhibited cortex. we tested whether it has characteristics, such as age-dependency, similar to the plasticity in the normal cortex.Muscimol-treatment of adult visual cortex did not induce a loss of open eye response, suggesting that the ocular dominan … More ce plasticity in the inhibited cortex operates only in developing animals as in the normal cortex. Further study showed that the ocular dominance plasticity proceeds in slower time course than in the normal cortex. Three days MD did not induce the ocular dominance plasticity in the inhibited cortex, while it exerted a saturated effect in the normal cortex.Binocular deprivation (BD) exerts a much weaker effect on cortical responses than MD and does not induce the retraction of afferent axons. Thus, we examined whether the retraction of geniculocortical axons in an inhibited cortex could be induced in the absence of binocular imbalance. We analyzed the morphology of geniculocortical axons in a pharmacologically inhibited visual cortex of animals with normal vision and binocularly deprived animals. In the normal vision animals, the axonal arbors in the inhibited cortex showed robust retraction. On the other hand, the arbors in binocularly deprived animals remained mostly intact. These results suggest that a homosynaptic associative mechanism, rather than a heterosynaptic competition between inputs, may play an important role in the ocular dominance plasticity. Less