双眼形觉剥夺成年大鼠视皮层可塑性与CSPGs和tPA表达关系的研究
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摘要
人类和哺乳动物出生后,视觉系统能根据周围的视觉环境调整和改变与生俱有的神经联系和突触结构,这一改变发生的最敏感时期,称为视皮层可塑性关键期。以往的研究认为,只有在关键期内弱视才能得到有效治疗,一旦错过则成年期残留的弱视不能得到恢复。但目前的研究与临床观察使这一观点越来越受到质疑,许多基础和临床研究发现,成年动物的视皮层可塑性是被抑制而非完全消失,在一些特定的情况下可被“再激活”。
在临床观察中发现,当单眼弱视的成年人,其健眼因疾病或外伤失明后,弱视眼的最佳矫正视力会逐渐提高,甚至可以接近正常,说明人类的成年弱视有治愈的可能。而通过动物研究,更是使用多种方法使成年大鼠视皮层恢复了可塑性。2002年,Pizzorusso等使用chABC酶降解成年期大鼠视皮层内硫酸软骨素蛋白多糖(chondroitin sulphate proteoglycans,CSPGs),首次成功恢复了成年期大鼠视皮层可塑性,并联合健眼反剥夺使成年大鼠弱视眼的视力恢复正常,首次证实了成年期大鼠视皮层可塑性可被“再激活”。随后,其他学者通过成年大鼠10天黑暗饲养、丰富环境法、服用5-羟色胺摄取抑制剂和降低皮层内抑制功能等方法,均成功恢复成年期大鼠视皮层可塑性,这些事实均说明成年期大鼠视皮层可塑性并未完全消失,而是被抑制,通过某些特定的方法,成年期视皮层可塑性可被“再激活”。本实验室以往的研究发现,双眼形觉剥夺可以抑制大鼠γ-氨基丁酸(γ-amino butyric acid, GABA)能抑制性突触传递功能发育,减弱成年大鼠视皮层内神经元抑制性突触传递的强度,调节视皮层抑制性和兴奋性神经递质受体的重新表达和分布。然而,双眼形觉剥夺所致的对GABA抑制环路功能的减弱是通过什么途径进行的,尚未进行进一步研究。以往的研究发现,以CSPGs聚集为主要构成的神经元周围网络(perineuronal net, PNNs)的成熟可以促进GABA抑制性环路功能的成熟,降解PNNs恢复成年大鼠视皮层可塑性后,视皮层内GABA能神经元对其靶细胞的抑制性功能降低,说明PNNs的减少是导致GABA环路抑制功能下降的原因之一。那么双眼形觉剥夺模型所致的GABA抑制性环路的功能降低是否是由于PNNs的减少所导致的呢?
组织型纤溶酶原激活剂(tissue-type plasminogen activator, tPA)是一种丝氨酸蛋白水解酶,是CSPGs天然的降解因子。以往的研究发现,在小鼠视皮层可塑性关键期内,单眼剥夺后,剥夺眼对侧视皮层内tPA的活性增高,说明异常的视觉环境可以影响tPA的活性。那么双眼形觉剥夺模型能不能对视皮层内tPA的活性产生影响呢?结合上述内容我们提出假设:成年大鼠双眼形觉剥夺后,视皮层内tPA活性增高,使CSPGs降解增多,减少PNNs的表达,“再激活”成年大鼠视皮层可塑性。
为此,本实验采用以下方法验证此假设:
1、采用图形视觉诱发电位的方法,记录视觉发育可塑性关键期结束前后,视皮层可塑性的变化以及视皮层可塑性结束的时间,然后予以行双眼形觉剥夺,记录不同剥夺时间对视皮层可塑性的影响,确定能稳定激活成年大鼠视皮层可塑性的时间。结果发现:(1)正常出生后5周以内的大鼠,短期3天单眼剥夺即可造成视皮层眼优势的移动,说明大鼠视皮层存在可塑性。(2)正常出生后6周大鼠,短期3天单眼剥夺,不能使眼优势发生移动,说明大鼠视皮层可塑性被抑制。(3)予以7周大鼠双眼形觉剥夺14天,短期3天单眼剥夺可以使视皮层眼优势发生移动,说明双眼形觉剥夺14天可以稳定的再激活成年期大鼠视皮层可塑性。(4)在后面两部分实验,将采用出生后7周大鼠行双眼形觉剥夺14天作为双眼形觉剥夺视皮层可塑性再激活组模型。
2、采用免疫荧光组织化学、免疫蛋白印迹和酶联免疫吸附法,检测在视皮层可塑性关键期前后,及行双眼形觉剥夺14天组大鼠视皮层内tPA的表达及活性变化。结果发现:(1)大鼠出生后1周,视皮层内仅有少量表达及活性,睁眼后其表达及活性明显升高,说明tPA的表达具有视觉经验依赖性。(2)在视皮层可塑性关键期高峰期以内,视皮层内tPA的表达及活性均较高,但到了关键期末和成年期,其表达及活性明显降低,说明其参与了视皮层可塑性,且与视皮层可塑性的终止有关。(3)双眼形觉剥夺组大鼠视皮层内的tPA表达和活性与同周龄及关键期结束前相比均升高,说明双眼形觉剥夺对视皮层内tPA的表达和活性均有影响。
3、采用免疫荧光组织化学双重标记技术,双重标记视皮层可塑性关键期前后及行双眼形觉剥夺14天组大鼠视皮层内tPA和CSPGs的表达变化。结果发现:(1)大鼠出生后1周,视皮层内未见CSPGs表达,睁眼后开始出现,随年龄增长逐渐增加,说明视皮层内CSPGs的表达受到视觉经验和年龄因素影响,与视皮层可塑性的终止有关。(2)双眼形觉剥夺组大鼠视皮层内CSPGs与同周龄大鼠及关键期结束前大鼠相比,其表达明显降低,说明双眼形觉剥夺对视皮层可塑性的影响与CSPGs有关。(3)大鼠视皮层内tPA和CSPGs双标阳性细胞随年龄增加逐渐增多,说明随着年龄增加,tPA对CSPGs水解降低,使CSPGs表达增多,参与了视皮层可塑性关键期的终止。(4)双眼形觉剥夺组大鼠与成年大鼠及关键期结束前大鼠相比,视皮层内tPA和CSPGs双标阳性细胞明显降低,说明双眼形觉剥夺可增加视皮层内tPA的表达和活性,对CSPGs降解增多,减少皮层内PNNs的形成,是“再激活”成年大鼠视皮层可塑性的途径之一。
本研究得到以下结论:
1、BFD可成功再激活成年大鼠视皮层可塑性,形觉剥夺和光觉剥夺一样可以终身增强其眼优势可塑性;
2、BFD14天可以使成年大鼠视皮层内tPA的表达和活性增加,加强对CSPGs的降解,减少PNNs的形成,可能是成年大鼠视皮层可塑性被“再激活”的机制之一。
After human and the mammalian’s born, visual system regulated the connection of neurons and structures of synaptics according to the visual environment, which is called the critical period of visual cortex plasticity. Researches in the past showed that amblyopia can be treated only in this critical period. Present researches showed that visual plasticity in the adult is just inhibited but not disappeared and it can be“reactivated”in some specific conditions.
In 2002, Pizzorusso degraded the CSPGs in adult rats’visual cortex by using chABC enzymes, which first successfully recovered adult rats’visual cortex plasticity, and raised the amblyopic eye’s visual acuity by deprivating inputs of the fellow eye. This study first confirmed that the plasticity of adult visual cortex can be“reactivated”. Thereafter, some studies which used 10 days’dark rearing、environment enrichment、the antidepressant drugs and reducing intracortical inhibition in adult rats can also recover adult visual cortex plasticity. Our researches in the past found that binocular form deprivation can inhibite the development of GABA circuit, reduce the strength of neuron synapses’transmission, and regulate the expression and distribution of inhibiting and exciting neurotransmitter receptors in adult visual cortex. Researches have showed that maturing of PNNs constituted by CSPGs can promote the maturing of GABA inhibition circuit, but degradation of PNNs can reduce the inhibition of GABA circuit. Therefore, reducing of PNNs is one of the ways to turn down inhibition of GABA circuit and whether it can also be caused by binocular form deprivation(BFD) is not known. TPA is one of the natural factors in CSPGs’degradation, and plays an important role in mediating the ocular dominance shift in response to monocular deprivation. Researches have showed that, the activity of tPA increased in contralateral visual cortex caused by monocular deprivation in critical period. Whether it can also happen in BFD is not known. Overall, we made this hypothesis: tPA activity increases in visual cortex in response to binocular form deprivation in adult rats, which degrades CSPGs, reduses expression of PNNs, and then“reactivates”adult visual cortex plasticity.
Therefore we applied the following methods to investigate this hypothesis:
1、Pattern visual evoked potentials(PVEPs) was applied to detect the OD shift in order to find out the end time of visual cortex plasticity and the proper time to reactive adult visual cortex plasticity by binocular form deprivation in adult rats. Results:(1) Brief 3 days monocular deprivation caused the OD shift in PW3、PW4 and PW5 rats, which showed the visual cortex plasticity existed. (2) The OD shift could not be observed in rats after PW6 after brief 3 days monocular deprevation, which showed the visual cortex plasticity was inhibited. (3) A significant OD shift was observed in PW7 rats after 14 days’BFD in response to brief 3 days monocular deprivation, which demonstrated a steady reactivation of visual cortex plasticity in adult rats. (4) 14 days’BFD was taken as the model in the following experiments.
2、With the use of immunofluorescence histochemistry, immunoblot and ELISA kit, we detected tPA expression and activity in visual cortex during the critical period and 14 days’BFD in adult rats. Results:(1) There were only a few cells expressing tPA in visual cortex in PW1, and increased significantly after eyes’open. The expression of tPA depended on the visual experience. (2) High expression and activity was detected in the peak of critical period, but lower one in adult visual cortex. TPA played a role in the end of visual cortex plasticity. (3) The expression and activity of tPA was increased in BFD, which showed BFD affected the expression and activity of tPA.
3、With the use of immunofluorescence histochemistry to double lable tPA and CSPGs in visual cortex during the critical period and 14 days’BFD in adult rats. Results:(1) No CSPGs was detected in PW1, and some were detected after eyes’open and then, increased with the age. The expression of CSPGs depended on the visual experience and the age, which are relevant to the end of visual cortex plasticity. (2) Expression of CSPGs decreased in response to BFD. (3) Double labled cells of tPA and CSPGs increased gradually according to the age, which played a role in the end of critical period. (4) A significant decreasing of double labled cells of tPA and CSPGs in visual cortex of 14 days’BFD adult rats, which showed the degradation of CSPGs in response to the increasing of expression and activity in tPA after BFD, is one of the ways to“reactive”the adult visual cortex plasticity.
Based on the results, we concluded:
1、Adult visual cortex plasticity can be“reactivated”by binocular form deprivation, and form deprivation can enhance the visual cortex plasticity as the same as light deprivation.
2、The expression and activity of tPA increases and CSPGs degrades in the adult visual cortex by 14 days’BFD, which may be one of the ways to“reactivate”the adult visual cortex plasticity.
在临床观察中发现,当单眼弱视的成年人,其健眼因疾病或外伤失明后,弱视眼的最佳矫正视力会逐渐提高,甚至可以接近正常,说明人类的成年弱视有治愈的可能。而通过动物研究,更是使用多种方法使成年大鼠视皮层恢复了可塑性。2002年,Pizzorusso等使用chABC酶降解成年期大鼠视皮层内硫酸软骨素蛋白多糖(chondroitin sulphate proteoglycans,CSPGs),首次成功恢复了成年期大鼠视皮层可塑性,并联合健眼反剥夺使成年大鼠弱视眼的视力恢复正常,首次证实了成年期大鼠视皮层可塑性可被“再激活”。随后,其他学者通过成年大鼠10天黑暗饲养、丰富环境法、服用5-羟色胺摄取抑制剂和降低皮层内抑制功能等方法,均成功恢复成年期大鼠视皮层可塑性,这些事实均说明成年期大鼠视皮层可塑性并未完全消失,而是被抑制,通过某些特定的方法,成年期视皮层可塑性可被“再激活”。本实验室以往的研究发现,双眼形觉剥夺可以抑制大鼠γ-氨基丁酸(γ-amino butyric acid, GABA)能抑制性突触传递功能发育,减弱成年大鼠视皮层内神经元抑制性突触传递的强度,调节视皮层抑制性和兴奋性神经递质受体的重新表达和分布。然而,双眼形觉剥夺所致的对GABA抑制环路功能的减弱是通过什么途径进行的,尚未进行进一步研究。以往的研究发现,以CSPGs聚集为主要构成的神经元周围网络(perineuronal net, PNNs)的成熟可以促进GABA抑制性环路功能的成熟,降解PNNs恢复成年大鼠视皮层可塑性后,视皮层内GABA能神经元对其靶细胞的抑制性功能降低,说明PNNs的减少是导致GABA环路抑制功能下降的原因之一。那么双眼形觉剥夺模型所致的GABA抑制性环路的功能降低是否是由于PNNs的减少所导致的呢?
组织型纤溶酶原激活剂(tissue-type plasminogen activator, tPA)是一种丝氨酸蛋白水解酶,是CSPGs天然的降解因子。以往的研究发现,在小鼠视皮层可塑性关键期内,单眼剥夺后,剥夺眼对侧视皮层内tPA的活性增高,说明异常的视觉环境可以影响tPA的活性。那么双眼形觉剥夺模型能不能对视皮层内tPA的活性产生影响呢?结合上述内容我们提出假设:成年大鼠双眼形觉剥夺后,视皮层内tPA活性增高,使CSPGs降解增多,减少PNNs的表达,“再激活”成年大鼠视皮层可塑性。
为此,本实验采用以下方法验证此假设:
1、采用图形视觉诱发电位的方法,记录视觉发育可塑性关键期结束前后,视皮层可塑性的变化以及视皮层可塑性结束的时间,然后予以行双眼形觉剥夺,记录不同剥夺时间对视皮层可塑性的影响,确定能稳定激活成年大鼠视皮层可塑性的时间。结果发现:(1)正常出生后5周以内的大鼠,短期3天单眼剥夺即可造成视皮层眼优势的移动,说明大鼠视皮层存在可塑性。(2)正常出生后6周大鼠,短期3天单眼剥夺,不能使眼优势发生移动,说明大鼠视皮层可塑性被抑制。(3)予以7周大鼠双眼形觉剥夺14天,短期3天单眼剥夺可以使视皮层眼优势发生移动,说明双眼形觉剥夺14天可以稳定的再激活成年期大鼠视皮层可塑性。(4)在后面两部分实验,将采用出生后7周大鼠行双眼形觉剥夺14天作为双眼形觉剥夺视皮层可塑性再激活组模型。
2、采用免疫荧光组织化学、免疫蛋白印迹和酶联免疫吸附法,检测在视皮层可塑性关键期前后,及行双眼形觉剥夺14天组大鼠视皮层内tPA的表达及活性变化。结果发现:(1)大鼠出生后1周,视皮层内仅有少量表达及活性,睁眼后其表达及活性明显升高,说明tPA的表达具有视觉经验依赖性。(2)在视皮层可塑性关键期高峰期以内,视皮层内tPA的表达及活性均较高,但到了关键期末和成年期,其表达及活性明显降低,说明其参与了视皮层可塑性,且与视皮层可塑性的终止有关。(3)双眼形觉剥夺组大鼠视皮层内的tPA表达和活性与同周龄及关键期结束前相比均升高,说明双眼形觉剥夺对视皮层内tPA的表达和活性均有影响。
3、采用免疫荧光组织化学双重标记技术,双重标记视皮层可塑性关键期前后及行双眼形觉剥夺14天组大鼠视皮层内tPA和CSPGs的表达变化。结果发现:(1)大鼠出生后1周,视皮层内未见CSPGs表达,睁眼后开始出现,随年龄增长逐渐增加,说明视皮层内CSPGs的表达受到视觉经验和年龄因素影响,与视皮层可塑性的终止有关。(2)双眼形觉剥夺组大鼠视皮层内CSPGs与同周龄大鼠及关键期结束前大鼠相比,其表达明显降低,说明双眼形觉剥夺对视皮层可塑性的影响与CSPGs有关。(3)大鼠视皮层内tPA和CSPGs双标阳性细胞随年龄增加逐渐增多,说明随着年龄增加,tPA对CSPGs水解降低,使CSPGs表达增多,参与了视皮层可塑性关键期的终止。(4)双眼形觉剥夺组大鼠与成年大鼠及关键期结束前大鼠相比,视皮层内tPA和CSPGs双标阳性细胞明显降低,说明双眼形觉剥夺可增加视皮层内tPA的表达和活性,对CSPGs降解增多,减少皮层内PNNs的形成,是“再激活”成年大鼠视皮层可塑性的途径之一。
本研究得到以下结论:
1、BFD可成功再激活成年大鼠视皮层可塑性,形觉剥夺和光觉剥夺一样可以终身增强其眼优势可塑性;
2、BFD14天可以使成年大鼠视皮层内tPA的表达和活性增加,加强对CSPGs的降解,减少PNNs的形成,可能是成年大鼠视皮层可塑性被“再激活”的机制之一。
After human and the mammalian’s born, visual system regulated the connection of neurons and structures of synaptics according to the visual environment, which is called the critical period of visual cortex plasticity. Researches in the past showed that amblyopia can be treated only in this critical period. Present researches showed that visual plasticity in the adult is just inhibited but not disappeared and it can be“reactivated”in some specific conditions.
In 2002, Pizzorusso degraded the CSPGs in adult rats’visual cortex by using chABC enzymes, which first successfully recovered adult rats’visual cortex plasticity, and raised the amblyopic eye’s visual acuity by deprivating inputs of the fellow eye. This study first confirmed that the plasticity of adult visual cortex can be“reactivated”. Thereafter, some studies which used 10 days’dark rearing、environment enrichment、the antidepressant drugs and reducing intracortical inhibition in adult rats can also recover adult visual cortex plasticity. Our researches in the past found that binocular form deprivation can inhibite the development of GABA circuit, reduce the strength of neuron synapses’transmission, and regulate the expression and distribution of inhibiting and exciting neurotransmitter receptors in adult visual cortex. Researches have showed that maturing of PNNs constituted by CSPGs can promote the maturing of GABA inhibition circuit, but degradation of PNNs can reduce the inhibition of GABA circuit. Therefore, reducing of PNNs is one of the ways to turn down inhibition of GABA circuit and whether it can also be caused by binocular form deprivation(BFD) is not known. TPA is one of the natural factors in CSPGs’degradation, and plays an important role in mediating the ocular dominance shift in response to monocular deprivation. Researches have showed that, the activity of tPA increased in contralateral visual cortex caused by monocular deprivation in critical period. Whether it can also happen in BFD is not known. Overall, we made this hypothesis: tPA activity increases in visual cortex in response to binocular form deprivation in adult rats, which degrades CSPGs, reduses expression of PNNs, and then“reactivates”adult visual cortex plasticity.
Therefore we applied the following methods to investigate this hypothesis:
1、Pattern visual evoked potentials(PVEPs) was applied to detect the OD shift in order to find out the end time of visual cortex plasticity and the proper time to reactive adult visual cortex plasticity by binocular form deprivation in adult rats. Results:(1) Brief 3 days monocular deprivation caused the OD shift in PW3、PW4 and PW5 rats, which showed the visual cortex plasticity existed. (2) The OD shift could not be observed in rats after PW6 after brief 3 days monocular deprevation, which showed the visual cortex plasticity was inhibited. (3) A significant OD shift was observed in PW7 rats after 14 days’BFD in response to brief 3 days monocular deprivation, which demonstrated a steady reactivation of visual cortex plasticity in adult rats. (4) 14 days’BFD was taken as the model in the following experiments.
2、With the use of immunofluorescence histochemistry, immunoblot and ELISA kit, we detected tPA expression and activity in visual cortex during the critical period and 14 days’BFD in adult rats. Results:(1) There were only a few cells expressing tPA in visual cortex in PW1, and increased significantly after eyes’open. The expression of tPA depended on the visual experience. (2) High expression and activity was detected in the peak of critical period, but lower one in adult visual cortex. TPA played a role in the end of visual cortex plasticity. (3) The expression and activity of tPA was increased in BFD, which showed BFD affected the expression and activity of tPA.
3、With the use of immunofluorescence histochemistry to double lable tPA and CSPGs in visual cortex during the critical period and 14 days’BFD in adult rats. Results:(1) No CSPGs was detected in PW1, and some were detected after eyes’open and then, increased with the age. The expression of CSPGs depended on the visual experience and the age, which are relevant to the end of visual cortex plasticity. (2) Expression of CSPGs decreased in response to BFD. (3) Double labled cells of tPA and CSPGs increased gradually according to the age, which played a role in the end of critical period. (4) A significant decreasing of double labled cells of tPA and CSPGs in visual cortex of 14 days’BFD adult rats, which showed the degradation of CSPGs in response to the increasing of expression and activity in tPA after BFD, is one of the ways to“reactive”the adult visual cortex plasticity.
Based on the results, we concluded:
1、Adult visual cortex plasticity can be“reactivated”by binocular form deprivation, and form deprivation can enhance the visual cortex plasticity as the same as light deprivation.
2、The expression and activity of tPA increases and CSPGs degrades in the adult visual cortex by 14 days’BFD, which may be one of the ways to“reactivate”the adult visual cortex plasticity.
引文
1. Berardi N, Pizzorusso T, Maffei L. Critical periods during sensory development[J]. Curr Opin Neurobiol. 2000, 10(1): 138-145.
2. Fox K, Caterson B. Neuroscience. Freeing the bain from the perineuronal net[J]. Science. 2002, 298(5596): 1187-1189.
3. Heynen AJ, Yoon BJ, Liu CH et al. Molecular mechanism for loss of visual cortical responsiveness following brief monocular deprivation[J]. Nat Neurosci. 2003, 6(8): 854-862.
4. Muir DW, Mitchell DE. Visual resolution and experience: acuity deficits in cats following early selective visual deprivation[J]. Science. 1973, 180(84): 420-422.
5. Frenkel MY, Bear MF. How monocular deprivation shifts ocular dominance in visual cortex of young mice[J]. Neuron. 2004, 44(6): 917-923.
6. Sawtell NB, Frenkel MY, Philpot BD et al. NMDA receptor-dependent ocular dominance plasticity in adult visual cortex[J]. Neuron. 2003, 38(6): 977-985.
7. Pizzorusso T, Medini P, Berardi N et al. Reactivation of ocular dominance plasticity in the adult visual cortex[J]. Science. 2002, 298(5596): 1248-1251.
8. Maya Vetencourt JF, Sale A, Viegi A et al. The antidepressant fluoxetine restores plasticity in the adult visual cortex[J]. Science. 2008, 320(5874): 385-388.
9. Harauzov A, Spolidoro M, DiCristo G et al. Reducing intracortical inhibition in the adult visual cortex promotes ocular dominance plasticity[J]. J Neurosci. 2010, 30(1): 361-371.
10. He HY, Hodos W, Quinlan EM. Visual deprivation reactivates rapid ocular dominance plasticity in adult visual cortex[J]. J Neurosci. 2006, 26(11):2951-2955.
11. Mainardi M, Landi S, Gianfranceschi L et al. Environmental enrichment potentiates thalamocortical transmission and plasticity in the adult rat visual cortex[J]. J Neurosci Res. 2010, 88(14): 3048-3059.
12. Fagiolini M, Hensch TK. Inhibitory threshold for critical-period activation in primary visual cortex[J]. Nature. 2000, 404(6774): 183-186.
13. Yin ZQ, Crewther SG, Yang M et al. Distribution and localization of NMDA receptor subunit 1 in the visual cortex of strabismic and anisometropic amblyopic cats[J]. Neuroreport. 1996, 7(18): 2997-3003.
14.阴正勤,余涛,陈莉.斜视性弱视猫发育过程中视皮层神经元NMDA-R1表达的免疫组织化学电镜观察[J].中华眼科杂志. 2002, 38(8): 472-475.
15.秦伟,阴正勤,王仕军等.正常和双眼形觉剥夺大鼠发育过程中视皮层神经元NR-1的表达。[J].第三军医大学学报. 2003, 25(21): 1924-1926.
16. Huber KM, Sawtell NB, Bear MF. Brain-derived neurotrophic factor alters the synaptic modification threshold in visual cortex[J]. Neuropharmacology. 1998, 37(4-5): 571-579.
17. Cohen-Cory S, Fraser SE. Effects of brain-derived neurotrophic factor on optic axon branching and remodelling in vivo[J]. Nature. 1995, 378(6553): 192-196.
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19. Lander C, Kind P, Maleski M et al. A family of activity-dependent neuronal cell-surface chondroitin sulfate proteoglycans in cat visual cortex[J]. J Neurosci. 1997, 17(6): 1928-1939.
20. Sale A, Maya Vetencourt JF, Medini P et al. Environmental enrichment in adulthood promotes amblyopia recovery through a reduction of intracortical inhibition[J]. Nat Neurosci. 2007, 10(6): 679-681.
21. Hensch TK. Critical period plasticity in local cortical circuits[J]. Nat Rev Neurosci. 2005, 6(11): 877-888.
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23. Werb Z. ECM and cell surface proteolysis: regulating cellular ecology[J]. Cell. 1997, 91(4): 439-442.
24. Mataga N, Nagai N, Hensch TK. Permissive proteolytic activity for visual cortical plasticity[J]. Proc Natl Acad Sci U S A. 2002, 99(11): 7717-7721.
25. Z.Q.YIN SZ. GABAergic neurons co-localize with perineuronal nets and tPA immunoreactivity in rat visual cortex during postnatal development.[J]. Invest.Ophthalmol.Vis.Sci. 2008, 49:E-Abstract 3620.
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27. Qin W, Yin ZQ, Wang S et al. Effects of binocular form deprivation on the excitatory post-synaptic currents mediated by N-methyl-D-aspartate receptors in rat visual cortex[J]. Clin Experiment Ophthalmol. 2004, 32(3): 289-293.
28.余涛,阴正勤,翁传煌等.双眼形觉剥夺对成年大鼠视皮层兴奋性递质受体表达和分布的影响[J]。眼科新进展. 2009, 9(2): 84-89.
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32. Fagiolini M, Pizzorusso T, Berardi N et al. Functional postnataldevelopment of the rat primary visual cortex and the role of visual experience: dark rearing and monocular deprivation[J]. Vision Res. 1994, 34(6): 709-720.
33.余涛,阴正勤,翁传煌.双眼形觉剥夺后成年大鼠视皮层可塑性再激活模型建立[J].眼科新进展. 2009, 29,(7): 481-484.
34. Porciatti V, Pizzorusso T, Maffei L. The visual physiology of the wild type mouse determined with pattern VEPs[J]. Vision Res. 1999, 39(18): 3071-3081.
35. Cerri C, Restani L, Caleo M. Callosal contribution to ocular dominance in rat primary visual cortex[J]. Eur J Neurosci. 2010, 32(7): 1163-1169.
36. Dyer RS, Clark CC, Boyes WK. Surface distribution of flash-evoked and pattern reversal-evoked potentials in hooded rats[J]. Brain Res Bull. 1987, 18(2): 227-234.
37. Gordon JA, Stryker MP. Experience-dependent plasticity of binocular responses in the primary visual cortex of the mouse[J]. J Neurosci. 1996, 16(10): 3274-3286.
38. Hanover JL, Huang ZJ, Tonegawa S et al. Brain-derived neurotrophic factor overexpression induces precocious critical period in mouse visual cortex[J]. J Neurosci. 1999, 19(22): RC40.
39. W原著,诸葛启钏主译GPC.大鼠脑立体定位图谱[J].北京:人民卫生出版社. 2005.
40. Nicole O, Docagne F, Ali C et al. The proteolytic activity of tissue-plasminogen activator enhances NMDA receptor-mediated signaling[J]. Nat Med. 2001, 7(1): 59-64.
41. Muller CM, Griesinger CB. Tissue plasminogen activator mediates reverse occlusion plasticity in visual cortex[J]. Nat Neurosci. 1998, 1(1): 47-53.
42. Krystosek A, Seeds NW. Plasminogen activator release at the neuronal growth cone[J]. Science. 1981, 213(4515): 1532-1534.
43. Seeds NW, Basham ME, Haffke SP. Neuronal migration is retarded in micelacking the tissue plasminogen activator gene[J]. Proc Natl Acad Sci U S A. 1999, 96(24): 14118-14123.
44. Siconolfi LB, Seeds NW. Induction of the plasminogen activator system accompanies peripheral nerve regeneration after sciatic nerve crush[J]. J Neurosci. 2001, 21(12): 4336-4347.
45. Mataga N, Mizuguchi Y, Hensch TK. Experience-dependent pruning of dendritic spines in visual cortex by tissue plasminogen activator[J]. Neuron. 2004, 44(6): 1031-1041.
46. Zheng S, Yin ZQ, Zeng YX. Developmental profile of tissue plasminogen activator in postnatal Long Evans rat visual cortex[J]. Mol Vis. 2008, 14: 975-982.
47. Shiosaka S, Yoshida S. Synaptic microenvironments--structural plasticity, adhesion molecules, proteases and their inhibitors[J]. Neurosci Res. 2000, 37(2): 85-89.
48. Lochner JE, Kingma M, Kuhn S et al. Real-time imaging of the axonal transport of granules containing a tissue plasminogen activator/green fluorescent protein hybrid[J]. Mol Biol Cell. 1998, 9(9): 2463-2476.
49. Fiumelli H, Jabaudon D, Magistretti PJ et al. BDNF stimulates expression, activity and release of tissue-type plasminogen activator in mouse cortical neurons[J]. Eur J Neurosci. 1999, 11(5): 1639-1646.
50. Wannier-Morino P, Rager G, Sonderegger P et al. Expression of neuroserpin in the visual cortex of the mouse during the developmental critical period[J]. Eur J Neurosci. 2003, 17(9): 1853-1860.
51. McGee AW, Yang Y, Fischer QS et al. Experience-driven plasticity of visual cortex limited by myelin and Nogo receptor[J]. Science. 2005, 309(5744): 2222-2226.
1. Hensch TK. Critical period regulation[J]. Annu Rev Neurosci. 2004, 27: 549-579.
2. Berardi N, Pizzorusso T, Maffei L. Critical periods during sensory development[J]. Curr Opin Neurobiol. 2000, 10(1): 138-145.
3. Prusky GT, Douglas RM. Developmental plasticity of mouse visual acuity[J]. Eur J Neurosci. 2003, 17(1): 167-173.
4. McGee AW, Yang Y, Fischer QS et al. Experience-driven plasticity of visual cortex limited by myelin and Nogo receptor[J]. Science. 2005, 309(5744): 2222-2226.
5. Pizzorusso T, Medini P, Berardi N et al. Reactivation of ocular dominance plasticity in the adult visual cortex[J]. Science. 2002, 298(5596): 1248-1251.
6. Hockfield S, Kalb RG, Zaremba S et al. Expression of neural proteoglycans correlates with the acquisition of mature neuronal properties in the mammalian brain[J]. Cold Spring Harb Symp Quant Biol. 1990, 55: 505-514.
7. Hensch TK, Fagiolini M, Mataga N et al. Local GABA circuit control of experience-dependent plasticity in developing visual cortex[J]. Science. 1998, 282(5393): 1504-1508.
8. Hensch TK. Critical period plasticity in local cortical circuits[J]. Nat Rev Neurosci. 2005, 6(11): 877-888.
9. Soghomonian JJ, Martin DL. Two isoforms of glutamate decarboxylase: why?[J]. Trends Pharmacol Sci. 1998, 19(12): 500-505.
10. Fagiolini M, Hensch TK. Inhibitory threshold for critical-period activation in primary visual cortex[J]. Nature. 2000, 404(6774): 183-186.
11. Fagiolini M, Fritschy JM, Low K et al. Specific GABAA circuits for visual cortical plasticity[J]. Science. 2004, 303(5664): 1681-1683.
12. Katagiri H, Fagiolini M, Hensch TK. Optimization of somatic inhibition at critical period onset in mouse visual cortex[J]. Neuron. 2007, 53(6): 805-812.
13. Sugiyama S, Di Nardo AA, Aizawa S et al. Experience-dependent transfer of Otx2 homeoprotein into the visual cortex activates postnatal plasticity[J]. Cell. 2008, 134(3):508-520.
14. Huang ZJ, Kirkwood A, Pizzorusso T et al. BDNF regulates the maturation of inhibition and the critical period of plasticity in mouse visual cortex[J]. Cell. 1999, 98(6): 739-755.
15. Morales B, Choi SY, Kirkwood A. Dark rearing alters the development of GABAergic transmission in visual cortex[J]. J Neurosci. 2002, 22(18): 8084-8090.
16. Bradbury EJ, Moon LD, Popat RJ et al. Chondroitinase ABC promotes functional recovery after spinal cord injury[J]. Nature. 2002, 416(6881): 636-640.
17. Silver J, Miller JH. Regeneration beyond the glial scar[J]. Nat Rev Neurosci. 2004, 5(2): 146-156.
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22. Mataga N, Mizuguchi Y, Hensch TK. Experience-dependent pruning of dendritic spines in visual cortex by tissue plasminogen activator[J]. Neuron. 2004, 44(6): 1031-1041.
23. Harauzov A, Spolidoro M, DiCristo G et al. Reducing intracortical inhibition in the adult visual cortex promotes ocular dominance plasticity[J]. J Neurosci. 2010, 30(1): 361-371.
24. Sale A, Maya Vetencourt JF, Medini P et al. Environmental enrichment in adulthood promotes amblyopia recovery through a reduction of intracortical inhibition[J]. Nat Neurosci. 2007, 10(6): 679-681.
25. Mainardi M, Landi S, Gianfranceschi L et al. Environmental enrichment potentiatesthalamocortical transmission and plasticity in the adult rat visual cortex[J]. J Neurosci Res. 2010, 88(14): 3048-3059.
26. Maya Vetencourt JF, Sale A, Viegi A et al. The antidepressant fluoxetine restores plasticity in the adult visual cortex[J]. Science. 2008, 320(5874): 385-388.
27. He HY, Hodos W, Quinlan EM. Visual deprivation reactivates rapid ocular dominance plasticity in adult visual cortex[J]. J Neurosci. 2006, 26(11): 2951-2955.
2. Fox K, Caterson B. Neuroscience. Freeing the bain from the perineuronal net[J]. Science. 2002, 298(5596): 1187-1189.
3. Heynen AJ, Yoon BJ, Liu CH et al. Molecular mechanism for loss of visual cortical responsiveness following brief monocular deprivation[J]. Nat Neurosci. 2003, 6(8): 854-862.
4. Muir DW, Mitchell DE. Visual resolution and experience: acuity deficits in cats following early selective visual deprivation[J]. Science. 1973, 180(84): 420-422.
5. Frenkel MY, Bear MF. How monocular deprivation shifts ocular dominance in visual cortex of young mice[J]. Neuron. 2004, 44(6): 917-923.
6. Sawtell NB, Frenkel MY, Philpot BD et al. NMDA receptor-dependent ocular dominance plasticity in adult visual cortex[J]. Neuron. 2003, 38(6): 977-985.
7. Pizzorusso T, Medini P, Berardi N et al. Reactivation of ocular dominance plasticity in the adult visual cortex[J]. Science. 2002, 298(5596): 1248-1251.
8. Maya Vetencourt JF, Sale A, Viegi A et al. The antidepressant fluoxetine restores plasticity in the adult visual cortex[J]. Science. 2008, 320(5874): 385-388.
9. Harauzov A, Spolidoro M, DiCristo G et al. Reducing intracortical inhibition in the adult visual cortex promotes ocular dominance plasticity[J]. J Neurosci. 2010, 30(1): 361-371.
10. He HY, Hodos W, Quinlan EM. Visual deprivation reactivates rapid ocular dominance plasticity in adult visual cortex[J]. J Neurosci. 2006, 26(11):2951-2955.
11. Mainardi M, Landi S, Gianfranceschi L et al. Environmental enrichment potentiates thalamocortical transmission and plasticity in the adult rat visual cortex[J]. J Neurosci Res. 2010, 88(14): 3048-3059.
12. Fagiolini M, Hensch TK. Inhibitory threshold for critical-period activation in primary visual cortex[J]. Nature. 2000, 404(6774): 183-186.
13. Yin ZQ, Crewther SG, Yang M et al. Distribution and localization of NMDA receptor subunit 1 in the visual cortex of strabismic and anisometropic amblyopic cats[J]. Neuroreport. 1996, 7(18): 2997-3003.
14.阴正勤,余涛,陈莉.斜视性弱视猫发育过程中视皮层神经元NMDA-R1表达的免疫组织化学电镜观察[J].中华眼科杂志. 2002, 38(8): 472-475.
15.秦伟,阴正勤,王仕军等.正常和双眼形觉剥夺大鼠发育过程中视皮层神经元NR-1的表达。[J].第三军医大学学报. 2003, 25(21): 1924-1926.
16. Huber KM, Sawtell NB, Bear MF. Brain-derived neurotrophic factor alters the synaptic modification threshold in visual cortex[J]. Neuropharmacology. 1998, 37(4-5): 571-579.
17. Cohen-Cory S, Fraser SE. Effects of brain-derived neurotrophic factor on optic axon branching and remodelling in vivo[J]. Nature. 1995, 378(6553): 192-196.
18. Bradbury EJ, Moon LD, Popat RJ et al. Chondroitinase ABC promotes functional recovery after spinal cord injury[J]. Nature. 2002, 416(6881): 636-640.
19. Lander C, Kind P, Maleski M et al. A family of activity-dependent neuronal cell-surface chondroitin sulfate proteoglycans in cat visual cortex[J]. J Neurosci. 1997, 17(6): 1928-1939.
20. Sale A, Maya Vetencourt JF, Medini P et al. Environmental enrichment in adulthood promotes amblyopia recovery through a reduction of intracortical inhibition[J]. Nat Neurosci. 2007, 10(6): 679-681.
21. Hensch TK. Critical period plasticity in local cortical circuits[J]. Nat Rev Neurosci. 2005, 6(11): 877-888.
22. Basham ME, Seeds NW. Plasminogen expression in the neonatal and adult mouse brain[J]. J Neurochem. 2001, 77(1): 318-325.
23. Werb Z. ECM and cell surface proteolysis: regulating cellular ecology[J]. Cell. 1997, 91(4): 439-442.
24. Mataga N, Nagai N, Hensch TK. Permissive proteolytic activity for visual cortical plasticity[J]. Proc Natl Acad Sci U S A. 2002, 99(11): 7717-7721.
25. Z.Q.YIN SZ. GABAergic neurons co-localize with perineuronal nets and tPA immunoreactivity in rat visual cortex during postnatal development.[J]. Invest.Ophthalmol.Vis.Sci. 2008, 49:E-Abstract 3620.
26. Morales B, Choi SY, Kirkwood A. Dark rearing alters the development of GABAergic transmission in visual cortex[J]. J Neurosci. 2002, 22(18): 8084-8090.
27. Qin W, Yin ZQ, Wang S et al. Effects of binocular form deprivation on the excitatory post-synaptic currents mediated by N-methyl-D-aspartate receptors in rat visual cortex[J]. Clin Experiment Ophthalmol. 2004, 32(3): 289-293.
28.余涛,阴正勤,翁传煌等.双眼形觉剥夺对成年大鼠视皮层兴奋性递质受体表达和分布的影响[J]。眼科新进展. 2009, 9(2): 84-89.
29. Ducati A, Fava E, Motti ED. Neuronal generators of the visual evoked potentials: intracerebral recording in awake humans[J]. Electroencephalogr Clin Neurophysiol. 1988, 71(2): 89-99.
30. Iny K, Heynen AJ, Sklar E et al. Bidirectional modifications of visual acuity induced by monocular deprivation in juvenile and adult rats[J]. J Neurosci. 2006, 26(28): 7368-7374.
31. Wiesel TN, Hubel DH. Single-Cell Responses in Striate Cortex of Kittens Deprived of Vision in One Eye[J]. J Neurophysiol. 1963, 26: 1003-1017.
32. Fagiolini M, Pizzorusso T, Berardi N et al. Functional postnataldevelopment of the rat primary visual cortex and the role of visual experience: dark rearing and monocular deprivation[J]. Vision Res. 1994, 34(6): 709-720.
33.余涛,阴正勤,翁传煌.双眼形觉剥夺后成年大鼠视皮层可塑性再激活模型建立[J].眼科新进展. 2009, 29,(7): 481-484.
34. Porciatti V, Pizzorusso T, Maffei L. The visual physiology of the wild type mouse determined with pattern VEPs[J]. Vision Res. 1999, 39(18): 3071-3081.
35. Cerri C, Restani L, Caleo M. Callosal contribution to ocular dominance in rat primary visual cortex[J]. Eur J Neurosci. 2010, 32(7): 1163-1169.
36. Dyer RS, Clark CC, Boyes WK. Surface distribution of flash-evoked and pattern reversal-evoked potentials in hooded rats[J]. Brain Res Bull. 1987, 18(2): 227-234.
37. Gordon JA, Stryker MP. Experience-dependent plasticity of binocular responses in the primary visual cortex of the mouse[J]. J Neurosci. 1996, 16(10): 3274-3286.
38. Hanover JL, Huang ZJ, Tonegawa S et al. Brain-derived neurotrophic factor overexpression induces precocious critical period in mouse visual cortex[J]. J Neurosci. 1999, 19(22): RC40.
39. W原著,诸葛启钏主译GPC.大鼠脑立体定位图谱[J].北京:人民卫生出版社. 2005.
40. Nicole O, Docagne F, Ali C et al. The proteolytic activity of tissue-plasminogen activator enhances NMDA receptor-mediated signaling[J]. Nat Med. 2001, 7(1): 59-64.
41. Muller CM, Griesinger CB. Tissue plasminogen activator mediates reverse occlusion plasticity in visual cortex[J]. Nat Neurosci. 1998, 1(1): 47-53.
42. Krystosek A, Seeds NW. Plasminogen activator release at the neuronal growth cone[J]. Science. 1981, 213(4515): 1532-1534.
43. Seeds NW, Basham ME, Haffke SP. Neuronal migration is retarded in micelacking the tissue plasminogen activator gene[J]. Proc Natl Acad Sci U S A. 1999, 96(24): 14118-14123.
44. Siconolfi LB, Seeds NW. Induction of the plasminogen activator system accompanies peripheral nerve regeneration after sciatic nerve crush[J]. J Neurosci. 2001, 21(12): 4336-4347.
45. Mataga N, Mizuguchi Y, Hensch TK. Experience-dependent pruning of dendritic spines in visual cortex by tissue plasminogen activator[J]. Neuron. 2004, 44(6): 1031-1041.
46. Zheng S, Yin ZQ, Zeng YX. Developmental profile of tissue plasminogen activator in postnatal Long Evans rat visual cortex[J]. Mol Vis. 2008, 14: 975-982.
47. Shiosaka S, Yoshida S. Synaptic microenvironments--structural plasticity, adhesion molecules, proteases and their inhibitors[J]. Neurosci Res. 2000, 37(2): 85-89.
48. Lochner JE, Kingma M, Kuhn S et al. Real-time imaging of the axonal transport of granules containing a tissue plasminogen activator/green fluorescent protein hybrid[J]. Mol Biol Cell. 1998, 9(9): 2463-2476.
49. Fiumelli H, Jabaudon D, Magistretti PJ et al. BDNF stimulates expression, activity and release of tissue-type plasminogen activator in mouse cortical neurons[J]. Eur J Neurosci. 1999, 11(5): 1639-1646.
50. Wannier-Morino P, Rager G, Sonderegger P et al. Expression of neuroserpin in the visual cortex of the mouse during the developmental critical period[J]. Eur J Neurosci. 2003, 17(9): 1853-1860.
51. McGee AW, Yang Y, Fischer QS et al. Experience-driven plasticity of visual cortex limited by myelin and Nogo receptor[J]. Science. 2005, 309(5744): 2222-2226.
1. Hensch TK. Critical period regulation[J]. Annu Rev Neurosci. 2004, 27: 549-579.
2. Berardi N, Pizzorusso T, Maffei L. Critical periods during sensory development[J]. Curr Opin Neurobiol. 2000, 10(1): 138-145.
3. Prusky GT, Douglas RM. Developmental plasticity of mouse visual acuity[J]. Eur J Neurosci. 2003, 17(1): 167-173.
4. McGee AW, Yang Y, Fischer QS et al. Experience-driven plasticity of visual cortex limited by myelin and Nogo receptor[J]. Science. 2005, 309(5744): 2222-2226.
5. Pizzorusso T, Medini P, Berardi N et al. Reactivation of ocular dominance plasticity in the adult visual cortex[J]. Science. 2002, 298(5596): 1248-1251.
6. Hockfield S, Kalb RG, Zaremba S et al. Expression of neural proteoglycans correlates with the acquisition of mature neuronal properties in the mammalian brain[J]. Cold Spring Harb Symp Quant Biol. 1990, 55: 505-514.
7. Hensch TK, Fagiolini M, Mataga N et al. Local GABA circuit control of experience-dependent plasticity in developing visual cortex[J]. Science. 1998, 282(5393): 1504-1508.
8. Hensch TK. Critical period plasticity in local cortical circuits[J]. Nat Rev Neurosci. 2005, 6(11): 877-888.
9. Soghomonian JJ, Martin DL. Two isoforms of glutamate decarboxylase: why?[J]. Trends Pharmacol Sci. 1998, 19(12): 500-505.
10. Fagiolini M, Hensch TK. Inhibitory threshold for critical-period activation in primary visual cortex[J]. Nature. 2000, 404(6774): 183-186.
11. Fagiolini M, Fritschy JM, Low K et al. Specific GABAA circuits for visual cortical plasticity[J]. Science. 2004, 303(5664): 1681-1683.
12. Katagiri H, Fagiolini M, Hensch TK. Optimization of somatic inhibition at critical period onset in mouse visual cortex[J]. Neuron. 2007, 53(6): 805-812.
13. Sugiyama S, Di Nardo AA, Aizawa S et al. Experience-dependent transfer of Otx2 homeoprotein into the visual cortex activates postnatal plasticity[J]. Cell. 2008, 134(3):508-520.
14. Huang ZJ, Kirkwood A, Pizzorusso T et al. BDNF regulates the maturation of inhibition and the critical period of plasticity in mouse visual cortex[J]. Cell. 1999, 98(6): 739-755.
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