| 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. |
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