| Background:Amblyopia is a common cause of monocular vision impairment, and its incidence is about 1.3-3.6%. The common methods in treating amblyopia are optical correction, covering method and atropine depressive therapy, etc. Atropine depressive therapy is widely used in treating mild-to-moderate amblyopia and easy to accept for patients and their parents. If patients miss the follow-up during the critical period of visual development, atropine may impact the visual function of the normal eye. Studying the effects of monocular atropinization in critical period will help us understand the mechanism of amblyopia, and provides a theoretical basis in preventing the damage caused by long-term atropinization.The connection of the neurons in mammalian visual system is one of the common models in neurobiological research. The function of the visual system depends on the normal development and transmission of the synapses. By adjusting the number ofsynaptic or synaptic efficacy, the composition and function of neurons in a loop can be changed, namely the synaptic plasticity. Synaptic plasticity is a relatively short period of time changing the activities of the neurons, but the overall excitability of the neurons remains stable in a long time. With the development of the synaptic research, the homeostatic synaptic plasticity(HSP) can balance the excitability or depression and prevent the long- term potentiation(LTP) or the long-term depression(LTD). The presynaptic and postsynaptic changes occur in the homeostatic compensation. It is found that the changes of amplitude exist both in vivo and vitro. Blocking the synaptic activity in neuromuscular junction can increase the neurotransmitter release rate among the central synaptic junction. The change of presynaptic effectiveness is usually associated with the rise of postsynaptic receptors, suggesting that a functional coordination exists between the presynaptic and postsynaptic synapses miniature excitatory postsynaptic currents(m EPSCs) is the best index to measure the homeostatic synaptic plasticity. It has been confirmed that the abnormal visual environment like dark raring and monocular form-deprivation can change the m EPSCs mediated by a-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid(AMPA) receptors in layerⅡ/Ⅲ pyramidal neurons of developmental rat visual cortex, which effect the homeostatic synaptic plasticity. The changes of the HSP may show the potential mechanism of amblyopia. Does the long-term atropinization change the HSP which leading to the amblyopia? But the related research has not been reported that how monocular atropinization impact the HSP of rats.Objective:1. To investigate the changes of visual cortex by using the monocular atropinization model of the abnormal visual experiment in rats.2. To investigate the changes of monocular atropinization for miniature excitatory postsynaptic currents mediated by AMPA receptors in layer Ⅱ/Ⅲ pyramidal neurons of developmental rat visual cortex, and indicate the potential mechanism of the amblyopia.Methods:1. Normal SD rats were randomly divided into two groups: control group andatropinization group. Atropinization group was produced by atropine of left eyes in ten rats, and the right eyes of atropinization group and the control group was produced by normal saline. The flash visual evoked potentials(F-VEP) and retinoscopy refraction of the rats’ both eyes in atropinization group and left eyes in the control group were detected at five time points: 0 d, 7 d, 14 d, 21 d, 28 d after atropinization, respectively.2. Six rats were randomly selected from both groups and each group had three rats after 28 d. The expression of the c-fos m RNA was observed in visual cortexes. Another six rats were chosen for the same test after 2-day dark environment with 2-hour light later.3. Postnatal 14 days SD rats were randomly divided into two groups: control group and atropinization group. Atropinization group was produced by atropine of the left eyes and divided into five groups(0 d, 7 d, 14 d, 21 d and 28 d) after atropinization, respectively. By infrared auxiliary brain slice of patch clamp whole cell recording technique, miniature excitatory postsynaptic currents(m EPSCs) of each group after atropinization has been observed and analyzed, respectively.Results:1. Anisometropia was formed at 14 d after atropinization(P<0.05) and the peak time of P1 wave in atropinization group were extended compared to the control group. The difference was 88.9+1.889 ms and statistically significant(P<0.05). The expression of the c-fos m RNA in left visual cortex of the atropinization group was higher than that of the right one without differences after 28 days. But it was significantly increased for 5 times than that of the right sides after the rats came back from the 2-day dark environment for 2 hours.2. The amplitude of mEPSCs in the right side of the experiment groups was enhanced with the time of atropinization(F=9.79,P<0.05). The m EPSCs frequency decreased with the time of atropinization(F=6.79,P<0.05). Both the amplitude and frequency of the m EPSCs between 0 d and 21 d groups had their significant differences on the right side of the experiment groups(P<0.05). There were no significant differences between the normal groups and the experiment groups regarding the rise time and decay time(P>0.05). Theresults indicate that the monocular atropinization can reduce the reaction to the light and damage the function of the visual cortex.Conclusions:1. Anisometropia can be formed by monocular atropinization of rats during the visual development which may delay the transmission of the optic nerve and the normal development.2. Monocular atropinization can lead to the up-scaling of synaptic homeostatic plasticity to the side of the disposed eyes in pyramidal cells of layer Ⅱ/Ⅲ in primary visual cortex and little impact to the side of undisposed eyes. This result shows that monocular atropinization lead to anisometropia which depressed the development of the visual cortex, and enhance the HSP of the visual cortex, indicating that the potential mechanisms of amblyopia by long-term atropinization and the importance of the follow-up to the patients with amblyopia. |
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