The Changes Of Ultrastructure And NGF Expression In Visual Cortex Area17of Optical Strabismus Cats

ObjectiveTo investigate the changes of synaptic ultrastructure and nerve growth factor (nervegrowth factor NGF) expression in visual cortex area17of optical strabismus cats, wholack of binocular fusion, so that we can find the probable mechanism of the binocularfusion and its related influencing factors.MethodsOrdinary domestic cats were randomly divided into three groups: normal control group,optical strabismus group and amblyopia group. During the critical period, by wearing the15△base-in prisms and suturing the right eye, we established the optical strabismusmodels and the monocular deprivation amblyopia models, respectively. Then we screenedthe animals by detecting VEP until6months of age. According to the three-dimensionalcat brain stereotactic atlas,we drawn on the visual cortex of area17，followed by fixation,embedding, production of electron microscope specimen and paraffin sections. Weobserved the changes of synaptic ultrastructure and NGF expression visual cortex area17. By using the Image Pro-plus, we measured the width of the synaptic cleft, the synapticdense material thickness, the chord length and arc length of the postsynaptic membrane.All experimental data were statistically analyzed using SPSS17.0statistical software.Results1. P-VEP test results: monocular P100wave amplitude and latency of normal group werenormal, binocular amplitude was2times greater than the monocular amplitude; monocularP100amplitude and latency of optical strabismus group, had no significant differences tothe normal group (P>0.05), binocular amplitude was less than the monocularamplitude;compared with the normal group, there were no statistical significance in P100amplitude and latency of the left eye of the amblyopic group(P>0.05), but the right eye isless than the normal group and strabismus group, the latency was longer than thenormal group and strabismus group, the difference was statistically significant (P<0.05),binocular amplitude was less than the monocular amplitude.2. Toluidine blue staining results: the normal group and the optical strabismus groupvisual cortex area17stratified clear. Area17was divided into six layers from shallow todeep: the molecular layer, the external granular layer, external pyramidal cell layer,internal granular layer, internal pyramidal cell layer and polymorphonuclear cell layer.The granular layer cells in normal group were more intensive than optical strabismusgroup. The stratification of visual cortex in amplyopia group was not obvious, mainlyfilled with light staining and small immature cells.3.Synaptic ultrastructure changes: to compare the differences of the synaptic cleft, thepostsynaptic membrane curvature and the postsynaptic membrane dense materialthickness of the normal group and the optical strabismus group, difference there wereno statistical significance(P>0.05). Compared with the normal group and the opticalstrabismus group, the synaptic gap in amblyopia group widened, the interface curvaturedecreased, the postsynaptic membrane dense thickened, the differences were statistically significant (P<0.05).4. Immunohistochemical staining results: all cortical Area17layers were available to seeNGF-positive cells. Immunoreactive neurons in optical strabismus group and inmonocular visual deprivation amblyopia group stained lighter than in normal group, thenumber of positive neurons was decreased, the difference was statistically significant(P<0.05); the number of positive neurons in amblyopia group was less than thestrabismus group, the difference was statistically significant (P <0.05).Conclusion1. Established optical strabismus cats in the critical period of visual cortex plasticity anddestructed its fusion, but did not cause changes of synaptic structure parameters, Whilethe monocular form deprivation amblyopia caused variations of the synaptic structureparameters, we speculate that the structural basis of fusion damage mechanisms andmonocular deprivation amblyopia mechanism of is different.2. Destruction of fusion and monocular form deprivation amblyopia caused decreasedexpression of NGF in the visual cortex area17, the amblyopia group expressed less thanthe strabismus group, proved that the expression of NGF and binocular vision had a closerelationship.