Relationship Between The Effects Of BFD On The Synaptic Plasticity Of Rat Visual Cortex And The Neurotransmitters And Receptors

Visual development, a branch of neuroscience, is an important field for clinical and theoretical research in ophthalmology. Investigation of visual development will help interpret the principle of brain working, and provide theoretical basis for the visual reconstruction of adult visual damage and the treatment of infant-eye-disease. During the critical period of visual development, abnormal visual environment such as dark-rearing influences the experience-dependent plasticity of visual cortex. However, transmitters and receptors, which are involved in the changes of visual cortical plasticity, are still unclear. N-methyl-D-aspartate (NMDA) receptors and aminobutyric acid (GABA) receptors mediate respectively the excitatory and inhibitory synaptic transmission in cerebral cortex. To date, no report has been published as to how the NMDA or GABAA receptors involve in the effects of binocular form deprivation (BFD) on the synaptic transmission in the visual cortex Therefore, we applied the following methods and techniques to investigate the relationship between the effects of BFD on the synaptic plasticity of visual cortex and the neurotransmitters and receptors.1. With the use of patch-clamp whole-cell-recording technique, we recorded the postsynaptic currents (PSCs) of visual cortical neurons in normal and BFD rats during the critical period of visual development, then isolated pharmacologically the excitatory postsynaptic currents mediated by glutamate receptors (glutamate-EPSCs) by adding bicuculline methiodide (20 μM, BMI), a blocker of GABAA receptor, into artificial cerebrospinal fluid (ACSF); and isolated the EPSCs mediated by NMDA receptors (NMDA-EPSCs) by adding BMI (20 μM) and 6-cyano-7-nitroquinoxaline-2, 3-dione (20 μM, CNQX), a blocker of AMPA receptor, into artificial cerebrospinal fluids (ACSF). For each cell, we calculated the ratio of the peak currents mediated by NMDA receptors to that mediated by glutamate receptors. The results showed that: ⑴ The input resistance (IR) of visual cortical neurons declined significantly with age in normal rats (P < 0.05), but not in BFD group ( P > 0.05); the IR became smaller 1 week after opening the sutured eyelids (VsPW4 of BFD group, P < 0.05). ⑵The decay time of NMDA-EPSCs of visual cortical neurons became shorter with age in normal rats (P < 0.05), but not in BFD group (P > 0.05); the decay time had a tendency of becoming smaller after opening the sutured eyelids (Vs PW4 of BFD group, P = 0.06). ⑶The rise time and peak value of NMDA-EPSCs of visual cortical neurons in normal, BFD and removed BFD rats did not change with age (P > 0.05). ⑷The ratios of NMDA-EPSCs to glutamate-EPSCs of visual cortex declined significantly with age in normal rats (P < 0.05), but not in BFD group ( P > 0.05); the ratios became smaller after opening the sutured eyelids (Vs PW4 of BFD group, P < 0.05). The results indicated that BFD influenced the functional plasticity of excitatory synaptic transmission of rat visual cortex with the role of NMDA receptors.2. With the use of patch-clamp whole-cell-recording technique, we recorded the PSCs of visual cortical neurons in normal and BFD rats during the critical period of visual development, then isolated pharmacologically the inhibitory postsynaptic currents mediated by GABAA receptors (GABA-IPSCs) by adding D, L-2-amino-5-phosphonovalerate (50 μM, AP-5), a blocker of NMDA receptor, and CNQX (20 μM) into ACSF. As a result, the peak value and decay time of neuronal GABA-IPSCs of visual cortex increased gradually with age in normal rats (P < 0.05), but not in BFD group (P > 0.05); after opening the binocular eyelids suture, they became smaller (Vs PW4 of BFD group, P < 0.05 and P = 0.059). The rise time of neuronal GABA-IPSCs of visual cortex did not change with age in normal, BFD and removed BFD rats (P > 0.05). The results indicated that BFD had effects on the functional plasticity of inhibitory synaptic transmission in rat visual cortex with the role of GABAA receptors.3. Intracellular labeling was perfor...