摘要
BACKGROUND: Affected signal convection of synaptophysin on motor neurons may cause injury of motor neurons and then induce neurodegeneration and cell death in the end. OBJECTIVE: To investigate the number and density of synaptophysin on motor neurons in the anterior horn of lumbar spinal cord and sensorimotor cortex of the transgenic mouse model of amyotrophic lateral sclerosis (ALS). DESIGN: Randomized controlled animal study. SETTING: Brain Injury and Repair Group, HFI Institute of Melbourne University. MATERIALS: Transgenic mice expressing a mutated human superoxide dismutase 1 (SOD-1) were taken as ALS group (n =36), while those derived from the B6SJL-TgN gene line were taken as control group (n =36), according to the difference of gender and three postnatal time points (postnatal 60, 90 and 120 days), twelve mice of either gender were allocated in each subgroup. METHODS: The experiment was carried out in Brain Injury and Repair Group, HFI Institute of Melbourne University from November 2003 to June 2004. ① Fluorogold labeling was used for the motor neurons in the lumbar and sensorimotor cortex. ② Immunofluorescence was applied for the labeling of synaptophysin; positive control sections were represented by adding the synaptophysin antibody and the staining, showing a positive result. For negative controls, the synaptophysin antibody was omitted. ③ Stereological counting system was adopted in the statistical analysis. MAIN OUTCOME MEASURES: ① Fluorogold labeling of motor neurons; ② number of synaptophysin on the motor neurons. RESULTS: ① Fluorogold labeling of motor neurons: The motor neurons in the lumbar and sensorimotor cortex were clearly labeled by fluorogold under the detection of fluorescent microscope. ② The number of synaptophysin on the motor neurons: The number statistically decreased at the mid stage (postnatal 90 days) and late stage (postnatal 120 days) [motor neuron somas at lumbar spinal cord: (0.75±0.06), (0.59±0.09)/μm; motor neuron dendrite at lumbar spinal cord: (0.71±0.06), (0.55±0.03)/μm; motor neuron somas at sensorimotor cortex: (0.79±0.03), (0.63±0.08)/μm; motor neuron dendrite at sensorimotor cortex: (0.76±0.07), (0.61±0.08)/μm, P < 0.01]. The reduction of synaptophysin was parallel between the gender differences. CONCLUSION: Loss of synaptophysin on motor neurons is directly related to the progression of ALS.
BACKGROUND: Affected signal convection of synaptophysin on motor neurons may cause injury of motor neurons and then induce neurodegeneration and cell death in the end. OBJECTIVE: To investigate the number and density of synaptophysin on motor neurons in the anterior horn of lumbar spinal cord and sensorimotor cortex of the transgenic mouse model of amyotrophic lateral sclerosis (ALS). DESIGN: Randomized controlled animal study. SETTING: Brain Injury and Repair Group, HFI Institute of Melbourne University. MATERIALS: Transgenic mice expressing a mutated human superoxide dismutase 1 (SOD-1) were taken as ALS group (n =36), while those derived from the B6SJL-TgN gene line were taken as control group (n =36), according to the difference of gender and three postnatal time points (postnatal 60, 90 and 120 days), twelve mice of either gender were allocated in each subgroup. METHODS: The experiment was carried out in Brain Injury and Repair Group, HFI Institute of Melbourne University from November 2003 to June 2004. ① Fluorogold labeling was used for the motor neurons in the lumbar and sensorimotor cortex. ② Immunofluorescence was applied for the labeling of synaptophysin; positive control sections were represented by adding the synaptophysin antibody and the staining, showing a positive result. For negative controls, the synaptophysin antibody was omitted. ③ Stereological counting system was adopted in the statistical analysis. MAIN OUTCOME MEASURES: ① Fluorogold labeling of motor neurons; ② number of synaptophysin on the motor neurons. RESULTS: ① Fluorogold labeling of motor neurons: The motor neurons in the lumbar and sensorimotor cortex were clearly labeled by fluorogold under the detection of fluorescent microscope. ② The number of synaptophysin on the motor neurons: The number statistically decreased at the mid stage (postnatal 90 days) and late stage (postnatal 120 days) [motor neuron somas at lumbar spinal cord: (0.75±0.06), (0.59±0.09)/μm; motor neuron dendrite at lumbar spinal cord: (0.71±0.06), (0.55±0.03)/μm; motor neuron somas at sensorimotor cortex: (0.79±0.03), (0.63±0.08)/μm; motor neuron dendrite at sensorimotor cortex: (0.76±0.07), (0.61±0.08)/μm, P < 0.01]. The reduction of synaptophysin was parallel between the gender differences. CONCLUSION: Loss of synaptophysin on motor neurons is directly related to the progression of ALS.
