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Objective To observe the change of expression of neuroligin1 (NL1) in injured spinal cord in rats. Methods A total of 60 adult female Sprague-Dawley rats were randomly divided into control group (n=30) and experi-ment group (n=30), and both groups were further arranged into three days, seven days, 14 days, 21 days, and 28 days subgroups. The control group accepted T9-11 laminectomy, while the experiment group was injured at T10 spi-nal cord hit by Allen's technique (10 g×25 mm). They were assessed with Basso, Beattie & Bresnahan locomotor rating scale (BBB scale), in their time-points, while Golgi-Cox staining was used to observe the variation of den-drites and density of dendritic spine in the white matter located at upper end of spinal cord injured center, and im-munofluorescence staining was used to detect the expression of NL1. Results The score of BBB scale reduced in the experiment group compared with that in the control group in every sub-group (P<0.001). Compared to the control group, both dendrites and density of dendritic spine in the white mat-ter decreased with time after injury (P<0.001), while the level of NL1 increased three days after injury, peaked on the 14th day after injury (P<0.05). Conclusion NL1 increases spontaneously after spinal cord injury, but it is not enough to promote synaptic regeneration.
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Objective To observe whether ketamine improves the symptoms of post-traumatic stress disorder (PTSD).Methods Sixty male SD rats were randomized into four groups:groups CN,CK,PN and PK,15 in each.PTSD animal model was established by inescapable foot shock (IFS) procedure.In groups PK and CK,rats were treated with ketamine 2.5 mg/kg by intraperitoneal injection beginning at 30 min after the IFS procedure once a day for 14 days.Twelve rats were used for be havioral tests,and the others were sacrificed to collect hippocampus tissues for Western blot in each group 14 d after IFS procedure,respectively.The expression of neuroligin (NLGN)-1 was detected by Western blot.Results In the fear conditioning test,compared with group CN,the percent age of freezing time in total time in group PN was significantly increased (P＜0.01).Compared with group PN,the percent age of freezing time in PK group was significantly decreased (P＜0.01).In the water maze test,compared with group CN,the escape latency of group PN was significantly increased on day 2,3,4,5 of training period (P＜0.05).Compared with group PN,the escape latency of group PK was significantly decreased on day 2,4,5 of training period (P＜0.05).There was no significant difference in the time spent in the target quadrant.The expression of NLGN-1 in the hippocampus was significantly increased in PN group compared with group CN (P＜0.05);compared with group PN,the expression of NLGN-1 in the hippocampus was significantly decreased in PK group (P＜0.05).Conclusion The study suggest that the fear memory is significantly,increased and the hippo campus-dependent spatial learning capacity is impaired in the PTSD model rats.And the increased ex pression of hippocampal NLGN-1 may be involved in the development of PTSD.Ketamine mediated down regulation of NLGN-1 in the hippocampus might contribute to attenuating the fear memory and improving the hippocampus dependent spatial learning in the PTSD model rats.
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OBJECTIVE: To explore the effects of sub-chronic aluminum exposure on the combination of hippocampus neuroligin 1( NL1) with N-methyl-D-aspartate receptor( NMDAR) and the effects of correlated bonding to long-term potentiation( LTP) in rats. METHODS: Ninety healthy male specific pathogen free SD rats were selected and randomly divided into blank control group,solvent control group and low-,medium-and high-dose groups,with 18 rats in each group. The rats in blank control group received no treatment. Rats in solvent control group were given 0. 9% sodium chloride solution by concentration of 1 m L/kg body weight( bw). The low-,medium-and high-dose group rats were given the mass concentration of 0. 41,0. 81,1. 62 mg/kg bw maltol aluminum solution by intraperitoneal injection every other day for 1,2,and 3 months,respectively. After maltol aluminum exposure,LTP was detected in the CA1 region of rat hippocampus,aluminum levels were detected by the graphite furnace atomic absorption spectrometry,and the protein relative expression of NL1 combined with NMDAR1 and NMDAR2B were detected by immunoprecipitation and immunoblotting. RESULTS: The LTP in the solvent control group and the low-,medium-,high-dose groups were all lower than that in the blank control group( P < 0. 01). The LTP in the high-dose group was lower than those in the solvent control group and the low-and medium-dose groups( P < 0. 05). The aluminum levels in the hippocampus of rats in the low-,medium-and high-dose groups were higher than those of the blank control group and the solvent control group( P <0. 01). The protein relative expression of NMDAR1 and NMDAR2B combined with NL1 in treatment groups was lower than those in the blank control group and solvent control group at the same exposure time points( P < 0. 01). The protein relative expression of NMDAR1 and NMDAR2B combined with NL1 in treatment groups at time point of 2 months was lower than those at time point of 1 month in the same dose group( P < 0. 01). The protein relative expression of NMDAR1 and NMDAR2 B combined with NL1 at time point of 3 months was lower than those at time points of 1 and 2 months in the same dose group( P < 0. 01). CONCLUSION: Maltol aluminum can prevent the normal combination of NL1 with NMDAR1 and NMDAR2B,affecting LTP regulated by NMDAR1 and NMDAR2B,resulting in a LTP decline,as well as learning and memory impairment.
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All information processing and transmission in the brain involves synapses, the synaptic cell adhesion molecules play an important role in the formation, maturation and maintenance of synapses. Neuroligin1 ( NL1) is excitatory postsynaptic trans?membrane cell adhesion molecules. The interaction between NL1 and other molecules, such as Neurexin1 ( NRXN1) , involves in the formation, plasticity and function of synapses. NL1 knockout or overexpression displayed impairment in learning and memory, thus sug?gesting that NL1 participates in the pathophysiology of neuropsychiatric disease with cognitive dysfunction. Therefore, study of NL1 will open up new avenues to understand pathogenesis of cognitive dysfunction, and may provide a novel insight into prevention and treatment of cognitive dysfunction?associated diseases.