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Objective:To explore the effects of acute sleep fragmentation (SF) on cognitive function and the relationship between hippocampal Homer1a and synaptic plasticity in aged rats.Methods:One hundred and eight SPF grade male SD rats aged 22 to 24 months were divided into three groups according to random number table: control group (Control group), non-sleep fragmentation group (NSF group) and sleep fragmentation group (SF group), with 36 rats in each group.A sleep fragmentation model was established by sleep deprivation rod method.Morris water maze and novel object recognition tests were used to evaluate the learning and memory function of rats.Homer1a expression in hippocampus was detected by Western blot, and its distribution in CA1 area of hippocampus was observed by immunohistochemical staining.Golgi staining was used to observe the density of dendritic spines in CA1 area of hippocampus, and in vitro electrophysiological patch clamp test was used to detect the slope of field excitatory postsynaptic potential(fEPSP) from CA3 to CA1 in hippocampus.SPSS 22.0 and GraphPad Prism 9.3 softwares were used for data statistical analysis and mapping.One-way ANOVA was used for comparison among groups, and Tukey-Kramer test was used for further pairwise comparison. Results:(1)In the behavioral tests, there were statistical differences in the times of crossing the original platform, the target quadrant residence time and the new object recognition index at 1 h and 24 h among the three groups( F=13.63, 11.34, 21.26, 16.22, all P<0.01). The times of crossing the original platform in SF group((2.00±1.27) times) was lower than that of Control group ((5.67±2.16) times) and NSF group ((6.50±2.35) times) (both P<0.05). The target quadrant residence time in SF group ((9.02±4.84) s) was shorter than that in Control group ((24.73±7.37) s) and NSF group ((27.81±8.37)s) (both P<0.05). The new object recognition index at 1 h and 24 h in SF group were lower than those in Control group and NSF group (all P<0.05). (2) In Western blot assay, the expression of Homer1a protein in hippocampus of SF group(0.91±0.13) was higher than that of Control group(0.70±0.05) and NSF group(0.74±0.04)(both P<0.05). (3) In immunohistochemical staining, the optical density value of the Homer1a protein in CA1 area of hippocampus in the SF group was higher than that in the Control group and NSF group(both P<0.05). (4) In Golgi staining, the density of dendritic spines in CA1 area of hippocampus in SF group was lower than that in Control group and NSF group (both P<0.05). (5) In vitro electrophysiological test showed that the slope of fEPSP in CA3-CA1 area of hippocampus in SF group were lower than that in Control group and NSF group (both P<0.05). Conclusion:Acute SF intervention in aged rats can cause cognitive impairment, which may be associated with the inhibition of hippocampal synaptic plasticity induced by hippocampal Homer1a overexpression.
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A single infusion of ketamine has sustained antidepressant effects and significantly de-creases the risk of suicide,and the effects can last up for 7-10 days,but the underlying mechanism is un-clear. The mechanism was reviewed underlying the antidepressant effects of ketamine,and found that ket-amine may exert its antidepressant effect by regulating sleep/wake cycle,synaptic pruning,molecular path-ways,and neural circuits for treatment-refractory depression. Further studies are needed to investigate the ge-netic,molecular mechanisms underlying the sustained antidepressant effect of ketamine,and the associated imaging findings through in vivo imaging of animals and imaging genetics techniques,explore the optimal time for administration of ketamine,and then provide accurate scientific basis for enhancing its anti-depressant effect.
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Objective To study the Homer1a protein expression and its relationship with neurological deficit and neuronal apoptosis in craniocerebral trauma patients. Methods Forty-two craniocerebral trauma patients, admitted to our hospital from May 2012 to March 2016, were selected as craniocerebral trauma group; 50 healthy subjects accepted physical examination at the same period in our hospital were selected as normal control group (n=50). Immediately after admission, serum contents of Homer1a protein and nerve function damage indices (neurospecific estrogenase [NSE]), fatty acid binding protein [FABP], insulin-like growth factor [IGF-1], and S100B protein) were measured by enzyme linked immunosorbent assay (ELISA). Serum apoptotic indices (soluble apoptotic factor [(sFas)], sFas ligand [sFasL], and cell lymphoma-2 [Bcl-2]) were detected by radioimmunoassay. Results Immediately after admission, serum content of Homer1a protein content in craniocerebral trauma group ([113.27±12.19] pg/mL) was significantly higher than that in normal control group ([53.93±4.06] pg/mL, P<0.05); the median serum Homer1a protein level was 115.302 pg/mL, and according to this level, the patients from the craniocerebral trauma group were further divided into high Homer1a group and low Homer1a group. Serum NSE, FABP, S100B, sFas and sFasL levels in the high Homer1a group, low Homer1a group and normal control group were decreased in sequence, and IGF-1 and Bcl-2 levels increased in sequence, with significant differences (P<0.05). Conclusion Expression of Homer1a protein is increased in patients with traumatic brain injury, and its content is directly related to nerve injury and neuron apoptosis.