ABSTRACT
Anti-α-amino-3-hydroxy-5-methyl-4-isoxazolipropionic acid receptor (AMPAR) encephalitis is an autoimmune encephalitis that is resistant to neuron cell surface antigen, and the clinical incidence is rare. We report a new case of AMPAR encephalitis with clinical features and management. A male patient, 56 years old, presented with progressive dizziness with difficulty swallowing disorder in acute onset. Chest CT examination revealed thymoma and thymic tumor resection was done. Postoperative dizziness and swallowing difficulties were still in progression, with abnormal mental behavior, disturbance of consciousness, seizures, etc. Cerebral MRI showed multiple long T1 and long T2 signals, as well as high fluid attenuated inversion recovery signal lesions in bilateral parietal lobe, bilateral frontal lobe, left occipital lobe, bilateral temporal lobe and right hippocampus. Serum glutamate receptor (AMPA2) antibody IgG was found positive. Based on the patient′s clinical manifestations, auxiliary examination and literature review, the patient was diagnosed as AMPAR encephalitis and received immunotherapy. After active treatment, the patient′s symptoms improved and he then discharged from hospital. Serum or cerebrospinal fluid antibody detection is helpful for early diagnosis and treatment of the disease.
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Objective:To investigate themechanism on NF-κB mediates the injection coryadlis decumbens pers ( ICDP ) participated in neuroprotection after ischemia reperfusion of rats .Methods:The SD rats were rando mly divided into several groups as follows:Sham operation group,Model group,1.0 ml/kg ICDP group(Low-dose,ICDP-L),2.5 ml/kg ICDP group(Middle-dose,ICDP-M),5 ml/kg ICDP group(High-dose,ICDP-H),and NF-κB inhibitor group(BAY11-7082).24 h after anesthetize,the volume of infarct sections in different groups were detected by TCC staining ,and the phosphorylated NF-κB expression in rats brain was observed by im-munohistochemistry and Western blot .Results:The TTC staining showed that different concentration of ICDP and BAY 11-7082 could reduce the brain infarction volume significantly .There was no significant different effect among the ICDP-H group,ICDP-M group and inhibitor group ,however ,the effect in these three groups was more effective than that in the ICDP-M group.In addition ,the results of im-munohistochemistry indicated that phosphorylated NF-κB p65 expressed in brain tissue located mainly at the nucleus neuronal cells in the CA1 region of hippocampusin model rats ,and the expression of phosphorylated NF-κB were significantly reduced inICDP groups and BAY11-7082 group.Conclusion: The ICDP can reduce brain infarct volume after ischemia reperfusion of rats .The neuralprotection mechanism of ICDP may relative toinhibits thehyperphosphorylation of NF-κB.
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Objective To use the whole-cell patch clamp recording to observe the effect of adenosine on hippocampus pyramidal neurons epileptiform discharge from lithium chloride-pilocarpine induced epileptic rats.Methods Twenty adult male and female SD rats (weighing about 200 g) were selected and were narcotized by 10％ chloral hydrate intraperitoneal injection.The whole brain was removed, then chopped into 350 μm thick slices.The brain slices were transferred to 37 ℃ preheated artificial cerebrospinal fluid for 1 h and then transferred to 23 ℃ for 30 min.Action potentials (AP) and evoked excitatory postsynaptic currents (eEPSCs) of brain slices neurons were recorded by whole-cell patch clamp, in addition, 25 μmol/L adenosine was used to observe its effect on AP and eEPSCs.Results With the application of current clamp technique, the application of adenosine (25 μmol/L) significandy decreased the numbers of AP in epileptic neurons (P ＜ 0.01) compared with the normal neurons ((0.50 ± 0.06) nA), and eEPSCs amplitude of epileptic neurons increased significantly ((1.44 ± 0.06) nA;independent sample t test, t =30.99, P ＜ 0.01) by voltage clamp.Bath application of adenosine (25 μmol/L) significantly reduced eEPSCs amplitude ((0.66 × 0.06) nA), while application of A1 receptor inhibitor DPCPX partially reversed this effect ((0.92 × 0.06) nA;one-way analysis of variance and q test, F =266.3, q =9.81, P ＜ 0.01).Conclusion Adenosine possesses a strong inhibitory effect on epileptic hippocampal brain slices discharge, which is mediated by its effect on eEPSCs.
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Objective To observe the phosphorylation level and nuclear translocation of signal transducer and activator of transcription factor-3 (STAT3) in hippocampal neurons induced by oxygen and glucose deprivation in vitro and discuss the dynamic changes of STAT3 signal pathway in an in vitro cell model of brain hypoxia and ischemia.Methods Hippocampal neurons from newly born SD rats (within 24 hours from birth) were cultured with DMEM/F12 for nine days,and then were transferred to oxygen and glucose deprivation environment for four hours to establish experimental cell models.The distribution of phosphorylated STAT3 (p-STAT3) in the hippocampal neurons in different groups was observed under laser scanning confocal microscope after immunofluorescence staining.Expression intensity of p-STAT3 at different time points after oxygen and glucose deprivation in the hippocampal neurons was detected by Western blotting.Results Expression of p-STAT3 was unobvious in the nucleus of the control group,but it was observed in the nucleus of the model group one hour after modeling,and peaked at three hour.Expression levels of p-STAT3 in the hippocampal neurons at each time point between the two groups showed significant difference (P ＜ 0.05).Conclusion Oxygen and glucose deprivation induces noticeable up-regulation of p-STAT3 in the hippocampal neuronal nucleus,which indicates the overactivation of signal transduction pathway of STAT3.
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Objective To observe the phosphorylation of extraceUular signal-regulated kinase (p-ERK1/2) and its nuclear translocation at different time points after the hippocampal neurons were cul-tured in the magnesium-free medium, and discuss the changes of ERK1/2 signal pathway after epileptic injury of hippocampal neurons. Methods Hippocampal neurons from newly-born Wistar rats were cul-tured with NB medium and B-27 for 9 days, and then were transferred to the magnesium-free medium to induce epileptic injury to the hippocampal neurons. The distribution of p-ERK1/2 in the hippocampal neurons before and after the epileptic injury was observed under laser scanning confocal microscope, and the expression of p-ERK1/2 at different time points after culturing the hippocampal neurons in the magne-sium-free medium was detected by Western blot. Results Before the epileptic injury of hippocampal neurons, p-ERK1/2 mainly expressed in the cytoplasm and axoplasm of the neurons. While after the epi-leptic injury, the expression of p-ERK1/2 was detected in the cytoplasm, axoplasm and nucleus of the neurons. The expression of p-ERK1/2 was increased one hour after the epileptic injury, and peaked at hour 3 (p-ERK1:2.2838±0.1 186; p-ERK2:4.1 273±0.0 927). There was significant difference in the expression of p-ERK1/2 between the hippocampal neurons cultured with or without magnesium-free medium (P < 0.05). Conclusion Epileptic injury may induce increased expression of p-ERK1/2 in hippocampal neurons, and the activated ERK1/2 signal pathway may be associated with the epileptic dis-charge in neurons.
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Objective:To establish an ex-vivo epileptic model by investigating hippocampal neurons epileptiform discharge induced by magnesium-free extracellular fluid. Methods:Neonatal Wistar rats(