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Objective To study the effects of transcranial magnetic stimulation (TMS) on learning and memory, and angiogenesis and the dendritic structure of hippocampal CA3 pyramidal neurons after cerebral infarction. Methods Forty-eight male Sprague-Dawley rats were divided into a sham operated group, a model group and a TMS group (n = 16). Rat models of focal cerebral infarction were established with unilateral middle cerebral artery (MCA) suture occlusion in the model and TMS groups. The rats of the TMS group were given 4 weeks of TMS treatment beginning 1 day after the infarction (2 times per day, 30 pulses per time). Their learning and memory abilities were tested with a Y-maze. Angiogenesis and the dendritic structure of their hippocampal CA3 pyramidal neurons were detected after 4 weeks. Results Compared with the model group, learning and memory improved significantly in the TMS group. The average microvessel density of the hippocampus in the TMS group was significantly more than in the model group. The total length of apical dendrites of hippocampal CA3 pyramidal neurons in TMS group was significantly longer than in the model group. Conclusions The improved learning and memory observed following TMS treatment are likely to be related to changes in angiogenesis, the dendritic.structure of the hippocampal CA3 pyramidal neurons, and enhanced synaptic plasticity.
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ObjectiveTo investigate the role of N-methyl-D-aspartate receptor subunit 2B (NR2B) antagonist CP-101.606 in behaviour and expression of related signal proteins in a rat model of levodopa-induced motor complications.MethodsThe hemi-parkinsonian rat model was produced by injecting stereotaxically 6-OHDA to right medial forebrain bundle.Then,rats were intraperitoneally treated with levodopa (50 mg/kg with benserazide 12.5 mg/kg,twice daily) for 22 days.On 23th day,rats received CP-101.606 before levodopa administration.Rotational duration was estimated.After sacrificed,phosphorylated NR2B and Ca2+/calmodulin-dependent protein kinase Ⅱ (CaMKⅡ) and glutamate receptor 1 ( GluR1S831 ) were observed by western blot.ResultsThe results showed that NR2B antagonist CP-101.606 reversed the levodopa-induced shortened rotational duration.Chronic levodopa treatment increased abundance of the phosphorylated NR2B and downstream related signal proteins CaMKⅡ and GluR1S831 to (145.3±6.5)％ and (132.5±5.7)％ and (105.6±6.3)％,respectively.Moreover,CP-101.606 could reduce hyperphosphorylation of NR2B and CaMKⅡ and GluR1 S831 to (102 ± 4.9 )％,(98.4±3.9)％ and (49.5 ± 4.2 )％,respectively.ConclusionsThese results indicate that the enhancement of N-methyl-D-aspartate (NMDA) receptor function mediated by NR2B phosphorylation contribute to development of motor complications,through a mechanism that involved the downstream signal mediators of NMDA receptor overactivation.Pharmaceuticals which act to inhibit NR2B may be useful in the treatment of the motor complications in parkinsonian patients.
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Objective To investigate the alteration of phosphorylated GluR1Ser831 and behavioural effects in a rat model of levodopa-induced motor complications after Ca2 +/calmodulin-dependent protein kinase Ⅱ (CaMKⅡ) inhibitor KN-93 treatment. Methods The hemi-parkinsonian rat model was produced by injecting stereotaxically 6-OHDA to right medial forebrain bundle. Then, rats were intraperitoneally treated with levodopa ( 50 mg/kg with benserazide 12.5 mg/kg,twice daily) for 22 days. On day 23 ,rats received KN-93 before levodopa administration. Rotational duration was estimated. After sacrificed, subcellualr distribution of GluR1 and phosphorylated GluR1Ser831 were observed by western blot. Results The study showed that CaMKⅡ inhibitor KN-93 prolonged rotational duration. Moreover, KN-93 could regulate subcellular distribution of GluR1 and reduce hyperphosphorylation of GluR1 Ser831, which was closely associated with levodopa-induced motor complications. The expression of membrane GluR1 and phosphorylated GluR1Ser831 was (83.4 ±4.2)% and (47.2 ±5.2)% ,respectively. Conclusions These results indicated that activation of CaMKⅡ contributed to development of motor complications, through a mechanism that involved an increase in phosphorylated GluR1 Ser831. Pharmaceuticals which act to inhibit CaMKⅡ may be useful in the treatment of the motor complications in parkinsonian patients.
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Objective To study the clinical characteristics of epidemic Japanese encephalitis in 4 adult patients and to improve the level of diagnosis.Methods The clinical characteristics, laboratory results and MRI features of 4 adult patients with epidemic Japanese encephalitis hospitalized in our hospital between 2007 and 2008 was retrospectively reviewed and analyzed.Results All patients were sporadic.Two were female and others were male with the age from 34 to 68 years old and onset in summer and autumn.One patient had diarrhea at onset while others had fever and headache at onset.All patients had high fever and psychiatric symptoms.Two patients had respiratory failure.Obvious elevation of white cells in cerebrospinal fluid was seen in all patients and Japanese viral antibody of IgM was all positive whereas the image of MRI was abnormal only in one patient.Two patients had neurological sequelae.Conclusions The clinical manifestations of epidemic Japanese encephalitis in adults are severe and untypical and the respiratory failure is likely to occur.