کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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6022565 | 1580687 | 2012 | 6 صفحه PDF | دانلود رایگان |
The functional effects of cerebrospinal fluid (CSF) from patients with anti-NMDA receptor (NMDAR) encephalitis on the NMDAR-mediated synaptic plasticity were evaluated by using mouse hippocampus slices. Anti-NMDAR antibody detection system was established by immunostaining recombinant NMDAR heteromers expressed in HEK cell culture as well as native NMDARs in cultured hippocampal neurons. Under a complete blind manner for the clinical information, CSF and sera collected from 36 pre-diagnosed patients were tested for anti-NMDAR antibodies. With this test, thirteen patients were diagnosed as anti-NMDAR encephalitis. CSF positive for anti-NMDAR antibodies suppressed induction of long-term potentiation (LTP) at Schaffer collateral-CA1 synapses in mouse hippocampal slices. LTP induction was not suppressed by CSF collected from herpes simplex virus (HSV) encephalitis or non-encephalitis control patients. Antibody absorption with NMDAR-expressing HEK cell culture reversed the suppression of LTP by anti-NMDAR encephalitis patients' CSF, confirming that anti-NMDAR antibodies suppressed LTP. The present experiments firmly support the proposal that the anti-NMDAR encephalitis autoantibody is responsible for cognitive disorders like amnesia accompanying this disease.
⺠Cerebrospinal fluid was collected from anti-NMDAR encephalitis patients with amnesia as a symptom. ⺠Presence of anti-NMDAR antibodies in the fluid was confirmed. ⺠Application of the fluid suppressed long-term potentiation in mouse hippocampal slices. ⺠Antibody absorption from the fluid reversed the suppression of long-term potentiation. ⺠Anti-NMDAR autoantibody is likely to be responsible for amnesia accompanying this disease.
Journal: Neurobiology of Disease - Volume 45, Issue 1, January 2012, Pages 610-615