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Hippocampal Neuronal Cultures to Detect and Study New Pathogenic Antibodies Involved in Autoimmune Encephalitis
Published on: June 2, 2022
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Hippocampal epileptogenesis in autoimmune encephalitis
Michele Romoli1,2, Paraskevi Krashia3,4, Arjune Sen5,6
1Neurology Clinic, Department of Medicine, University of Perugia, Perugia, Italy.
Annals of Clinical and Translational Neurology
|October 17, 2019
Summary
Autoantibodies targeting LGI1 and CASPR2 increase hippocampal neuron excitability, leading to epileptiform activity in encephalitis. GABAB R antibodies did not affect neuronal function in this study.
Area of Science:
- Neuroscience
- Immunology
- Pathophysiology
Background:
- Autoantibody-mediated encephalitis (AE) causes neurological disorders with seizures.
- The electrophysiological impact of AE autoantibodies on neurons is poorly understood.
Purpose of the Study:
- To investigate the epileptogenic potential of autoantibodies found in AE.
- To assess the effects of CSF containing specific autoantibodies on hippocampal neuron function.
Main Methods:
- CSF from AE patients with LGI1, CASPR2, or GABAB R antibodies were stereotactically inoculated into mouse hippocampi.
- Ex vivo electrophysiology, including whole-cell patch-clamp and extracellular recordings, was performed on hippocampal neurons.
Main Results:
- CSF with LGI1 and CASPR2 antibodies increased glutamate release and induced epileptiform activity.
- CASPR2 antibodies also increased spontaneous firing in CA1 pyramidal neurons.
- CSF with GABAB R antibodies did not alter intrinsic neuronal activity or field potentials.
Conclusions:
- Antibodies against LGI1 and CASPR2 enhance hippocampal neuron excitability, contributing to epileptogenesis in AE.
- These findings offer in vivo insights into the mechanisms of neuronal dysfunction in AE.
