Leucine-rich glioma inactivated 1 (LGI1) is a soluble secreted protein which links Adam22/23 proteins across the synaptic cleft and is also abundant in the axon initial segments of in the hippocampus. Anti-LGI1 autoantibodies have been found in CSF and serum of acquired epilepsy patients with symptoms of limbic encephalitis with amnesia and seizures. Previous studies showed human LGI1 autoantibodies co-precipitated with voltage-gated (VG) potassium channel complexes in rodent tissue. As VG-ion channels help maintain homeostasis in hippocampal action potentials, dysregulation of these channels may be causal in triggering LGI1 autoantibody-induced neuropathophysiology. Our aim is to detect changes in either the distribution or numbers of VG-ion channels when mice are exposed to LGI1 autoantibodies. In mice injected with monoclonal LGI1-antibody into the hippocampus, epileptic seizures were induced, while no symptoms were observed in mice injected with control antibody. Immunolabeling of replicas with colloidal gold antibodies quantified Cav2.1 calcium channels and Kv1.1 potassium channels in axon initial segments and mossy fiber active zones (AZ). Results showed that Cav2.1 was slightly reduced in AZ of LGI1-autoantibody-injected animals, compared to controls, while Kv1.1 density was low in both groups. This suggests that Cav2.1 and Kv1.1 may not be causing mossy fiber hyperactivity at synapses. However, a significant reduction in synaptic vesicle numbers was observed in mossy fiber boutons in LGI1-autoantibody-injected mice with epilepsy symptoms compared to controls. This shows that our model will be useful in investigating if alteration of ion channels trigger hyperexcitability of neurons and contributing to epilepsy in LGI1 autoimmune encephalitis.