Optogenetic control of perforant pathway kindled seizures by photoinhibition of CA3 after insertion of Jaws into CA3 neuronal cells.

Medial temporal lobe epilepsy (MTLE) is among the most common and most drug-resistant types of epilepsies associated with remodeling of the trisynaptic circuit of the hippocampus. The cornu ammonis (CA)3 region, as the "pacemaker" of the circuit, and CA3 → CA1 synapse (Schaffer collaterals) are potential targets for suppression of MTLE. We examined optogenetic manipulation of CA3 neurons in controlling the perforant pathway kindled seizures.

The Lentiviral Vector Pseudotyped by Modified Rabies Glycoprotein Does Not Cause Reactive Gliosis and Neurodegeneration in Rat Hippocampus.

Background: A human immunodeficiency virus type 1 (HIV-1)-based lentiviral vector (LV) pseudotyped by a variant of rabies envelope glycoprotein, FUG-B2, has previously been prepared and used in transfection of hippocampal CA1 ("Cornu Ammonis" area 1) neurons. This study aimed to verify reactive gliosis and neuronal damage after injection of the vector into the rat hippocampus.

Methods: HEK 293T cells were transfected with transfer (fck-Jaws-GFP-ER2), envelope (FUG-B2), and packaging (pMDLg/pRRE, pRSV-Rev) plasmids, and the vector was injected into CA1 of the rat hippocampus.

Transduction efficacy and retrograde movement of a lentiviral vector pseudotyped by modified rabies glycoprotein throughout the trisynaptic circuit of the rat hippocampus.

Background: The trisynaptic circuit (entorhinal cortex-dentate gyrus-CA3-CA1) is a key unidirectional network in the hippocampus. Damage to the hippocampus interrupts this circuit and causes neurological disorders. Efficient delivery of therapeutic genes into this network is of great interest with respect to treating trisynaptic circuit pathologies.