Morpho-physiologic characteristics of dorsal subicular network in mice after pilocarpine-induced status epilepticus.
The goal of this study was to examine the morpho-physiologic changes in the dorsal subiculum network in the mouse model of temporal lobe epilepsy using extracellular recording, juxtacellular and immunofluorescence double labeling, and anterograde tracing methods. A significant loss of total dorsal subicular neurons, particularly calbindin, parvalbumin (PV) and immunopositive interneurons, was found at 2 months after pilocarpine-induced status epilepticus (SE). However, the sprouting of axons from lateral entorhinal cortex (LEnt) was observed to contact with surviving subicular neurons. These neurons had two predominant discharge patterns: bursting and fast irregular discharges. The bursting neurons were mainly pyramidal cells, and their dendritic spine density and bursting discharge rates were increased significantly in SE mice compared with the control group. Fast irregular discharge neurons were PV-immunopositive interneurons and had less dendritic spines in SE mice when compared with the control mice. When LEnt was stimulated, bursting and fast irregular discharge neurons had much shorter latency and stronger excitatory response in SE mice compared with the control group. Our results illustrate that morpho-physiologic changes in the dorsal subiculum could be part of a multilevel pathologic network that occurs simultaneously in many brain areas to contribute to the generation of epileptiform activity.
He
De Fu
DF
Epilepsy Research Lab, National Neuroscience Institute, 11 Jalan Tan Tock Seng, Singapore, Singapore.
Ma
Dong Liang
DL
Tang
Yong Cheng
YC
Engel
Jerome
J
Bragin
Anatol
A
Tang
Feng Ru
FR
D000818:Animals; D001522:Behavior, Animal / Q000187:drug effects; D064032:Calbindin 2; D064026:Calbindins; D004268:DNA-Binding Proteins; D003627:Data Interpretation, Statistical; D003712:Dendrites / Q000473:pathology; D049229:Dendritic Spines / Q000473:pathology; D004594:Electrophysiology; D018728:Entorhinal Cortex / Q000473:pathology; D004833:Epilepsy, Temporal Lobe / Q000139:chemically induced / Q000473:pathology; D005260:Female; D005455:Fluorescent Antibody Technique; D006624:Hippocampus / Q000473:pathology*; D007150:Immunohistochemistry; D008297:Male; D051379:Mice; D018721:Muscarinic Agonists; D009415:Nerve Net / Q000473:pathology*; D009419:Nerve Tissue Proteins / Q000096:biosynthesis; D009434:Neural Pathways / Q000473:pathology; D009474:Neurons / Q000473:pathology; D009687:Nuclear Proteins / Q000096:biosynthesis; D010320:Parvalbumins / Q000096:biosynthesis; D010835:Phytohemagglutinins; D010862:Pilocarpine; D064030:S100 Calcium Binding Protein G / Q000096:biosynthesis; D013226:Status Epilepticus / Q000139:chemically induced* / Q000473:pathology* / Q000523:psychology
D064032:Calbindin 2; D064026:Calbindins; D004268:DNA-Binding Proteins; D018721:Muscarinic Agonists; D009419:Nerve Tissue Proteins; C492380:NeuN protein, mouse; D009687:Nuclear Proteins; D010320:Parvalbumins; D010835:Phytohemagglutinins; D064030:S100 Calcium Binding Protein G; C100156:leukoagglutinins, plants; D010862:Pilocarpine