Spatiotemporal characteristics of astroglial death in the rat hippocampo-entorhinal complex following pilocarpine-induced status epilepticus.
Recently we reported that astroglial loss and subsequent gliogenesis in the dentate gyrus play a role in epileptogenesis following pilocarpine-induced status epilepticus (SE). In the present study we investigated whether astroglial damages in the hippocampo-entorhinal complex following SE are relevant to pathological or electrophysiological properties of temporal lobe epilepsy. Astroglial loss/damage was observed in the entorhinal cortex and the CA1 region at 4 weeks and 8 weeks after SE, respectively. These astroglial responses in the hippocampo-entorhinal cortex were accompanied by hyperexcitability of the CA1 region (impairment of paired-pulse inhibition and increase in excitability ratio). Unlike the dentate gyrus and the entorhinal cortex, CA1 astroglial damage was protected by conventional anti-epileptic drugs. alpha-Aminoadipic acid (a specific astroglial toxin) infusion into the entorhinal cortex induced astroglial damage and changed the electrophysiological properties in the CA1 region. Astroglial regeneration in the dentate gyrus and the stratum oriens of the CA1 region was found to originate from gliogenesis, while that in the entorhinal cortex and stratum radiatum of the CA1 region originated from in situ proliferation. These findings suggest that regional specific astroglial death/regeneration patterns may play an important role in the pathogenesis of temporal lobe epilepsy.
Kim
Duk-Soo
DS
Department of Anatomy and Neurobiology, College of Medicine, Hallym University, Chunchon 200-702, South Korea.
Kim
Ji-Eun
JE
Kwak
Sung-Eun
SE
Choi
Kyung-Chan
KC
Kim
Dae-Won
DW
Kwon
Oh-Shin
OS
Choi
Soo-Young
SY
Kang
Tae-Cheon
TC
D015074:2-Aminoadipic Acid / Q000633:toxicity; D000818:Animals; D001253:Astrocytes / Q000473:pathology*; D016923:Cell Death / Q000502:physiology; D049109:Cell Proliferation; D003292:Convulsants; D004195:Disease Models, Animal; D018450:Disease Progression; D018728:Entorhinal Cortex / Q000473:pathology / Q000503:physiopathology*; D004827:Epilepsy / Q000139:chemically induced / Q000473:pathology / Q000503:physiopathology*; D018691:Excitatory Amino Acid Antagonists / Q000633:toxicity; D006624:Hippocampus / Q000473:pathology / Q000503:physiopathology*; D008297:Male; D008564:Membrane Potentials / Q000502:physiology; D009433:Neural Inhibition / Q000502:physiology; D010862:Pilocarpine; D051381:Rats; D017207:Rats, Sprague-Dawley; D012038:Regeneration / Q000502:physiology; D013226:Status Epilepticus / Q000139:chemically induced / Q000473:pathology / Q000503:physiopathology*; D013997:Time Factors
D003292:Convulsants; D018691:Excitatory Amino Acid Antagonists; D010862:Pilocarpine; D015074:2-Aminoadipic Acid