title: Selective loss and axonal sprouting of GABAergic interneurons in the sclerotic hippocampus induced by LiCl-pilocarpine.
abstract: In this study, we performed immunohistochemistry for somatostatin (SS), neuropeptide Y (NPY), and parvalbumin (PV) in LiCl-pilocarpine-treated rats to observe quantitative changes and axonal sprouting of GABAergic interneurons in the hippocampus, especially in the sclerotic hippocampus. Fluoro-Jade B (FJB) was performed to detect the specific degeneration of GABAergic interneurons. Compared with age-matched control rats, there were fewer SS/NPY/PV-immunoreactive (IR) interneurons in the hilus of the sclerotic hippocampus in pilocarpine-treated rats; hilar dentritic inhibitory interneurons were most vulnerable. FJB stain revealed degeneration was evident at 2 months after status epilepticus. Some SS-IR and NPY-IR interneurons were also stained for FJB, but there was no evidence of degeneration of PV-IR interneurons. Axonal sprouting of GABAergic interneurons was present in the hippocampus of epileptic rats, and a dramatic increase of SS-IR fibers was observed throughout all layers of CA1 region in the sclerotic hippocampus. These results confirm selective loss and degeneration of a specific subset of GABAergic interneurons in specific subfields of the hippocampus. Axonal sprouting of inhibitory GABAergic interneurons, especially numerous increase of SS-IR neutrophils within CA1 region of the sclerotic hippocampus, may constitute the aberrant inhibitory circum and play a significant role in the generation and compensation of temporal lobe epilepsy.
authors.affiliation: Department of Neurology, Xiangya Hospital, Central South University, Changsha, Hunan, China.
authors.forename: Lili
authors.initials: L
authors.lastname: Long
authors.forename: Bo
authors.initials: B
authors.lastname: Xiao
authors.forename: Li
authors.initials: L
authors.lastname: Feng
authors.forename: Fang
authors.initials: F
authors.lastname: Yi
authors.forename: Guoliang
authors.initials: G
authors.lastname: Li
authors.forename: Shuyu
authors.initials: S
authors.lastname: Li
authors.forename: M Abuhamed
authors.initials: MA
authors.lastname: Mutasem
authors.forename: Si
authors.initials: S
authors.lastname: Chen
authors.forename: Fangfang
authors.initials: F
authors.lastname: Bi
authors.forename: Yi
authors.initials: Y
authors.lastname: Li
mesh_terms: D000818:Animals; D001369:Axons / Q000473:pathology*; D004195:Disease Models, Animal; D006624:Hippocampus / Q000187:drug effects / Q000378:metabolism / Q000473:pathology*; D007395:Interneurons / Q000378:metabolism / Q000473:pathology*; D018021:Lithium Chloride; D008297:Male; D009410:Nerve Degeneration / Q000378:metabolism*; D009478:Neuropeptide Y / Q000378:metabolism; D010320:Parvalbumins / Q000378:metabolism; D010862:Pilocarpine; D051381:Rats; D017207:Rats, Sprague-Dawley; D012598:Sclerosis / Q000139:chemically induced / Q000378:metabolism / Q000473:pathology*; D013004:Somatostatin / Q000378:metabolism; D013226:Status Epilepticus / Q000139:chemically induced / Q000378:metabolism / Q000401:mortality / Q000473:pathology*; D005680:gamma-Aminobutyric Acid / Q000378:metabolism*
chemical_list: D009478:Neuropeptide Y; D010320:Parvalbumins; D010862:Pilocarpine; D013004:Somatostatin; D005680:gamma-Aminobutyric Acid; D018021:Lithium Chloride