title: Preferential interneuron survival in the transition zone of 3-NP-induced striatal injury in rats.
abstract: Histology, immunohistochemistry, and Western blotting were used to characterize the changes in morphology, distribution pattern, and marker protein expression of striatal interneurons in the transition zone of striatal injury induced by 3-NP. The 3-NP treatment in rats yielded movement, motor coordination, and cognitive dysfunction. The 3-NP-induced lesion core was unvaryingly in the dorsolateral striatum, with a transition zone of lesser damage around the lesion core, in which medium-sized neurons were significantly decreased in abundance, but larger neurons survived. In both the transition zone and the lesion core, many TUNEL-positive cells negative for the interneuron markers were detected, indicating widespread projection neuron death. Immunohistochemical staining for the four interneuron types (parvalbuminergic, cholinergic, calretinergic, and neuropeptide Y-neuronal nitric oxide synthase cocontaining) showed that few immunolabeled interneurons were observed in the lesion core, but interneuron perikarya showed no evident loss in the transition zone. Consistently with this, Western blotting showed that the five interneuron protein markers were significantly decreased in the striatum after 3-NP treatment. Transition-zone calretinergic and neuropeptide Y-neuronal nitric oxide synthase-cocontaining interneurons, however, possessed more processes and varicosities than normal. These results show that, although striatal interneurons survive in the transition zone after 3-NP-mediated striatal injury, they have enhanced marker protein levels in their processes.
authors.affiliation: Department of Anatomy, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, China.
authors.forename: Shuhua
authors.initials: S
authors.lastname: Mu
authors.forename: Lisi
authors.initials: L
authors.lastname: OuYang
authors.forename: Bingbing
authors.initials: B
authors.lastname: Liu
authors.forename: Yaxi
authors.initials: Y
authors.lastname: Zhu
authors.forename: Keyi
authors.initials: K
authors.lastname: Li
authors.forename: Mali
authors.initials: M
authors.lastname: Zhan
authors.forename: Zongwei
authors.initials: Z
authors.lastname: Liu
authors.forename: Yu
authors.initials: Y
authors.lastname: Jia
authors.forename: Wanlong
authors.initials: W
authors.lastname: Lei
authors.forename: A
authors.initials: A
authors.lastname: Reiner
mesh_terms: D000818:Animals; D002470:Cell Survival / Q000187:drug effects / Q000502:physiology; D003342:Corpus Striatum / Q000378:metabolism / Q000473:pathology*; D004195:Disease Models, Animal; D006816:Huntington Disease / Q000378:metabolism / Q000473:pathology*; D007395:Interneurons / Q000187:drug effects / Q000378:metabolism / Q000473:pathology*; D008297:Male; D009410:Nerve Degeneration / Q000139:chemically induced / Q000473:pathology*; D009498:Neurotoxins / Q000633:toxicity*; D009574:Nitro Compounds / Q000633:toxicity*; D011422:Propionates / Q000633:toxicity*; D051381:Rats; D017207:Rats, Sprague-Dawley; D011930:Reaction Time / Q000187:drug effects / Q000502:physiology
chemical_list: D009498:Neurotoxins; D009574:Nitro Compounds; D011422:Propionates; C015392:3-nitropropionic acid