title: Neuropeptide Y and somatostatin participate differently in the seizure-generating mechanisms following trimethyltin-induced hippocampal damage.
abstract: Trimethyltin (TMT) is an organic metal known to induce neuronal degeneration in the hippocampus, and abnormal behavior characterized by seizures, increased aggression and memory deficits. We administered TMT to rats and studied the changes of neuropeptide Y (NPY) and somatostatin (SOM) in the hippocampus. Phenobarbital (PB) was administered as an anticonvulsant to assess the effect of seizures on neuropeptide expressions in both dorsal and ventral hippocampus. Histochemically, NPY-immunoreactivity increased 4 days after TMT treatment in the hilus of the hippocampus, then progressively decreased and dropped to a level below control 16 days after TMT treatment. Detection of NPY mRNA by in situ hybridization preceded the detection of NPY by immunohistochemistry. NPY mRNA signals increased in the hilus 2 days after TMT treatment. SOM-immunoreactivity also increased in the hilus of the hippocampus 2 days after TMT treatment, then decreased rapidly to a normal level. Similar changes in SOM mRNA were demonstrated by in situ hybridization. PB treatment significantly inhibited changes of NPY in terms of both immunoreactivity and mRNA expression; however, the same treatment failed to affect changes in SOM expression. This suggests that NPY and SOM act by different mechanisms in TMT-induced neurodegeneration.
authors.affiliation: Division of Cortical Function Disorders, National Institute of Neuroscience, NCNP, 4-1-1 Ogawahigashi, Kodaira, 187-8502, Tokyo, Japan.
authors.forename: Nako
authors.initials: N
authors.lastname: Ishikura
authors.forename: Koichi
authors.initials: K
authors.lastname: Tsunashima
authors.forename: Kei ichiro
authors.initials: Ki
authors.lastname: Watanabe
authors.forename: Tsutomu
authors.initials: T
authors.lastname: Nishimura
authors.forename: Yoshio
authors.initials: Y
authors.lastname: Minabe
authors.forename: Nobumasa
authors.initials: N
authors.lastname: Kato
mesh_terms: D000818:Animals; D000927:Anticonvulsants / Q000494:pharmacology; D048588:Benzoxazines; D002452:Cell Count; D004396:Coloring Agents; D006624:Hippocampus / Q000187:drug effects / Q000378:metabolism / Q000473:pathology*; D007150:Immunohistochemistry; D017403:In Situ Hybridization; D008297:Male; D009478:Neuropeptide Y / Q000096:biosynthesis / Q000502:physiology*; D010078:Oxazines; D010634:Phenobarbital / Q000494:pharmacology; D012333:RNA, Messenger / Q000096:biosynthesis; D051381:Rats; D017207:Rats, Sprague-Dawley; D012640:Seizures / Q000139:chemically induced* / Q000503:physiopathology*; D013004:Somatostatin / Q000096:biosynthesis / Q000502:physiology*; D014298:Trimethyltin Compounds / Q000633:toxicity*
chemical_list: D000927:Anticonvulsants; D048588:Benzoxazines; D004396:Coloring Agents; D009478:Neuropeptide Y; D010078:Oxazines; D012333:RNA, Messenger; D014298:Trimethyltin Compounds; C046488:trimethyltin; C028911:cresyl violet; D013004:Somatostatin; D010634:Phenobarbital