PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
9330376-3	1997	(1) Morphologically, trimethyltin produced a progressive loss of hippocampal CA3 and CA4 pyramidal cells, starting from four days after peroral treatment with trimethyltin hydroxide (9 mg/kg), as described previously.	trimethyltin	21-33	carbonic anhydrase 3	Rattus norvegicus	77-80	
11520118-3	2001	Peroral administration of a single dose of TMT (9 mg/kg body wt) induced the extensive loss of CA3 pyramidal neurons and reactive astrocytosis in the hippocampus, as evidenced by results of vimentin and glial fibrillary acidic protein immunohistochemistry, and the effects were profoundly exacerbated by bilateral adrenalectomy.	trimethyltin	43-46	carbonic anhydrase 3	Rattus norvegicus	95-98	
9330376-8	1997	(4) Neurochemically, trimethyltin treatment caused changes of neurochemical markers, which were manifested by the elevation of neuropeptide Y content in the entorhinal cortex, and of choline acetyltransferase in the hippocampal CA3 subfield.	trimethyltin	21-33	carbonic anhydrase 3	Rattus norvegicus	228-231	
12490135-9	2002	The above results were substantiated by histological experiments, revealing that Ampakine treatment prevented TMT-induced cell loss in CA3 and DG.	trimethyltin	110-113	carbonic anhydrase 3	Rattus norvegicus	135-138	
19083469-4	2008	Peroral administration of a single dose of trimethyltin (8.5 mg/kg) induced spatial memory loss and the extensive loss of CA3 pyramidal neurons in hippocampi, as indicated by the results of a Morris water maze task and histologic examination, respectively.	trimethyltin	43-55	carbonic anhydrase 3	Rattus norvegicus	122-125