PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
8931001-11	1996	Our results show that GDNF specifically protects a subpopulation of striatal calbindin-immunoreactive neurons against quinolinate lesion, suggesting that GDNF administration may have a potential therapeutic application in the prevention and treatment of striatonigral degenerative disorders.	Quinolinic Acid	118-129	calbindin 1	Rattus norvegicus	77-86	
10585160-3	1999	Immunohistochemical studies showed a total loss of calbindin immunoreactivity, a known marker of GABAergic striatal projection neurons, throughout the full extent of the quinolinic acid lesion within 24 h. Similarly, within 24 h, there was a total loss of somatostatin/neuropeptide Y cells in the centre of the lesion but in the periphery of the lesion these cells remained unaltered at all survival times.	Quinolinic Acid	170-185	calbindin 1	Rattus norvegicus	51-60	
10585160-7	1999	This study shows that following quinolinic acid lesions of the striatum there is a major loss of calbindin and somatostatin/neuropeptide Y immunoreactive cells in the striatum within 24 h, and a marked increase in GABA(A) receptors in the substantia nigra within 2 h. These findings are similar to the changes in the basal ganglia in Huntington"s disease and provide further evidence supporting the use of the quinolinic acid lesioned rat as an animal model of Huntington"s disease.	Quinolinic Acid	32-47	calbindin 1	Rattus norvegicus	97-106	
7777157-7	1995	In the rat brain, two weeks after intrastriatal injection of quinolinic acid (6-20 ng), surviving medium-spiny neurons in the transition zone around the lesion core exhibited a marked increase in calbindin immunoreactivity similar to that seen in Huntington"s disease spiny neurons.	Quinolinic Acid	61-76	calbindin 1	Rattus norvegicus	196-205	
7777157-10	1995	In 12 day old postnatal striatal cultures, 2-6 h exposures to quinolinic acid (0.5 mM) significantly increased the length of neurites exhibiting calbindin immunoreactivity when compared to untreated controls.	Quinolinic Acid	62-77	calbindin 1	Rattus norvegicus	145-154	
7523988-0	1994	Chronic intrastriatal quinolinic acid produces reversible changes in perikaryal calbindin and parvalbumin immunoreactivity.	Quinolinic Acid	22-37	calbindin 1	Rattus norvegicus	80-89	
7523988-3	1994	The present findings show that chronic dialytic delivery of quinolinic acid also produces a Huntington"s disease-like pattern of reduced calbindin and parvalbumin perikaryal immunoreactivity that is reversed in rats allowed four to eight weeks" recovery after cessation of quinolinic acid.	Quinolinic Acid	60-75	calbindin 1	Rattus norvegicus	137-146	
7523988-5	1994	These results suggest that changes in calbindin and parvalbumin perikaryal immunoreactivity provide a relatively sensitive measure of quinolinic acid induced neurotoxicity.	Quinolinic Acid	134-149	calbindin 1	Rattus norvegicus	38-47	
1829975-2	1991	The results showed that both ibotenic acid and quinolinic acid affected calbindin and parvalbumin cells to the same extent.	Quinolinic Acid	47-62	calbindin 1	Rattus norvegicus	72-81