PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
29342042-0	2018	Long-term Administration of Salicylate-induced Changes in BDNF Expression and CREB Phosphorylation in the Auditory Cortex of Rats.	Salicylates	28-38	brain-derived neurotrophic factor	Rattus norvegicus	58-62	
8724989-5	1996	Systemic administration of NGF, BDNF and bFGF, but not NT-3 attenuated MPP+ induced increases in hydroxyl radical generation as assessed by the conversion of salicylate to 2,3- or 2,5-dihydroxybenzoic acid (DHBA).	Salicylates	158-168	brain-derived neurotrophic factor	Rattus norvegicus	32-36	
29342042-1	2018	HYPOTHESIS: We investigated whether salicylate induces tinnitus through alteration of the expression levels of brain-derived neurotrophic factor (BDNF), proBDNF, tyrosine kinase receptor B (TrkB), cAMP-responsive element-binding protein (CREB), and phosphorylated CREB (p-CREB) in the auditory cortex (AC).	Salicylates	36-46	brain-derived neurotrophic factor	Rattus norvegicus	111-144	
29342042-6	2018	METHODS: Salicylate-induced tinnitus-like behavior in rats was confirmed using gap prepulse inhibition of acoustic startle and prepulse inhibition testing, followed by comparison of the expression levels of BDNF, proBDNF, TrkB, CREB, and p-CREB.	Salicylates	9-19	brain-derived neurotrophic factor	Rattus norvegicus	207-211	
29342042-8	2018	RESULTS: BDNF and p-CREB were upregulated along with ultrastructural changes at the synapses in the AC of rats treated chronically with salicylate (p < 0.05, compared with control group).	Salicylates	136-146	brain-derived neurotrophic factor	Rattus norvegicus	9-13	
29342042-10	2018	CONCLUSION: Long-term administration of salicylate increased BDNF expression and CREB activation, upregulated synaptic efficacy, and changed synaptic ultrastructure in the AC.	Salicylates	40-50	brain-derived neurotrophic factor	Rattus norvegicus	61-65	
26886762-9	2016	We observed that the GAP-43 expression, predominantly from medial olivocochlear (MOC) neurons, was significantly up-regulated, and that BDNF- and Iba-1-immunoreactive cells were persistently decreased after salicylate administration.	Salicylates	207-217	brain-derived neurotrophic factor	Rattus norvegicus	136-140	
18524887-0	2008	Midazolam reverses salicylate-induced changes in brain-derived neurotrophic factor and arg3.1 expression: implications for tinnitus perception and auditory plasticity.	Salicylates	19-29	brain-derived neurotrophic factor	Rattus norvegicus	49-82	
18524887-6	2008	Regardless of the mode of salicylate application, a common pattern became evident: 1) BDNF mRNA expression was increased in the spiral ganglion neurons of the cochlea; and 2) Arg3.1 expression was significantly reduced in the auditory cortex.	Salicylates	26-36	brain-derived neurotrophic factor	Rattus norvegicus	86-90	
18524887-7	2008	Local application of the GABA(A) receptor modulator midazolam resulted in the reversal not only of salicylate-induced changes in cochlear BDNF expression, but also in cortical Arg3.1 expression, indicating that the tinnitus-associated changes in cochlear BDNF expression trigger the decline of cortical Arg3.1 expression.	Salicylates	99-109	brain-derived neurotrophic factor	Rattus norvegicus	138-142	
18524887-7	2008	Local application of the GABA(A) receptor modulator midazolam resulted in the reversal not only of salicylate-induced changes in cochlear BDNF expression, but also in cortical Arg3.1 expression, indicating that the tinnitus-associated changes in cochlear BDNF expression trigger the decline of cortical Arg3.1 expression.	Salicylates	99-109	brain-derived neurotrophic factor	Rattus norvegicus	255-259