PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
30414004-0	2019	GM1 Ameliorates Lead-Induced Cognitive Deficits and Brain Damage Through Activating the SIRT1/CREB/BDNF Pathway in the Developing Male Rat Hippocampus.	G(M1) Ganglioside	0-3	brain-derived neurotrophic factor	Rattus norvegicus	99-103	
31934908-14	2020	CONCLUSIONS: Our data suggest that the exogenous GM1 acts on BDNF signaling pathway to ameliorate the cognitive impairment and hippocampal apoptosis induced by ketamine in young rats.	G(M1) Ganglioside	49-52	brain-derived neurotrophic factor	Rattus norvegicus	61-65	
30414004-8	2019	Furthermore, we found that GM1 upregulated the expression of SIRT1, CREB phosphorylation, and BDNF, which underlie learning and memory in the lead-treated developing rat hippocampus.	G(M1) Ganglioside	27-30	brain-derived neurotrophic factor	Rattus norvegicus	94-98	
30414004-9	2019	In conclusion, our study demonstrated that GM1 exerts a protective effect on lead-induced cognitive deficits via antioxidant activity, preventing apoptosis, and activating SIRT1/CREB/BDNF in the developing rat hippocampus, implying a novel potential assistant therapy for lead poisoning.	G(M1) Ganglioside	43-46	brain-derived neurotrophic factor	Rattus norvegicus	183-187	
25453740-0	2015	Exogenous GM1 ganglioside increases accumbal BDNF levels in rats.	G(M1) Ganglioside	10-25	brain-derived neurotrophic factor	Rattus norvegicus	45-49	
25453740-4	2015	This study was performed to investigate the possibility that GM1 may induce changes in BDNF levels in the nucleus accumbens (NAc), a core structure in the brain"s reward circuitry, of rats submitted to three conditioning sessions with cocaine (10 mg/kg, i.p.).	G(M1) Ganglioside	61-64	brain-derived neurotrophic factor	Rattus norvegicus	87-91	
25453740-5	2015	The results demonstrate that GM1 administration, which showed no rewarding effect by itself in the CPP, induced a significant increase of BDNF protein levels in the NAc, which may account for the increased rewarding effect of cocaine shown in the CPP paradigm.	G(M1) Ganglioside	29-32	brain-derived neurotrophic factor	Rattus norvegicus	138-142	
16084500-3	2005	In situ, GM1 induced a rapid and transient activation of ERK1 and ERK 2 in both young and aged rats, and a similar effect was observed after stimulation with the neurotrophins NGF and BDNF.	G(M1) Ganglioside	9-12	brain-derived neurotrophic factor	Rattus norvegicus	184-188	
9849885-4	1998	The amount of associated GM1 decreased by about 33% also after concomitant treatment with phorbol ester and brain-derived neurotrophic factor, but in this case the neurotrophin was unable to enhance receptor tyrosine phosphorylation.	G(M1) Ganglioside	25-28	brain-derived neurotrophic factor	Rattus norvegicus	108-141	
8264958-4	1993	More importantly, subthreshold amounts of BDNF were rendered efficacious in the presence of ganglioside GM1: loss of tyrosine hydroxylase positive cells was reduced from 80% to only 20%.	G(M1) Ganglioside	104-107	brain-derived neurotrophic factor	Rattus norvegicus	42-46