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 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 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 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 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