PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 11334998-3 2001 In addition to this, TH induction and DA plus DOPAC production was observed in foetal human and rat cerebral cortex by using glial-cell derived neurotrophic factor (GDNF) in place of BDNF. 3,4-Dihydroxyphenylacetic Acid 46-51 glial cell derived neurotrophic factor Rattus norvegicus 125-163 11277973-9 2001 GDNF pretreatment also protected against 6-hydroxydopamine-induced reductions in striatal DOPAC levels in all age groups. 3,4-Dihydroxyphenylacetic Acid 90-95 glial cell derived neurotrophic factor Rattus norvegicus 0-4 11334998-3 2001 In addition to this, TH induction and DA plus DOPAC production was observed in foetal human and rat cerebral cortex by using glial-cell derived neurotrophic factor (GDNF) in place of BDNF. 3,4-Dihydroxyphenylacetic Acid 46-51 glial cell derived neurotrophic factor Rattus norvegicus 165-169 9449424-7 1997 Consistent with the behavioral changes, levels of DA and the metabolite dihydroxyphenylacetic acid (DOPAC) were elevated (by 98% and 65%, respectively) in the SN, but not the striatum of Ad-GDNF-injected rats. 3,4-Dihydroxyphenylacetic Acid 100-105 glial cell derived neurotrophic factor Rattus norvegicus 190-194 11085315-9 2000 Basal levels of DOPAC and HVA were also elevated on the GDNF-treated side of the brain. 3,4-Dihydroxyphenylacetic Acid 16-21 glial cell derived neurotrophic factor Rattus norvegicus 56-60 9753113-8 1998 Post-mortem neurochemical analysis at 13 weeks after surgery found that GDNF significantly inhibited 6-OHDA-induced loss of dopamine, 3,4-dihydroxyphenylacetic acid and homovanillic acid in the ipsilateral striatum. 3,4-Dihydroxyphenylacetic Acid 134-164 glial cell derived neurotrophic factor Rattus norvegicus 72-76 11085910-4 2000 In the 10 microgram GDNF-treated rats, there was a significant increase in the peak DA output in response to the second versus first K(+) infusion, a significant increase in both basal and overall K(+)-evoked DOPAC responses, and significantly increased striatal DA and DOPAC contents compared with vehicle- or 1 microgram GDNF-treated rats. 3,4-Dihydroxyphenylacetic Acid 209-214 glial cell derived neurotrophic factor Rattus norvegicus 20-24 11085910-4 2000 In the 10 microgram GDNF-treated rats, there was a significant increase in the peak DA output in response to the second versus first K(+) infusion, a significant increase in both basal and overall K(+)-evoked DOPAC responses, and significantly increased striatal DA and DOPAC contents compared with vehicle- or 1 microgram GDNF-treated rats. 3,4-Dihydroxyphenylacetic Acid 270-275 glial cell derived neurotrophic factor Rattus norvegicus 20-24 9449424-9 1997 These results suggest that virally delivered GDNF promotes the recovery of nigral dopaminergic tone (i.e.: increased DA and DOPAC levels) and improves behavioral performance (i.e.: decreased rotations, increased locomotion) in rodents with extensive nigrostriatal dopaminergic denervation. 3,4-Dihydroxyphenylacetic Acid 124-129 glial cell derived neurotrophic factor Rattus norvegicus 45-49 9262339-3 1997 In vivo microdialysis studies showed that basal extracellular levels of dopamine (DA) and its metabolites, 3,4-dihydroxyphenylacetic acid and homovanillic acid, were significantly increased in the striatum of the GDNF-treated rats. 3,4-Dihydroxyphenylacetic Acid 107-137 glial cell derived neurotrophic factor Rattus norvegicus 213-217 9042532-8 1997 GDNF significantly increased striatal (approximately 28%) and nigral (up to 40%) dopamine, as well as regulated the dopamine metabolites homovanillic acid and dihydroxyphenylacetic acid. 3,4-Dihydroxyphenylacetic Acid 159-185 glial cell derived neurotrophic factor Rattus norvegicus 0-4