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Loss\u2010of\u2010function mutations in parkin are the major cause of the early onset familial form of the disease. Although rodents deficient in parkin (parkin<jats:sup>(\u2212\/\u2212)<\/jats:sup>) have some dopaminergic system dysfunction associated with central oxidative stress and energy metabolism deficiencies, these animals only display nigrostriatal pathway degeneration under inflammatory conditions. This study investigated the impact of the inflammatory stimulus induced by lypopolisaccharide (LPS) on tetrahydrobiopterin (BH4) synthesizing enzymes (de novo and salvage pathways), since this cofactor is essential for dopamine synthesis. The mitochondrial content and architecture was investigated in the striatum of LPS\u2010exposed parkin<jats:sup>(\u2212\/\u2212)<\/jats:sup> mice. As expected, the LPS (0.33\u2009mg\/kg; i.p.) challenge compromised spontaneous locomotion and social interaction with juvenile parkin<jats:sup>(\u2212\/\u2212)<\/jats:sup> and WT mice. Moreover, the genotype impacted the kinetics of the investigation of the juvenile. The inflammatory scenario did not induce apparent changes in mitochondrial ultrastructure; however, it increased the quantity of mitochondria, which were of smaller size, and provoked the perinuclear distribution of the organelle. Furthermore, the BH4 de novo biosynthetic pathway failed to be up\u2010regulated in the LPS challenge, a well\u2010known stimulus for its activation. The LPS treatment increased sepiapterin reductase (SPR) expression, suggesting compensation by the salvage pathway. This might indicate that dopamine synthesis is compromised in parkin<jats:sup>(\u2212\/\u2212)<\/jats:sup> mice under inflammatory conditions. Finally, this scenario impaired the striatal expression of the transcription factor BDNF, possibly favoring cell death.<\/jats:p><\/jats:sec>","DOI":"10.1002\/cbin.10969","type":"journal-article","created":{"date-parts":[[2018,4,6]],"date-time":"2018-04-06T22:56:40Z","timestamp":1523055400000},"page":"725-733","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":14,"title":["De novo tetrahydrobiopterin biosynthesis is impaired in the inflammed striatum of parkin<sup>(\u2212\/\u2212)<\/sup> mice"],"prefix":"10.1002","volume":"42","author":[{"given":"Roberta","family":"de Paula Martins","sequence":"first","affiliation":[{"name":"Laborat\u00f3rio de Bioenerg\u00e9tica e Estresse Oxidativo\u2014LABOX Departamento de Bioqu\u00edmica, Centro de Ci\u00eancias Biol\u00f3gicas, Universidade Federal de Santa Catarina Florian\u00f3polis 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Neurosciences Paris France"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Rita","family":"Raisman\u2010Vozari","sequence":"additional","affiliation":[{"name":"Institut de Cerveau et de la Moelle Epini\u00e8re H\u00f4pital de la Piti\u00e9 Salp\u00eatri\u00e8re Paris France"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Olga","family":"Corti","sequence":"additional","affiliation":[{"name":"Institut de Cerveau et de la Moelle Epini\u00e8re H\u00f4pital de la Piti\u00e9 Salp\u00eatri\u00e8re Paris France"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ana Lucia","family":"De Paul","sequence":"additional","affiliation":[{"name":"Centro de Microscopia Electr\u00f3nica, Instituto de Investigaciones en Ciencias de la Salud (INICSA\u2010CONICET) Facultad de Ciencias M\u00e9dicas, Universidad Nacional de C\u00f3rdoba C\u00f3rdoba Argentina"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Rodrigo Augusto","family":"da 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