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The DJ\u20101 gene trap\u2010induced null mutants exhibit less dopamine\u2010producing neurons in the ventral tegmental area (VTA). They also exhibit slight changes in behaviour, i.e. diminished rearing behaviour and impairments in object recognition. Furthermore, we detected subtle phenotypes, which suggest that these animals compensate for the loss of DJ\u20101. First, we found a significant upregulation of mitochondrial respiratory enzyme activities, a mechanism known to protect against oxidative stress. Second, a close to significant increase in c\u2010Jun N\u2010terminal kinase 1 phosphorylation in old DJ\u20101\u2010deficient mice hints at a differential activation of neuronal cell survival pathways. Third, as no change in the density of tyrosine hydroxylase (TH)\u2010positive terminals in the striatum was observed, the remaining dopamine\u2010producing neurons likely compensate by increasing axonal sprouting. In summary, the present data suggest that DJ\u20101 is implicated in major non\u2010motor symptoms of PD appearing in the early phases of the disease\u2014such as subtle impairments in motivated behaviour and cognition\u2014and that under basal conditions the loss of DJ\u20101 is compensated<\/jats:bold> <\/jats:p>","DOI":"10.1111\/j.1601-183x.2009.00559.x","type":"journal-article","created":{"date-parts":[[2009,12,17]],"date-time":"2009-12-17T22:50:38Z","timestamp":1261090238000},"page":"305-317","source":"Crossref","is-referenced-by-count":72,"title":["DJ\u20101\u2010deficient mice show less TH\u2010positive neurons in the ventral tegmental area and exhibit non\u2010motoric behavioural impairments"],"prefix":"10.1111","volume":"9","author":[{"given":"T. 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