Antisense (AS) transcripts are RNA molecules that are transcribed from the 
opposite strand to sense (S) genes forming S/AS pairs. The most prominent 
configuration is when a lncRNA is antisense to a protein coding gene. Increasing 
evidences prove that antisense transcription may control sense gene expression 
acting at distinct regulatory levels. However, its contribution to brain 
function and neurodegenerative diseases remains unclear. We have recently 
identified AS Uchl1 as an antisense to the mouse Ubiquitin carboxy-terminal 
hydrolase L1 (Uchl1) gene (AS Uchl1), the synthenic locus of UCHL1/PARK5. This 
is mutated in rare cases of early-onset familial Parkinson's Disease (PD) and 
loss of UCHL1 activity has been reported in many neurodegenerative diseases. 
Importantly, manipulation of UchL1 expression has been proposed as tool for 
therapeutic intervention. AS Uchl1 induces UchL1 expression by increasing its 
translation. It is the representative member of SINEUPs (SINEB2 sequence to 
UP-regulate translation), a new functional class of natural antisense lncRNAs 
that activate translation of their sense genes. Here we take advantage of 
FANTOM5 dataset to identify the transcription start sites associated to S/AS 
pair at Uchl1 locus. We show that AS Uchl1 expression is under the regulation of 
Nurr1, a major transcription factor involved in dopaminergic cells' 
differentiation and maintenance. Furthermore, AS Uch1 RNA levels are strongly 
down-regulated in neurochemical models of PD in vitro and in vivo. This work 
positions AS Uchl1 RNA as a component of Nurr1-dependent gene network and target 
of cellular stress extending our understanding on the role of antisense 
transcription in the brain.