During brain development, excess neurons that are formed die by apoptosis. cln3 
was recently identified as the gene defective in juvenile Batten disease, an 
inherited neurodegenerative disease of childhood. In this disease, neurons die 
by apoptosis. Overexpression of this gene increases survival of human NT2 
neuronal precursor cells. We, therefore, hypothesized that cln3 may be present 
in developing neurons and may play an important role in regulating the 
developmental process. NT2 neuronal cells were induced to develop into mature 
neurons. We evaluated cln3 expression by reverse transcription PCR and 
immunohistochemistry over a 7-wk period of differentiation. Also, cln3 
expression was characterized in neonatal rat brain during the first week of life 
(P-1, P0, P4, and P8) and at P30. cln3 was differentially expressed during 
neuronal development into nondividing post-mitotic neurons. The greatest 
expression was noted during wk 6 and then dropped to predifferentiation levels 
during wk 7. cln3 expression was detected in all the rat brain developmental 
stages evaluated. The greatest expression was seen at P0 and was double compared 
with the other stages. We conclude that cln3 is present during critical periods 
of neuronal cell differentiation and brain development. As cln3 is 
antiapoptotic, we hypothesize that cln3 plays an important role in regulating 
brain development. These findings may have implications for identifying 
strategies aimed at neuroprotection and neuronal survival during development.