We previously developed a highly sensitive method to assess in situ repair
kinetics of ultraviolet (UV)-induced DNA photoproducts in epidermal cells u
sing monoclonal antibodies specific for cyclobutane pyrimidine dimers (CPDs
) and pyrimidine-pyrimidone (6-4) photoproducts (64PPs) by immunohistochemi
stry. In order to determine whether nucleotide excision repair capacity is
operative in postmitotic mature neurons, brain surfaces of adult mice were
exposed to UVB, and induction and removal of CPDs and 64PPs in Purkinje cel
l DNA were assessed immunohistochemically. UVB penetrated brain tissue to a
depth sufficient to allow quantitative study. CPDs but not 64PPs were clea
rly detectable in the nuclei of Purkinje cells at doses >500 J/m(2), in a d
ose-dependent manner. A time course experiment showed a statistically signi
ficant decrease of CPDs with time after irradiation. Although there was no
apparent removal on Day 1, about half of CPDs were removed within 5 days, a
nd the repair was essentially completed by Day 10. We conclude that non-div
iding cerebellar neuronal cells can indeed repair UV-induced DNA damage, bu
t with relatively low efficiency as compared with dividing epidermal cells.