While dopamine is likely to modulate hippocampal synaptic plasticity, there
has been little information about how dopamine affects synaptic transmissi
on in the hippocampus. The expression of IEGs including c-fos has been asso
ciated with late phase LTP in the CA1 region of the hippocampus, The induct
ion of c-fos by dopaminergic receptor activation in the rat hippocampus was
investigated ba using semiquantitative RT-PCR and immunocytochemistry. The
hippocampal slices which were not treated with dopamine showed little expr
ession of c-fos mRNA. However, the induction of c-fos mRNA was detected as
early as 5 min after dopamine treatment, peaked at 60 min, and remained ele
vated 5 h after treatment. Temporal profiles of increases in c-fos mRNA by
R(+)-SKF-38393 (50 muM) and forskolin (50 muM) were similar to that of dopa
mine. An increase in [cAMP] was observed in dopamine-, SKF-, or forskolin-t
reated hippocampal slices. By immunocytochemical studies, control hippocamp
al cells showed little expression of c-Fos immunoreactivity. However, when
cells were treated with dopamine, an increase in the expression of c-Fos im
munoreactivity was observed after treatment for 2 h, The treatment of hippo
campal neurons with R(+)-SKF-38393 (50 muM) or forskolin (50 muM) also indu
ced a significant increase in c-Fos expression. These results indicate that
the dopamine D1 receptor-mediated cAMP dependant pathway is associated wit
h the expression of c-Fos in the hippocampal neurons. These data are consis
tent with the possible role of endogenous dopamine on synaptic plasticity v
ia the regulation of gene expression. Furthermore, these results imply that
dopamine might control the process of memory storage in the hippocampus th
rough gene expression.