An amino-terminal fragment peptide of acidic fibroblast growth factor modulates synaptic transmission in rat hippocampal slices

Effects of acidic fibroblast growth factor (aFGF) fragments such as aminoterminal aFGF (1–15) and carboxyl-terminal aFGF (114–140) on synaptic transmission were investigated in rat hippocampal slices. Stimulation was applied to Schaffer collateral/commissural afferents, and evoked population spikes were recorded in the CA1 pyramidal cell layer. Continuous perfusion of slices with aFGF (1–15) slightly decreased the basal amplitude of population spikes and significantly increased the paired-pulse facilitation. When brief tetanic stimulation (7 pulses at 100 Hz) was applied 30 min after the perfusion of aFGF (1–15), aFGF (1–15)-treated slices enhanced the magnitude of short-term potentiation after the tetanus and facilitated a generation of long-term potentiation. These effects of aFGF (1–15) were dose-dependent. Perfusion of slices with aFGF (114–140) had no effect on the basal spike amplitude, paired-pulse facilitation, and short-term potentiation. Both aFGF (1–15) and aFGF (114–140) had no effect on the DNA synthesis stimulating activity in BALB/c 3T3-L1 cells. The results suggest that aFGF (1–15), which is not involved in mitogenic activity, is implicated in a modulatory mechanism of synaptic plasticity.