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.