Figure 3
Blocking SK channels only partially mimics the ability of β-adrenergic receptor activation to enable LTP induction in ventral hippocampal slices. (A) A 30 s-long train of TPS had no persistent effect on synaptic strength in control experiments (45 min post-TPS fEPSPS were 101 ± 3% of baseline, n = 7) but induced LTP in slices continuously bathed in ACSF containing SK channel blocker apamin (100 nM) (fEPSPs potentiated to 155 ± 9% of baseline, n = 8, t(13) = 5.622, **p = 8.31 × 10–5 compared to control). (B) Apamin enhances HFS-induced LTP. Field EPSPs were potentiated to 139 ± 4% of baseline in control experiments (n = 11) and 172 ± 8% of baseline in experiments where SK channels were blocked with apamin (n = 8, t(17) = 4.014, *p = 9.0 × 10–4 compared to control). (C and D) Apamin does not enable the induction of LTP by either brief (C) or long trains of TPS (D). Following a 5 s train of TPS, fEPSPs were 106 ± 5% of baseline in control experiments (n = 5) and 103 ± 3% of baseline in apamin-treated slices (n = 7, t(10) = 0.424, p = 0.68 compared to control). fEPSPs were 98 ± 3% of baseline 45 min after 3 min of TPS in control experiments (n = 7) and 99 ± 5% of baseline in slices bathed in ACSF containing apamin (n = 8, t(13) = 0.0217, p = 0.983 compared to control). Scatter plots show fEPSP slopes 45 min post-TPS or 60 min post-HFS in all experiments.
