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. Author manuscript; available in PMC: 2019 Nov 20.
Published in final edited form as: Neurosci Lett. 2018 Sep 13;687:31–36. doi: 10.1016/j.neulet.2018.09.017

Figure 2.

Figure 2.

Pretreatment with PKA inhibitors, KT5720 and PKI, blocks β-lactone-mediated enhancement in amounts of pCREB.

(A) Schematic outline of the experiment: after the recovery period of 120 min, hippocampal slices were treated with a PKA inhibitor (KT5720 or PKI) for 60 min. For the last 30 min of the PKA inhibitor treatment, β-lactone was added to the incubation solution. After chemical treatment, slices were transferred to the recording chamber and the slices were subjected to the 2 × 100 Hz protocol. Slices were then fixed and processed for immunohistochemistry. (B, D) Confocal images of pCREB immunoreactivities in the CA1 region of hippocampal slices without any treatment (control) or after β-lactone treatment followed by subthreshold LTP induction (β-lactone + 2 × 100 Hz), after PKA inhibitor treatment followed by subthreshold LTP induction (KT5720 or PKI + 2 × 100 Hz), or after PKA inhibitor and β-lactone pretreatment followed by subthreshold LTP induction (KT570 or PKI + β-lactone + 2 × 100 Hz). Scale bars: 20 μm. (C, E) Quantification of pCREB immunoreactivities shows that PKA inhibitor pretreatment blocks the β-lactone-mediated enhancement of CREB phosphorylation after subthreshold LTP. *p<0.05, **p<0.01, ***p<0.001 comparison between two groups as indicated by horizontal lines.