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<t>PKA</t> inhibition with <t>RPcAMP</t> or H89 largely restores the suppressed KCa-sAHP and IsAHP in chronic-phase post-SE neurons. Aa, b, Representative recordings of a KCa-sAHP evoked by a Ca2+ spike (shown in inset; a) and an IsAHP evoked by a depolarizing pulse (b) in a non-SE neuron. B, Same as in A, but recordings were made in a post-SE neuron. C, Same as in A, but recordings were made in non-SE slices treated for >1 h with the PKA inhibitor RPcAMP (100 μm). D, Same as in B, but recordings were made in post-SE slices treated for >1 h with the PKA inhibitor RPcAMP. E, Same as in C, but recordings were made in non-SE slices treated for >1 h with the PKA inhibitor H89 (10 μm). F, Same as in D, but recordings were made in post-SE slices treated for >1 h with the PKA inhibitor H89. Note that in this condition the KCa-sAHP and IsAHP in the non-SE and post-SE neurons appear similar in size. G, Summary bar diagram of KCa-sAHP amplitudes (measured at the peak of the sAHP) in non-SE and post-SE neurons recorded in normal aCSF and in RPcAMP or H89-containing aCSF. H, Summary bar diagram of IsAHP amplitudes (measured at peak current) in non-SE and post-SE neurons recorded in normal aCSF and RPcAMP or H89 containing aCSF. Note that both KCa-sAHP and IsAHP values are markedly and significantly reduced in post-SE neurons, and are largely restored by treating slices with PKA inhibitors (RPcAMP or H89). I, Spikes were evoked by a series of 1-s-long depolarizing current pulses in non-SE and post-SE neurons, all treated with H89. The two plots depict the number of spikes versus stimulus intensity in the two groups of neurons. Although post-SE neurons fire more spikes, the difference between the two plots is not significant, indicating that H89 treatment reduces the excitability of post-SE neurons to near the non-SE level. ***p ≤ 0.001. n.s., Not significant.
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PKA inhibition with RPcAMP or H89 largely restores the suppressed KCa-sAHP and IsAHP in chronic-phase post-SE neurons. Aa, b, Representative recordings of a KCa-sAHP evoked by a Ca2+ spike (shown in inset; a) and an IsAHP evoked by a depolarizing pulse (b) in a non-SE neuron. B, Same as in A, but recordings were made in a post-SE neuron. C, Same as in A, but recordings were made in non-SE slices treated for >1 h with the PKA inhibitor RPcAMP (100 μm). D, Same as in B, but recordings were made in post-SE slices treated for >1 h with the PKA inhibitor RPcAMP. E, Same as in C, but recordings were made in non-SE slices treated for >1 h with the PKA inhibitor H89 (10 μm). F, Same as in D, but recordings were made in post-SE slices treated for >1 h with the PKA inhibitor H89. Note that in this condition the KCa-sAHP and IsAHP in the non-SE and post-SE neurons appear similar in size. G, Summary bar diagram of KCa-sAHP amplitudes (measured at the peak of the sAHP) in non-SE and post-SE neurons recorded in normal aCSF and in RPcAMP or H89-containing aCSF. H, Summary bar diagram of IsAHP amplitudes (measured at peak current) in non-SE and post-SE neurons recorded in normal aCSF and RPcAMP or H89 containing aCSF. Note that both KCa-sAHP and IsAHP values are markedly and significantly reduced in post-SE neurons, and are largely restored by treating slices with PKA inhibitors (RPcAMP or H89). I, Spikes were evoked by a series of 1-s-long depolarizing current pulses in non-SE and post-SE neurons, all treated with H89. The two plots depict the number of spikes versus stimulus intensity in the two groups of neurons. Although post-SE neurons fire more spikes, the difference between the two plots is not significant, indicating that H89 treatment reduces the excitability of post-SE neurons to near the non-SE level. ***p ≤ 0.001. n.s., Not significant.

Journal: The Journal of Neuroscience

Article Title: Protein Kinase A-Mediated Suppression of the Slow Afterhyperpolarizing KCa3.1 Current in Temporal Lobe Epilepsy

doi: 10.1523/JNEUROSCI.1603-19.2019

Figure Lengend Snippet: PKA inhibition with RPcAMP or H89 largely restores the suppressed KCa-sAHP and IsAHP in chronic-phase post-SE neurons. Aa, b, Representative recordings of a KCa-sAHP evoked by a Ca2+ spike (shown in inset; a) and an IsAHP evoked by a depolarizing pulse (b) in a non-SE neuron. B, Same as in A, but recordings were made in a post-SE neuron. C, Same as in A, but recordings were made in non-SE slices treated for >1 h with the PKA inhibitor RPcAMP (100 μm). D, Same as in B, but recordings were made in post-SE slices treated for >1 h with the PKA inhibitor RPcAMP. E, Same as in C, but recordings were made in non-SE slices treated for >1 h with the PKA inhibitor H89 (10 μm). F, Same as in D, but recordings were made in post-SE slices treated for >1 h with the PKA inhibitor H89. Note that in this condition the KCa-sAHP and IsAHP in the non-SE and post-SE neurons appear similar in size. G, Summary bar diagram of KCa-sAHP amplitudes (measured at the peak of the sAHP) in non-SE and post-SE neurons recorded in normal aCSF and in RPcAMP or H89-containing aCSF. H, Summary bar diagram of IsAHP amplitudes (measured at peak current) in non-SE and post-SE neurons recorded in normal aCSF and RPcAMP or H89 containing aCSF. Note that both KCa-sAHP and IsAHP values are markedly and significantly reduced in post-SE neurons, and are largely restored by treating slices with PKA inhibitors (RPcAMP or H89). I, Spikes were evoked by a series of 1-s-long depolarizing current pulses in non-SE and post-SE neurons, all treated with H89. The two plots depict the number of spikes versus stimulus intensity in the two groups of neurons. Although post-SE neurons fire more spikes, the difference between the two plots is not significant, indicating that H89 treatment reduces the excitability of post-SE neurons to near the non-SE level. ***p ≤ 0.001. n.s., Not significant.

Article Snippet: To that end, we treated chronic-phase slices with the cell-permeable PKA inhibitor RPcAMP ( Dostmann et al., 1990 ; Wang et al., 1991 ).

Techniques: Inhibition