Figure 4

Prolonged inhibition of L-type VGCCs alone does not affect intrinsic excitability or mRNA levels of most K ⁺ channel genes. (A,B) Rat dissociated hippocampal neurons cultured at high density (DIV 12–14) were treated with L-type VGCC inhibitor Nif (20 μM), CaMKK inhibitor STO-609 (2 μM), or control (CTL-DMSO, 0.1% DMSO) for 48 h. (A) Representative spike trains are shown. (B) Average AP firing rates (Hz) measured in pyramidal neurons treated with CTL-DMSO (n = 12), Nif (n = 9), or STO-609 (n = 10) for 48 h. Nif or STO-609 treatment did not alter AP firing frequency compared to CTL-DMSO treatment. (C,D) QPCR validation of select genes that we identified by microarray analysis and have been implicated in intrinsic excitability (C) and synaptic transmission (D) identified by microarray analysis (n = 5 per treatment). Expression of intrinsic excitability genes was not altered by Nif or STO-609 treatment, except KCNJ12, KCNMB2, and KCNAB3. The ★ denotes genes whose protein products have not previously been implicated in homeostatic plasticity. Mean ± SEM (*p < 0.05).