Table 1.
PKA anchoring affects hippocampal neuron resting membrane properties
| Peak potential (mV) | Steady-state potential (mV) | “Sag” potential (mV) | Input resistance (MΩ) | |
|---|---|---|---|---|
| Ctrl (n = 10) | −104.5 ± 3.1 | −94.5 ± 3.3 | 9.8 ± 0.3 | 149.2 ± 5.8 |
| Ht31 (n = 8) | −83.7 ± 2.8* | −74.4 ± 2.6* | 9.3 ± 0.9 | 82.5 ± 2.6* |
| FK506 (n = 9) | −119.7 ± 4.3* | −110.2 ± 4.2* | 9.5 ± 0.3 | 198.6 ± 8.7* |
| 4-AP (n = 12) | −128.1 ± 6.6* | −118.7 ± 6.7* | 9.4 ± 0.9 | 245.7 ± 6.5* |
| 4-AP + Ht31 (n = 13) | −124.1 ± 3.8* | −114.4 ± 3.8* | 9.7 ± 0.5 | 210.9 ± 6.7* |
| 4-AP + FK506 (n = 12) | −127.8 ± 3.7* | −118.2 ± 4.8* | 9.6 ± 0.3 | 232.3 ± 10.4* |
Subthreshold voltage transients were generated in response to a +200 pA, 1000 ms current injection for control neurons, or neurons treated with Ht31 peptide, FK506, 4-AP, 4-AP + Ht31, or 4-AP + FK506. Compared with control neurons, both peak and steady-state responses are reduced in the Ht31 treatment group (n = 10 for Ctrl, n = 8 for Ht31 peptide) and enhanced in the FK506, 4-AP, 4-AP + Ht31, and 4-AP + FK506 groups, affecting cellular input resistance. The difference potential or “sag” between peak and steady-state voltages did not differ between experimental groups, indicating that the hyperpolarization-activated nonspecific cation current, Ih, was not affected.
*p < 0.05.