| First Author | Wang K | Year | 2016 |
| Journal | Elife | Volume | 5 |
| Pages | e11206 | PubMed ID | 26765773 |
| Mgi Jnum | J:229991 | Mgi Id | MGI:5755198 |
| Doi | 10.7554/eLife.11206 | Citation | Wang K, et al. (2016) IK1 channels do not contribute to the slow afterhyperpolarization in pyramidal neurons. Elife 5:e11206 |
| abstractText | In pyramidal neurons such as hippocampal area CA1 and basolateral amygdala, a slow afterhyperpolarization (sAHP) follows a burst of action potentials, which is a powerful regulator of neuronal excitability. The sAHP amplitude increases with aging and may underlie age related memory decline. The sAHP is due to a Ca(2+)-dependent, voltage-independent K(+) conductance, the molecular identity of which has remained elusive until a recent report suggested the Ca(2+)-activated K(+) channel, IK1 (KCNN4) as the sAHP channel in CA1 pyramidal neurons. The signature pharmacology of IK1, blockade by TRAM-34, was reported for the sAHP and underlying current. We have examined the sAHP and find no evidence that TRAM-34 affects either the current underling the sAHP or excitability of CA1 or basolateral amygdala pyramidal neurons. In addition, CA1 pyramidal neurons from IK1 null mice exhibit a characteristic sAHP current. Our results indicate that IK1 channels do not mediate the sAHP in pyramidal neurons. |
