Differential contributions of Ca2+‐activated K+ channels and Na+/K+‐ATPases to the generation of the slow afterhyperpolarization in CA1 pyramidal cells. Issue 5 (27th February 2018)

• Record Type: Journal Article
• Authors: Tiwari, Manindra Nath; Mohan, Sandesh; Biala, Yoav; Yaari, Yoel
• Is Part Of: Hippocampus. Volume 28:Issue 5(2018)
• Page Start: 338
• Page End: 357
• Publication Date: 2018-02-27
• Subjects: α1 Na+/K+‐ATPase -- CA1 -- KCa3.1 -- KV7 -- pyramidal cell -- slow afterhyperpolarization -- sodium pump; Hippocampus (Brain) -- Periodicals; 612.825
• DOI: 10.1002/hipo.22836
• Languages: English
• ISSNs: 1050-9631

Abstract

Abstract: In many types of CNS neurons, repetitive spiking produces a slow afterhyperpolarization (sAHP), providing sustained, intrinsically generated negative feedback to neuronal excitation. Changes in the sAHP have been implicated in learning behaviors, in cognitive decline in aging, and in epileptogenesis. Despite its importance in brain function, the mechanisms generating the sAHP are still controversial. Here we have addressed the roles of M‐type K + current ( I M ), Ca 2+ ‐gated K + currents ( I Ca(K) 's) and Na + /K + ‐ATPases (NKAs) current to sAHP generation in adult rat CA1 pyramidal cells maintained at near‐physiological temperature (35 °C). No evidence for I M contribution to the sAHP was found in these neurons. Both I Ca(K) 's and NKA current contributed to sAHP generation, the latter being the predominant generator of the sAHP, particularly when evoked with short trains of spikes. Of the different NKA isoenzymes, α1 ‐NKA played the key role, endowing the sAHP a steep voltage‐dependence. Thus normal and pathological changes in α1 ‐NKA expression or function may affect cognitive processes by modulating the inhibitory efficacy of the sAHP.