Dendritic potassium channels in hippocampal pyramidal neurons

Abstract

Potassium channels located in the dendrites of hippocampal CA1 pyramidal neurons control the shape and amplitude of back‐propagating action potentials, the amplitude of excitatory postsynaptic potentials and dendritic excitability. Non‐uniform gradients in the distribution of potassium channels in the dendrites make the dendritic electrical properties markedly different from those found in the soma. For example, the influence of a fast, calcium‐dependent potassium current on action potential repolarization is progressively reduced in the first 150 μm of the apical dendrites, so that action potentials recorded farther than 200 μm from the soma have no fast after‐hyperpolarization and are wider than those in the soma. The peak amplitude of back‐propagating action potentials is also progressively reduced in the dendrites because of the increasing density of a transient potassium channel with distance from the soma. The activation of this channel can be reduced by the activity of a number of protein kinases as well as by prior depolarization. The depolarization from excitatory postsynaptic potentials (EPSPs) can inactivate these A‐type K+ channels and thus lead to an increase in the amplitude of dendritic action potentials, provided the EPSP and the action potentials occur within the appropriate time window. This time window could be in the order of 15 ms and may play a role in long‐term potentiation induced by pairing EPSPs and back‐propagating action potentials.

Somato-dendritic mechanisms underlying the electrophysiological properties of hypothalamic magnocellular neuroendocrine cells: A multicompartmental model study

“…In the model, I A is most prominent in the secondary dendrites due to the increase in the maximum conductance of this current with distance from the soma (g A,s <g A,pd <g A, sd ), similar to that observed in hippocampal pyramidal neurons (Hoffman et al 1997;Johnston et al 2000). The Atype current may increase in the dendrites due not only to a corresponding increase in the density of Kv4-family α-subunits that form A-type channels, but also to changes in the distribution of Kv-channel interacting proteins (KChIPs), which may augment I A by a variety of mechanisms .…”

“…The temporal association of the opening times of N-type channels and BK channels indicates that these channels are in close proximity to one another. Taking into account the results of studies showing that, in hippocampal pyramidal neurons, BK channel distribution decreases with the distance from the soma (Johnston et al 2000), we did not include BK channels in the secondary dendrites of our model. We assumed that the [Ca 2+ ] in the vicinity of BK channels changed much faster than the bulk [Ca 2+ ] in the compartment.…”

A postsynaptic transient K + current modulated by arachidonic acid regulates synaptic integration and threshold for LTP induction in hippocampal pyramidal cells

“…AA suppresses Kv4-mediated I A in vertebrate neurons and expression systems (11)(12)(13)(14)(15), and the dendritic I A is down-regulated by AA and by means of phosphorylation by protein kinases A and C (12,16). Because I A can regulate dendritic excitability (10,17), these findings raise the possibility that AA, released by high-frequency activation of glutamatergic synapses, can enhance the impact of excitatory postsynaptic potentials (EPSPs) by inhibiting I A . If such modulation occurs, it would provide a positive feedback regulation of EPSP burst efficacy.…”

“…In hippocampal CA1 pyramidal cells, the apical dendrites express a high density of fast-inactivating K ϩ channels underlying the transient K ϩ current I A (10). AA suppresses Kv4-mediated I A in vertebrate neurons and expression systems (11)(12)(13)(14)(15), and the dendritic I A is down-regulated by AA and by means of phosphorylation by protein kinases A and C (12,16).…”

Photometric recording of transmembrane potential in outer hair cells

“…For example, a high density of sodium channels exists at the nodes of Ranvier and differences in the surface densities of channels between somata and neuronal processes have been reported Sugimori 1980a, 1980b). More recently, the discovery of potassium channel density gradients in the dendrites of pyramidal neurons has intensified the study of such functional inhomogeneities (Johnston et al 2000). Neither conventional microelectrode recordings nor patch-clamp recordings can assess regional variations in membrane voltage.…”