Modification of Current Transmitted From Apical Dendrite to Soma by Blockade of Voltage- and Ca2+-Dependent Conductances in Rat Neocortical Pyramidal Neurons
Authors: Schwindt Peter C. , Crill Wayne E. 
Published: December 2017

Schwindt, Peter C. and Wayne E. Crill. Modification of current transmitted from apical dendrite to soma by blockade of voltage- and Ca2+-dependent conductances in rat neocortical pyramidal neurons. J. Neurophysiol. 78: 187–198, 1997. The axial current transmitted to the soma during the long-lasting iontophoresis of glutamate at a distal site on the apical dendrite was measured by somatic voltage clamp of rat neocortical pyramidal neurons. Evidence for voltage- and Ca2+-gated channels in the apical dendrite was sought by examining the modification of this transmitted current resulting from the alteration of membrane potential and the application of channel-blocking agents. After N-methyl-d-aspartate receptor blockade, iontophoresis of glutamate on the soma evoked a current whose amplitude decreased linearly with depolarization to an extrapolated reversal potential near 0 mV. Under the same conditions, glutamate iontophoresis on the apical dendrite 241–537 μm from the soma resulted in a transmitted axial current that increased with depolarization over the same range of membrane potential (about −90 to −40 mV). Current transmitted from dendrite to soma was thus amplified during depolarization from resting potential (about −70 mV) and attenuated during hyperpolarization. After Ca2+ influx was blocked to eliminate Ca2+-dependent K+ currents, application of 10 mM tetraethylammonium chloride (TEA) altered the amplitude and voltage dependence of the transmitted current in a manner consistent with the reduction of dendritic voltage-gated K+ current. We conclude that dendritic, TEA-sensitive, voltage-gated K+ channels can be activated by tonic dendritic depolarization. The most prominent effects of blocking Ca2+ influx resembled those elicited by TEA application, suggesting that these effects were caused predominantly by blockade of a dendritic Ca2+-dependent K+ current. When cells were impaled with microelectrodes containing ethylene glycol-bis(β-amino-ethyl ether)- N,N′,N′-tetraacetic acid to prevent a rise in intracellular Ca2+ concentration, blockade of Ca2+ influx altered the tonic transmitted current in different manner consistent with the blockade of a inward dendritic current carried by high-threshold-activated Ca2+ channels. We conclude that the primary effect of Ca2+ influx during tonic dendritic depolarization is the activation of a dendritic Ca2+-dependent K+ current. The hyperpolarizing attenuation of transmitted current was unaffected by blocking all known voltage-gated inward currents except the hyperpolarization-activated cation current ( I h). Extracellular Cs+ (3 mM) reversibly abolished both the hyperpolarizing attenuation of transmitted current and I h measured at the soma. We conclude that activation of I h by hyperpolarization of the proximal apical dendrite would cause less axial current to arrive at the soma from a distal site than in a passive dendrite. Several functional implications of dendritic K+ and I h channels are discussed.