title: Impact of calcium-activated potassium channels on NMDA spikes in cortical layer 5 pyramidal neurons.
abstract: Active electrical events play an important role in shaping signal processing in dendrites. As these events are usually associated with an increase in intracellular calcium, they are likely to be under the control of calcium-activated potassium channels. Here, we investigate the impact of calcium-activated potassium channels onN-methyl-d-aspartate (NMDA) receptor-dependent spikes, or NMDA spikes, evoked by glutamate iontophoresis onto basal dendrites of cortical layer 5 pyramidal neurons. We found that small-conductance calcium-activated potassium channels (SK channels) act to reduce NMDA spike amplitude but at the same time, also decrease the iontophoretic current required for their generation. This SK-mediated decrease in NMDA spike threshold was dependent on R-type voltage-gated calcium channels and indicates a counterintuitive, excitatory effect of SK channels on NMDA spike generation, whereas the capacity of SK channels to suppress NMDA spike amplitude is in line with the expected inhibitory action of potassium channels on dendritic excitability. Large-conductance calcium-activated potassium channels had no significant impact on NMDA spikes, indicating that these channels are either absent from basal dendrites or not activated by NMDA spikes. These experiments reveal complex and opposing interactions among NMDA receptors, SK channels, and voltage-gated calcium channels in basal dendrites of cortical layer 5 pyramidal neurons during NMDA spike generation, which are likely to play an important role in regulating the way these neurons integrate the thousands of synaptic inputs they receive.
authors.affiliation: Eccles Institute of Neuroscience and Australian Research Council Centre of Excellence for Integrative Brain Function, John Curtin School of Medical Research, Australian National University, Canberra, Australia.
authors.forename: Tobias
authors.initials: T
authors.lastname: Bock
authors.affiliation: Eccles Institute of Neuroscience and Australian Research Council Centre of Excellence for Integrative Brain Function, John Curtin School of Medical Research, Australian National University, Canberra, Australia greg.stuart@anu.edu.au.
authors.forename: Greg J
authors.initials: GJ
authors.lastname: Stuart
mesh_terms: D000200:Action Potentials; D000818:Animals; D002540:Cerebral Cortex / Q000166:cytology / Q000378:metabolism* / Q000502:physiology; D051036:Large-Conductance Calcium-Activated Potassium Channels / Q000378:metabolism*; D017966:Pyramidal Cells / Q000378:metabolism* / Q000502:physiology; D051381:Rats; D017208:Rats, Wistar; D016194:Receptors, N-Methyl-D-Aspartate / Q000378:metabolism*; D051640:Small-Conductance Calcium-Activated Potassium Channels / Q000378:metabolism*; D013569:Synapses / Q000378:metabolism / Q000502:physiology
chemical_list: D051036:Large-Conductance Calcium-Activated Potassium Channels; D016194:Receptors, N-Methyl-D-Aspartate; D051640:Small-Conductance Calcium-Activated Potassium Channels
keywords: SK channel; cortex; dendrites; pyramidal neuron