The shaping of two distinct dendritic spikes by A-type voltage-gated K+ channels
Dendritic ion channels have been a subject of intense research in neuroscience because active ion channels in dendrites shape input signals. Ca2+-permeable channels including NMDA receptors (NMDARs) have been implicated in supralinear dendritic integration, and the IA conductance in sublinear integr...
| Main Authors: | , , |
|---|---|
| Format: | Article |
| Language: | English |
| Published: |
Frontiers Media S.A.
2015-12-01
|
| Series: | Frontiers in Cellular Neuroscience |
| Subjects: | |
| Online Access: | http://journal.frontiersin.org/Journal/10.3389/fncel.2015.00469/full |
| _version_ | 1818084411399208960 |
|---|---|
| author | Sungchil eYang Cha-min eTang Sunggu eYang |
| author_facet | Sungchil eYang Cha-min eTang Sunggu eYang |
| author_sort | Sungchil eYang |
| collection | DOAJ |
| description | Dendritic ion channels have been a subject of intense research in neuroscience because active ion channels in dendrites shape input signals. Ca2+-permeable channels including NMDA receptors (NMDARs) have been implicated in supralinear dendritic integration, and the IA conductance in sublinear integration. Despite their essential roles in dendritic integration, it has remained uncertain whether these conductances coordinate with, or counteract, each other in the process of dendritic integration. To address this question, experiments were designed in hippocampal CA1 neurons with a recent 3D digital holography system that has shown excellent performance for spatial photoactivation. The results demonstrated a role of IA as a key contributor to two distinct dendritic spikes, low- and high-threshold Ca2+ spikes, through a preferential action of IA on Ca2+-permeable channel-mediated currents, over fast AMPAR-mediated currents. It is likely that the rapid kinetics of IA provides feed-forward inhibition to counteract the delayed Ca2+ channel-mediated dendritic excitability. This research reveals one dynamic ionic mechanism of dendritic integration, and may contribute to a new understanding of neuronal hyperexcitability embedded in several neural diseases such as epilepsy, fragile X syndrome and Alzheimer's disease. |
| first_indexed | 2024-12-10T19:53:28Z |
| format | Article |
| id | doaj.art-dbf01cc57a204d76b465e2fc67cc3577 |
| institution | Directory Open Access Journal |
| issn | 1662-5102 |
| language | English |
| last_indexed | 2024-12-10T19:53:28Z |
| publishDate | 2015-12-01 |
| publisher | Frontiers Media S.A. |
| record_format | Article |
| series | Frontiers in Cellular Neuroscience |
| spelling | doaj.art-dbf01cc57a204d76b465e2fc67cc35772022-12-22T01:35:43ZengFrontiers Media S.A.Frontiers in Cellular Neuroscience1662-51022015-12-01910.3389/fncel.2015.00469167923The shaping of two distinct dendritic spikes by A-type voltage-gated K+ channelsSungchil eYang0Cha-min eTang1Sunggu eYang2City University of Hong KongUniversity of MarylandIncheon National UniversityDendritic ion channels have been a subject of intense research in neuroscience because active ion channels in dendrites shape input signals. Ca2+-permeable channels including NMDA receptors (NMDARs) have been implicated in supralinear dendritic integration, and the IA conductance in sublinear integration. Despite their essential roles in dendritic integration, it has remained uncertain whether these conductances coordinate with, or counteract, each other in the process of dendritic integration. To address this question, experiments were designed in hippocampal CA1 neurons with a recent 3D digital holography system that has shown excellent performance for spatial photoactivation. The results demonstrated a role of IA as a key contributor to two distinct dendritic spikes, low- and high-threshold Ca2+ spikes, through a preferential action of IA on Ca2+-permeable channel-mediated currents, over fast AMPAR-mediated currents. It is likely that the rapid kinetics of IA provides feed-forward inhibition to counteract the delayed Ca2+ channel-mediated dendritic excitability. This research reveals one dynamic ionic mechanism of dendritic integration, and may contribute to a new understanding of neuronal hyperexcitability embedded in several neural diseases such as epilepsy, fragile X syndrome and Alzheimer's disease.http://journal.frontiersin.org/Journal/10.3389/fncel.2015.00469/fullDendritecalcium channelDendritic excitabilityCA1 pyramidal neuronA-type K+ channels |
| spellingShingle | Sungchil eYang Cha-min eTang Sunggu eYang The shaping of two distinct dendritic spikes by A-type voltage-gated K+ channels Frontiers in Cellular Neuroscience Dendrite calcium channel Dendritic excitability CA1 pyramidal neuron A-type K+ channels |
| title | The shaping of two distinct dendritic spikes by A-type voltage-gated K+ channels |
| title_full | The shaping of two distinct dendritic spikes by A-type voltage-gated K+ channels |
| title_fullStr | The shaping of two distinct dendritic spikes by A-type voltage-gated K+ channels |
| title_full_unstemmed | The shaping of two distinct dendritic spikes by A-type voltage-gated K+ channels |
| title_short | The shaping of two distinct dendritic spikes by A-type voltage-gated K+ channels |
| title_sort | shaping of two distinct dendritic spikes by a type voltage gated k channels |
| topic | Dendrite calcium channel Dendritic excitability CA1 pyramidal neuron A-type K+ channels |
| url | http://journal.frontiersin.org/Journal/10.3389/fncel.2015.00469/full |
| work_keys_str_mv | AT sungchileyang theshapingoftwodistinctdendriticspikesbyatypevoltagegatedkchannels AT chaminetang theshapingoftwodistinctdendriticspikesbyatypevoltagegatedkchannels AT sunggueyang theshapingoftwodistinctdendriticspikesbyatypevoltagegatedkchannels AT sungchileyang shapingoftwodistinctdendriticspikesbyatypevoltagegatedkchannels AT chaminetang shapingoftwodistinctdendriticspikesbyatypevoltagegatedkchannels AT sunggueyang shapingoftwodistinctdendriticspikesbyatypevoltagegatedkchannels |