| First Author | Kis N | Year | 2024 |
| Journal | Proc Natl Acad Sci U S A | Volume | 121 |
| Issue | 46 | Pages | e2321501121 |
| PubMed ID | 39503887 | Mgi Jnum | J:365236 |
| Mgi Id | MGI:7782339 | Doi | 10.1073/pnas.2321501121 |
| Citation | Kis N, et al. (2024) Cholinergic regulation of dendritic Ca(2+) spikes controls firing mode of hippocampal CA3 pyramidal neurons. Proc Natl Acad Sci U S A 121(46):e2321501121 |
| abstractText | Active dendritic integrative mechanisms such as regenerative dendritic spikes enrich the information processing abilities of neurons and fundamentally contribute to behaviorally relevant computations. Dendritic Ca(2+) spikes are generally thought to produce plateau-like dendritic depolarization and somatic complex spike burst (CSB) firing, which can initiate rapid changes in spatial coding properties of hippocampal pyramidal cells (PCs). However, here we reveal that a morpho-topographically distinguishable subpopulation of rat and mouse hippocampal CA3PCs exhibits compound apical dendritic Ca(2+) spikes with unusually short duration that do not support the firing of sustained CSBs. These Ca(2+) spikes are mediated by L-type Ca(2+) channels and their time course is restricted by A- and M-type K(+) channels. Cholinergic activation powerfully converts short Ca(2+) spikes to long-duration forms, and facilitates and prolongs CSB firing. We propose that cholinergic neuromodulation controls the ability of a CA3PC subtype to generate sustained plateau potentials, providing a state-dependent dendritic mechanism for memory encoding and retrieval. |
