a-Calcium Calmodulin Kinase II Modulates the Temporal Structure of Hippocampal Bursting Patterns

Hdl Handle:
http://hdl.handle.net/10675.2/778
Title:
a-Calcium Calmodulin Kinase II Modulates the Temporal Structure of Hippocampal Bursting Patterns
Authors:
Cho, Jeiwon; Bhatt, Rushi; Elgersma, Ype; Silva, Alcino J.
Abstract:
The alpha calcium calmodulin kinase II (a-CaMKII) is known to play a key role in CA1/CA3 synaptic plasticity, hippocampal place cell stability and spatial learning. Additionally, there is evidence from hippocampal electrophysiological slice studies that this kinase has a role in regulating ion channels that control neuronal excitability. Here, we report in vivo single unit studies, with a-CaMKII mutant mice, in which threonine 305 was replaced with an aspartate (a-CaMKIIT305D mutants), that indicate that this kinase modulates spike patterns in hippocampal pyramidal neurons. Previous studies showed that a- CaMKIIT305D mutants have abnormalities in both hippocampal LTP and hippocampal-dependent learning. We found that besides decreased place cell stability, which could be caused by their LTP impairments, the hippocampal CA1 spike patterns of a-CaMKIIT305D mutants were profoundly abnormal. Although overall firing rate, and overall burst frequency were not significantly altered in these mutants, inter-burst intervals, mean number of intra-burst spikes, ratio of intra-burst spikes to total spikes, and mean intra-burst intervals were significantly altered. In particular, the intra burst intervals of place cells in a- CaMKIIT305D mutants showed higher variability than controls. These results provide in vivo evidence that besides its wellknown function in synaptic plasticity, a-CaMKII, and in particular its inhibitory phosphorylation at threonine 305, also have a role in shaping the temporal structure of hippocampal burst patterns. These results suggest that some of the molecular processes involved in acquiring information may also shape the patterns used to encode this information.
Editors:
Tsien, Joe Z.
Citation:
PLoS One. 2012 Feb 20; 7(2):e31649
Issue Date:
20-Feb-2012
URI:
http://hdl.handle.net/10675.2/778
DOI:
10.1371/journal.pone.0031649
PubMed ID:
22363696
PubMed Central ID:
PMC3282754
Type:
Article
ISSN:
1932-6203
Appears in Collections:
Department of Neurology: Faculty Research and Presentations

Full metadata record

DC FieldValue Language
dc.contributor.authorCho, Jeiwonen_US
dc.contributor.authorBhatt, Rushien_US
dc.contributor.authorElgersma, Ypeen_US
dc.contributor.authorSilva, Alcino J.en_US
dc.contributor.editorTsien, Joe Z.-
dc.date.accessioned2012-10-26T20:30:43Z-
dc.date.available2012-10-26T20:30:43Z-
dc.date.issued2012-02-20en_US
dc.identifier.citationPLoS One. 2012 Feb 20; 7(2):e31649en_US
dc.identifier.issn1932-6203en_US
dc.identifier.pmid22363696en_US
dc.identifier.doi10.1371/journal.pone.0031649en_US
dc.identifier.urihttp://hdl.handle.net/10675.2/778-
dc.description.abstractThe alpha calcium calmodulin kinase II (a-CaMKII) is known to play a key role in CA1/CA3 synaptic plasticity, hippocampal place cell stability and spatial learning. Additionally, there is evidence from hippocampal electrophysiological slice studies that this kinase has a role in regulating ion channels that control neuronal excitability. Here, we report in vivo single unit studies, with a-CaMKII mutant mice, in which threonine 305 was replaced with an aspartate (a-CaMKIIT305D mutants), that indicate that this kinase modulates spike patterns in hippocampal pyramidal neurons. Previous studies showed that a- CaMKIIT305D mutants have abnormalities in both hippocampal LTP and hippocampal-dependent learning. We found that besides decreased place cell stability, which could be caused by their LTP impairments, the hippocampal CA1 spike patterns of a-CaMKIIT305D mutants were profoundly abnormal. Although overall firing rate, and overall burst frequency were not significantly altered in these mutants, inter-burst intervals, mean number of intra-burst spikes, ratio of intra-burst spikes to total spikes, and mean intra-burst intervals were significantly altered. In particular, the intra burst intervals of place cells in a- CaMKIIT305D mutants showed higher variability than controls. These results provide in vivo evidence that besides its wellknown function in synaptic plasticity, a-CaMKII, and in particular its inhibitory phosphorylation at threonine 305, also have a role in shaping the temporal structure of hippocampal burst patterns. These results suggest that some of the molecular processes involved in acquiring information may also shape the patterns used to encode this information.en_US
dc.rightsCho et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.en_US
dc.subjectResearch Articleen_US
dc.subjectBiologyen_US
dc.subjectAnatomy and Physiologyen_US
dc.subjectBiochemistryen_US
dc.subjectComputational Biologyen_US
dc.subjectComputational Neuroscienceen_US
dc.subjectModel Organismsen_US
dc.subjectAnimal Modelsen_US
dc.subjectMolecular Cell Biologyen_US
dc.subjectCellular Typesen_US
dc.subjectSignal Transductionen_US
dc.subjectSignaling in Selected Disciplinesen_US
dc.subjectNeuroscienceen_US
dc.titlea-Calcium Calmodulin Kinase II Modulates the Temporal Structure of Hippocampal Bursting Patternsen_US
dc.typeArticleen_US
dc.identifier.pmcidPMC3282754en_US
dc.contributor.corporatenameDepartment of Neurology-
dc.contributor.corporatenameCollege of Graduate Studies-
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