dc.contributor.author
Klemz, Alexander
dc.contributor.author
Wildner, Florian
dc.contributor.author
Tütüncü, Ecem
dc.contributor.author
Gerevich, Zoltan
dc.date.accessioned
2022-03-23T13:53:13Z
dc.date.available
2022-03-23T13:53:13Z
dc.identifier.uri
https://refubium.fu-berlin.de/handle/fub188/34488
dc.identifier.uri
http://dx.doi.org/10.17169/refubium-34206
dc.description.abstract
Ion channels activated around the subthreshold membrane potential determine the likelihood of neuronal firing in response to synaptic inputs, a process described as intrinsic neuronal excitability. Long-term plasticity of chemical synaptic transmission is traditionally considered the main cellular mechanism of information storage in the brain; however, voltage- and calcium-activated channels modulating the inputs or outputs of neurons are also subjects of plastic changes and play a major role in learning and memory formation. Gamma oscillations are associated with numerous higher cognitive functions such as learning and memory, but our knowledge of their dependence on intrinsic plasticity is by far limited. Here we investigated the roles of potassium and calcium channels activated at near subthreshold membrane potentials in cholinergically induced persistent gamma oscillations measured in the CA3 area of rat hippocampal slices. Among potassium channels, which are responsible for the afterhyperpolarization in CA3 pyramidal cells, we found that blockers of SK (KCa2) and KV7.2/7.3 (KCNQ2/3), but not the BK (KCa1.1) and IK (KCa3.1) channels, increased the power of gamma oscillations. On the contrary, activators of these channels had an attenuating effect without affecting the frequency. Pharmacological blockade of the low voltage-activated T-type calcium channels (CaV3.1–3.3) reduced gamma power and increased the oscillation peak frequency. Enhancement of these channels also inhibited the peak power without altering the frequency of the oscillations. The presented data suggest that voltage- and calcium-activated ion channels involved in intrinsic excitability strongly regulate the power of hippocampal gamma oscillations. Targeting these channels could represent a valuable pharmacological strategy against cognitive impairment.
en
dc.rights.uri
https://creativecommons.org/licenses/by/4.0/
dc.subject.ddc
600 Technik, Medizin, angewandte Wissenschaften::610 Medizin und Gesundheit::610 Medizin und Gesundheit
dc.title
Regulation of Hippocampal Gamma Oscillations by Modulation of Intrinsic Neuronal Excitability
dc.type
Wissenschaftlicher Artikel
dcterms.bibliographicCitation.articlenumber
778022
dcterms.bibliographicCitation.doi
10.3389/fncir.2021.778022
dcterms.bibliographicCitation.journaltitle
Frontiers in Neural Circuits
dcterms.bibliographicCitation.originalpublishername
Frontiers Media SA
dcterms.bibliographicCitation.volume
15
refubium.affiliation
Charité - Universitätsmedizin Berlin
refubium.resourceType.isindependentpub
no
dcterms.accessRights.openaire
open access
dcterms.bibliographicCitation.pmid
35177966
dcterms.isPartOf.eissn
1662-5110