Inhibiting presynaptic calcium channel motility in the auditory cortex suppresses synchronized input processing.

Autor: Deane KE; Leibniz Institute for Neurobiology, Magdeburg, Germany.; University of California, Riverside, Riverside, CA, United States., Klymentiev R; Leibniz Institute for Neurobiology, Magdeburg, Germany.; Institute of Biology, Otto von Guericke University, Magdeburg, Germany., Heck J; Leibniz Institute for Neurobiology, Magdeburg, Germany.; European Molecular Biology Laboratory, Heidelberg, Germany., Mark MD; Faculty of Biology and Biotechnology, Ruhr-University Bochum, Bochum, Germany., Ohl FW; Leibniz Institute for Neurobiology, Magdeburg, Germany.; Institute of Biology, Otto von Guericke University, Magdeburg, Germany.; Center for Behavioral Brain Sciences (CBBS), Magdeburg, Germany., Heine M; Leibniz Institute for Neurobiology, Magdeburg, Germany.; Institute of Developmental Biology and Neurobiology, Johannes Gutenberg University Mainz, Mainz, Germany., Happel MFK; Leibniz Institute for Neurobiology, Magdeburg, Germany.; Center for Behavioral Brain Sciences (CBBS), Magdeburg, Germany.; MSB Medical School Berlin, Medical Faculty, Berlin, Germany.
Jazyk: angličtina
Zdroj: Frontiers in cellular neuroscience [Front Cell Neurosci] 2024 Apr 10; Vol. 18, pp. 1369047. Date of Electronic Publication: 2024 Apr 10 (Print Publication: 2024).
DOI: 10.3389/fncel.2024.1369047
Abstrakt: Introduction: The emergent coherent population activity from thousands of stochastic neurons in the brain is believed to constitute a key neuronal mechanism for salient processing of external stimuli and its link to internal states like attention and perception. In the sensory cortex, functional cell assemblies are formed by recurrent excitation and inhibitory influences. The stochastic dynamics of each cell involved is largely orchestrated by presynaptic CAV2.1 voltage-gated calcium channels (VGCCs). Cav2.1 VGCCs initiate the release of neurotransmitters from the presynaptic compartment and are therefore able to add variability into synaptic transmission which can be partly explained by their mobile organization around docked vesicles.
Methods: To investigate the relevance of Cav2.1 channel surface motility for the input processing in the primary auditory cortex (A1) in vivo, we make use of a new optogenetic system which allows for acute, reversable cross-linking Cav2.1 VGCCs via a photo-cross-linkable cryptochrome mutant, CRY2olig. In order to map neuronal activity across all cortical layers of the A1, we performed laminar current-source density (CSD) recordings with varying auditory stimulus sets in transgenic mice with a citrine tag on the N-terminus of the VGCCs.
Results: Clustering VGCCs suppresses overall sensory-evoked population activity, particularly when stimuli lead to a highly synchronized distribution of synaptic inputs.
Discussion: Our findings reveal the importance of membrane dynamics of presynaptic calcium channels for sensory encoding by dynamically adjusting network activity across a wide range of synaptic input strength.
Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
(Copyright © 2024 Deane, Klymentiev, Heck, Mark, Ohl, Heine and Happel.)
Databáze: MEDLINE