Dendrite-Specific Amplification of Weak Synaptic Input during Network Activity In Vivo
Leiron Ferrarese,
Jean-Sébastien Jouhanneau,
Michiel W.H. Remme,
Jens Kremkow,
Gergely Katona,
Balázs Rózsa,
Susanne Schreiber,
James F.A. Poulet
Affiliations
Leiron Ferrarese
Department of Neuroscience, Max Delbrück Center for Molecular Medicine in the Helmholtz Association (MDC), Berlin-Buch, Robert-Rössle-Str. 10, 13092 Berlin, Germany; Neuroscience Research Center and Cluster of Excellence NeuroCure, Charité-Universitätsmedizin Berlin, Charitéplatz 1, 10117 Berlin, Germany
Jean-Sébastien Jouhanneau
Department of Neuroscience, Max Delbrück Center for Molecular Medicine in the Helmholtz Association (MDC), Berlin-Buch, Robert-Rössle-Str. 10, 13092 Berlin, Germany; Neuroscience Research Center and Cluster of Excellence NeuroCure, Charité-Universitätsmedizin Berlin, Charitéplatz 1, 10117 Berlin, Germany
Michiel W.H. Remme
Department of Biology, Institute for Theoretical Biology, Humboldt-Universität zu Berlin and Bernstein Center for Computational Neuroscience Berlin, Philippstrasse 13, 10115 Berlin, Germany
Jens Kremkow
Department of Neuroscience, Max Delbrück Center for Molecular Medicine in the Helmholtz Association (MDC), Berlin-Buch, Robert-Rössle-Str. 10, 13092 Berlin, Germany; Neuroscience Research Center and Cluster of Excellence NeuroCure, Charité-Universitätsmedizin Berlin, Charitéplatz 1, 10117 Berlin, Germany; Department of Biology, Institute for Theoretical Biology, Humboldt-Universität zu Berlin and Bernstein Center for Computational Neuroscience Berlin, Philippstrasse 13, 10115 Berlin, Germany
Gergely Katona
Laboratory of 3D Functional Network and Dendritic Imaging, Institute of Experimental Medicine, Hungarian Academy of Sciences, Budapest 1083, Hungary; MTA-PPKE ITK-NAP B – 2p Measurement Technology Group, The Faculty of Information Technology, Pázmány Péter Catholic University, Budapest 1083, Hungary
Balázs Rózsa
Laboratory of 3D Functional Network and Dendritic Imaging, Institute of Experimental Medicine, Hungarian Academy of Sciences, Budapest 1083, Hungary; The Faculty of Information Technology, Pázmány Péter Catholic University, Budapest 1083, Hungary
Susanne Schreiber
Department of Biology, Institute for Theoretical Biology, Humboldt-Universität zu Berlin and Bernstein Center for Computational Neuroscience Berlin, Philippstrasse 13, 10115 Berlin, Germany
James F.A. Poulet
Department of Neuroscience, Max Delbrück Center for Molecular Medicine in the Helmholtz Association (MDC), Berlin-Buch, Robert-Rössle-Str. 10, 13092 Berlin, Germany; Neuroscience Research Center and Cluster of Excellence NeuroCure, Charité-Universitätsmedizin Berlin, Charitéplatz 1, 10117 Berlin, Germany; Corresponding author
Summary: Excitatory synaptic input reaches the soma of a cortical excitatory pyramidal neuron via anatomically segregated apical and basal dendrites. In vivo, dendritic inputs are integrated during depolarized network activity, but how network activity affects apical and basal inputs is not understood. Using subcellular two-photon stimulation of Channelrhodopsin2-expressing layer 2/3 pyramidal neurons in somatosensory cortex, nucleus-specific thalamic optogenetic stimulation, and paired recordings, we show that slow, depolarized network activity amplifies small-amplitude synaptic inputs targeted to basal dendrites but reduces the amplitude of all inputs from apical dendrites and the cell soma. Intracellular pharmacology and mathematical modeling suggests that the amplification of weak basal inputs is mediated by postsynaptic voltage-gated channels. Thus, network activity dynamically reconfigures the relative somatic contribution of apical and basal inputs and could act to enhance the detectability of weak synaptic inputs. : Ferrarese et al. investigate the impact of network activity on synaptic integration in cortical L2/3 pyramidal neurons in vivo. They report a reduction of apical dendritic inputs but an amplification of small-amplitude basal inputs during depolarized phases of slow network activity. The amplification is dependent on postsynaptic voltage-gated channels.