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Dendrite-Specific Amplification of Weak Synaptic Input during Network Activity In Vivo
Ferrarese, L.
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Jouhanneau, J.-S.
;
Remme, M.W.H.
;
Kremkow, J.
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Katona, G. [Katona, Gergely (Farmakológia), author] MTA-PPKE ITK-NAP B Two-photon measurement techn... (PPCU / ITK); Neuronhálózat és Dendritikus Aktivitás Kutatócs...
;
Rózsa, B. [Rózsa J., Balázs (Idegtudomány, fizika), author] Információs Technológiai és Bionikai Kar (PPCU); Neuronhálózat és Dendritikus Aktivitás Kutatócs...
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Schreiber, S.
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Poulet, J.F.A.
English Article (Journal Article) Scientific
Published:
CELL REPORTS 2639-1856 2211-1247
24
(13)
pp. 3455-3465.e5
2018
SJR Scopus - Biochemistry, Genetics and Molecular Biology (miscellaneous): D1
Identifiers
MTMT: 30309775
DOI:
10.1016/j.celrep.2018.08.088
WoS:
000445524700010
Scopus:
85053671433
PubMed:
30257207
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. © 2018 The Authors
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