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Neuron. 2018 Dec 5;100(5):1224-1240.e13. doi: 10.1016/j.neuron.2018.09.041. Epub 2018 Oct 25.

Dissecting the Synapse- and Frequency-Dependent Network Mechanisms of In Vivo Hippocampal Sharp Wave-Ripples.

Author information

1
Department of Physiology of Cognitive Processes, Max Planck Institute for Biological Cybernetics, Tübingen, Germany; Graduate School of Neural & Behavioral Sciences, International Max Planck Research School, Eberhard-Karls University of Tübingen, Tübingen, Germany.
2
Graduate School of Neural & Behavioral Sciences, International Max Planck Research School, Eberhard-Karls University of Tübingen, Tübingen, Germany; Werner-Reichardt Centre for Integrative Neuroscience, Tübingen, Germany; Hertie Institute for Clinical Brain Research, University of Tübingen, Tübingen, Germany.
3
Department of Physiology of Cognitive Processes, Max Planck Institute for Biological Cybernetics, Tübingen, Germany; Centre for Imaging Sciences, Biomedical Imaging Institute, The University of Manchester, Manchester, UK.
4
Department of Physiology of Cognitive Processes, Max Planck Institute for Biological Cybernetics, Tübingen, Germany; Department of Empirical Inference, Max Planck Institute for Intelligent Systems and Max Planck ETH Center for Learning Systems, Tübingen, Germany. Electronic address: michel.besserve@tuebingen.mpg.de.

Abstract

Hippocampal ripple oscillations likely support reactivation of memory traces that manifest themselves as temporally organized spiking of sparse neuronal ensembles. However, the network mechanisms concurring to achieve this function are largely unknown. We designed a multi-compartmental model of the CA3-CA1 subfields to generate biophysically realistic ripple dynamics from the cellular level to local field potentials. Simulations broadly parallel in vivo observations and support that ripples emerge from CA1 pyramidal spiking paced by recurrent inhibition. In addition to ripple oscillations, key coordination mechanisms involve concomitant aspects of network activity. Recurrent synaptic interactions in CA1 exhibit slow-gamma band coherence with CA3 input, thus offering a way to coordinate CA1 activities with CA3 inducers. Moreover, CA1 feedback inhibition controls the content of spontaneous replay during CA1 ripples, forming new mnemonic representations through plasticity. These insights are consistent with slow-gamma interactions and interneuronal circuit plasticity observed in vivo, suggesting a multifaceted ripple-related replay phenomenon.

KEYWORDS:

E-I balance; brain rhythms; compartmental models; hippocampus; learning; local field potentials; memory; plasticity; replay; sharp wave-ripples

PMID:
30482688
DOI:
10.1016/j.neuron.2018.09.041
[Indexed for MEDLINE]
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