Modeling the Spatial Reach of the LFP

Lindén, Henrik; Tetzlaff, Tom; Potjans, Tobias C.; Pettersen, Klas H.; Grün, Sonja; Diesmann, Markus; Einevoll, Gaute T.

doi:10.1016/j.neuron.2011.11.006

Cited by 421 publications

(556 citation statements)

References 52 publications

(80 reference statements)

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“…As shown in other studies, synchronization across such large areas of cortex is unlikely to be orchestrated by multiple LFP sources generated by uncorrelated synaptic activity or local field effects. 34 In support of this, we have shown that pathologic HFO networks have similar breakdown patterns across multiple seizure types (complex partial, generalized tonic-clonic, and secondarily generalized tonic-clonic) and therefore, likely manifest a common underlying epileptogenic process. This nonsynaptic mechanism is distinctly different from other well-described modes of generation of oscillatory activity, where intrinsic oscillatory dynamics of individual neurons coupled by gap junctions organize coherent oscillations, such as gamma oscillations.…”

Section: Discussionsupporting

confidence: 68%

High‐frequency brain networks undergo modular breakdown during epileptic seizures

et al. 2016

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SUMMARYObjective: Cortical high-frequency oscillations (HFOs; 100-500 Hz) play a critical role in the pathogenesis of epilepsy; however, whether they represent a true epileptogenic process remains largely unknown. HFOs have been recorded in the human cortex but their network dynamics during the transitional period from interictal to ictal phase remain largely unknown. We sought to determine the high-frequency network dynamics of these oscillations in patients with epilepsy who were undergoing intracranial electroencephalographic recording for seizure localization. Methods: We applied a graph theoretical analysis framework to high-resolution intracranial electroencephalographic recordings of 24 interictal and 24 seizure periods to identify the spatiotemporal evolution of community structure of high-frequency cortical networks at rest and during multiple seizure episodes in patients with intractable epilepsy. Results: Cortical networks at all examined frequencies showed temporally stable community architecture in all 24 interictal periods. During seizure periods, high-frequency networks showed a significant breakdown of their community structure, which was characterized by the emergence of numerous small nodal communities, not limited to seizure foci and encompassing the entire recorded network. Such network disorganization was observed on average 225 s before the electrographic seizure onset and extended on average 190 s after termination of the seizure. Gamma networks were characterized by stable community dynamics during resting and seizure periods. Significance: Our findings suggest that the modular breakdown of high-frequency cortical networks represents a distinct functional pathology that underlies epileptogenesis and corresponds to a cortical state of highest propensity to generate seizures.

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Section: Discussionsupporting

confidence: 68%

High‐frequency brain networks undergo modular breakdown during epileptic seizures

et al. 2016

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“…In recent experimental and modeling studies, there has been a lot of debate on the source and spatial extent of LFPs (1)(2)(3)(4)(5)(6)(7)(8)(9). However, most of these studies have used neurons with passive dendrites in their models and/or have largely focused on the contribution of spike-generating conductances to LFPs (7,8,10,11).…”

mentioning

confidence: 99%

HCN channels enhance spike phase coherence and regulate the phase of spikes and LFPs in the theta-frequency range

Sinha

Narayanan

2015

Proc. Natl. Acad. Sci. U.S.A.

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What are the implications for the existence of subthreshold ion channels, their localization profiles, and plasticity on local field potentials (LFPs)? Here, we assessed the role of hyperpolarizationactivated cyclic-nucleotide-gated (HCN) channels in altering hippocampal theta-frequency LFPs and the associated spike phase. We presented spatiotemporally randomized, balanced theta-modulated excitatory and inhibitory inputs to somatically aligned, morphologically realistic pyramidal neuron models spread across a cylindrical neuropil. We computed LFPs from seven electrode sites and found that the insertion of an experimentally constrained HCN-conductance gradient into these neurons introduced a location-dependent lead in the LFP phase without significantly altering its amplitude. Further, neurons fired action potentials at a specific theta phase of the LFP, and the insertion of HCN channels introduced large lags in this spike phase and a striking enhancement in neuronal spike-phase coherence. Importantly, graded changes in either HCN conductance or its half-maximal activation voltage resulted in graded changes in LFP and spike phases. Our conclusions on the impact of HCN channels on LFPs and spike phase were invariant to changes in neuropil size, to morphological heterogeneity, to excitatory or inhibitory synaptic scaling, and to shifts in the onset phase of inhibitory inputs. Finally, we selectively abolished the inductive lead in the impedance phase introduced by HCN channels without altering neuronal excitability and found that this inductive phase lead contributed significantly to changes in LFP and spike phase. Our results uncover specific roles for HCN channels and their plasticity in phase-coding schemas and in the formation and dynamic reconfiguration of neuronal cell assemblies.L ocal field potentials (LFPs) have been largely believed to be a reflection of the synaptic drive that impinges on a neuron. In recent experimental and modeling studies, there has been a lot of debate on the source and spatial extent of LFPs (1-9). However, most of these studies have used neurons with passive dendrites in their models and/or have largely focused on the contribution of spike-generating conductances to LFPs (7,8,10,11). Despite the widely acknowledged regulatory roles of subthreshold-activated ion channels and their somatodendritic gradients in the physiology and pathophysiology of synapses and neurons (12-17), the implications for their existence on LFPs and neuronal spike phase have surprisingly remained unexplored. This lacuna in LFP analysis is especially striking because local and widespread plasticity of these channels has been observed across several physiological and pathological conditions, translating to putative roles for these channels in neural coding, homeostasis, disease etiology and remedies, learning, and memory (16,(18)(19)(20)(21)(22)(23).In this study, we focus on the role of hyperpolarization-activated cyclic nucleotide-gated (HCN) channels that mediate the h current (I h ) in regulating LFPs and ...

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“…For correlated activity it is more difficult, but they concluded that "...the LFP recorded by an electrode is dominated by populations with substantial synaptic processes in the recording layer." [27]. Hence, nearby sources contribute most to the LFP and distant sources contributions are subject to strong attenuation.…”

Section: Origin Of Invasive Bci Signalsmentioning

confidence: 99%

On Similarities and Differences of Invasive and Non-Invasive Electrical Brain Signals in Brain-Computer Interfacing

Steyrl¹,

Kobler²,

Müller-Putz³

2016

JBiSE

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Modeling the Spatial Reach of the LFP

Cited by 421 publications

References 52 publications

High‐frequency brain networks undergo modular breakdown during epileptic seizures

High‐frequency brain networks undergo modular breakdown during epileptic seizures

HCN channels enhance spike phase coherence and regulate the phase of spikes and LFPs in the theta-frequency range

On Similarities and Differences of Invasive and Non-Invasive Electrical Brain Signals in Brain-Computer Interfacing

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