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Local field potential
Local field potential
Local field potential
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Local field potentials (LFP) are transient electrical signals generated in nerves and other tissues by the summed and synchronous electrical activity of the individual cells (e.g. neurons) in that tissue. LFP are "extracellular" signals, meaning that they are generated by transient imbalances in ion concentrations in the spaces outside the cells, that result from cellular electrical activity. LFP are 'local' because they are recorded by an electrode placed nearby the generating cells. As a result of the Inverse-square law, such electrodes can only 'see' potentials in a spatially limited radius. They are 'potentials' because they are generated by the voltage that results from charge separation in the extracellular space. They are 'field' because those extracellular charge separations essentially create a local electric field. LFP are typically recorded with a high-impedance microelectrode placed in the midst of the population of cells generating it. They can be recorded, for example, via a microelectrode placed in the brain of a human[1] or animal subject, or in an in vitro brain thin slice.

Background

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During local field potential recordings, a signal is recorded using an extracellular microelectrode placed sufficiently far from individual local neurons to prevent any particular cell from dominating the electrophysiological signal. This signal is then low-pass filtered, cut off at ~300 Hz, to obtain the local field potential (LFP) that can be recorded electronically or displayed on an oscilloscope for analysis. The low impedance and positioning of the electrode allows the activity of a large number of neurons to contribute to the signal. The unfiltered signal reflects the sum of action potentials from cells within approximately 50-350 μm from the tip of the electrode[2][3] and slower ionic events from within 0.5–3 mm from the tip of the electrode.[4] The low-pass filter removes the spike component of the signal and passes the lower frequency signal, the LFP.

The voltmeter or analog-to-digital converter to which the microelectrode is connected measures the electrical potential difference (measured in volts) between the microelectrode and a reference electrode. One end of the reference electrode is also connected to the voltmeter while the other end is placed in a medium which is continuous with, and compositionally identical to the extracellular medium. In a simple fluid, with no biological component present, there would be slight fluctuations in the measured potential difference around an equilibrium point, this is known as the thermal noise. This is due to the random movement of ions in the medium and electrons in the electrode. However, when placed in neural tissue the opening of an ion channel results in the net flow of ions into the cell from the extracellular medium, or out of the cell into the extracellular medium. These local currents result in larger changes in the electrical potential between the local extracellular medium and the interior of the recording electrode. The overall recorded signal thus represents the potential caused by the sum of all local currents on the surface of the electrode.

Synchronised input

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Spike-triggered averages
Spike-triggered averages of LFP from 4 recording sites. The spike is the sharp downward deflection at t = 0. The spike is preceded by slow oscillations (alpha), the spike happens at the trough of the LFP.[5]

The local field potential is believed to represent the sum of synaptic inputs into the observed area, as opposed to the spikes, which represents the output from the area. The fast fluctuations are mostly caused by the short inward and outward currents of action potentials, while the LFP is composed of the more sustained currents in the tissue that are generated by synaptic activity (EPSCs and IPSCs).[6] Data-driven models have shown a predictive relationship between the LFPs and spike activity.[7] A common method to investigate LFP oscillations that lead to spikes is to calculate spike-triggered averages (see figure). This is done after the recording (off line) by detecting the spikes as fast downward deflections, cutting out the temporal sections around the spike (+/- 250 ms) and averaging the spike-aligned traces for each recording site.[5] Alternatively, spikes can be removed from the extracellular recording traces by low-pass filtering, revealing the LFP.

Geometrical arrangement

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Which cells contribute to the slow field variations is determined by the geometric configuration of the cells themselves. In some cells, the dendrites face one direction and the soma another, such as the pyramidal cells. This is known as an open field geometrical arrangement. When there is simultaneous activation of the dendrites a strong dipole is produced. In cells where the dendrites are arranged more radially, the potential difference between individual dendrites and the soma tend to cancel out with diametrically opposite dendrites, this configuration is called a closed field geometrical arrangement. As a result the net potential difference over the whole cell when the dendrites are simultaneously activated tends to be very small. Thus changes in the local field potential represent simultaneous dendritic events in cells in the open field configuration.

Simple interpretation of LFP

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Interpreting LFP through the characteristics of neuronal activity remains a challenge. At the very least, it is clear that electrically compact neurons do not contribute to LFP. Consequently, the minimal model for calculating LFP is a two-compartment model. According to this model, the LFP is determined by the current flowing between the dendritic and somatic compartments. The synaptic component of this current is approximately proportional to the difference between the dendritic and somatic membrane potentials and is combined with the spiking component.[8]

Low-pass filtering of extracellular space

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Part of the low-pass filtering giving rise to local field potentials is due to complex electrical properties of extracellular space.[9] The fact that the extracellular space is not homogeneous, and is composed of a complex aggregate of highly conductive fluids and low-conductive and capacitive membranes, can exert strong low-pass filtering properties. Ionic diffusion, which plays an important role in membrane potential variations, can also act as a low-pass filter.

References

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Local field potential

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The local field potential (LFP) is a low-frequency extracellular electrical signal recorded from the using microelectrodes, reflecting the summed transmembrane currents—primarily synaptic inputs—from synchronized populations of neurons within a circumscribed volume of tissue, typically on the order of hundreds of micrometers to a few millimeters. Unlike single-unit recordings that capture individual action potentials, LFPs provide a population-level measure of subthreshold neural activity, including excitatory and inhibitory postsynaptic potentials, and are distinct from larger-scale signals like (EEG) due to their higher . These signals are , spanning frequencies from below 1 Hz to around 300 Hz, and are generated by the net flow of ionic currents across neuronal membranes in response to afferent inputs and intrinsic network dynamics. Biophysically, LFPs arise from the spatial and temporal of current sources and sinks in neuronal ensembles, where dendritic synaptic currents dominate over spike-related contributions, though the latter can influence higher-frequency components under conditions of strong synchrony. The signal's and are shaped by factors such as neuronal , tissue conductivity, and volume conduction, which allows contributions from both local and somewhat distant sources—extending laterally up to 6 mm and vertically toward the surface in some cases—challenging the traditional view of LFPs as strictly "local." Common misconceptions include assuming LFP polarity directly indicates excitatory versus inhibitory activity or that signal scales linearly with the number of active synapses; in reality, extensive cancellation of opposing currents and filtering effects often result in signals that are larger at a from the source in layered structures like the cortex or hippocampus. In research, LFPs are invaluable for probing neural oscillations—such as (4–8 Hz) and gamma (30–100 Hz) rhythms—that underpin cognitive processes like , , and sensory integration, offering insights into how populations coordinate information flow across networks. They also correlate with hemodynamic signals in (fMRI), linking electrical activity to metabolic demands, and serve as a bridge between invasive single-neuron recordings and non-invasive methods like EEG or (MEG). Applications extend to clinical domains, including brain-computer interfaces for motor restoration in and the study of pathological rhythms in disorders like , where LFP analysis reveals disrupted synchrony. Advances in high-density arrays have further enhanced LFP utility, enabling current source density (CSD) computations to localize activity sources with greater precision.

Fundamentals

Definition and Overview

The local field potential (LFP) is defined as the low-frequency component of extracellular voltage fluctuations recorded from neural tissue using microelectrodes, primarily reflecting the summed postsynaptic potentials arising from synaptic currents in nearby neuronal populations. These signals capture the collective electrical activity of ensembles of neurons within a confined volume, distinguishing LFPs as a measure of population-level dynamics rather than isolated cellular events. Key characteristics of LFPs include a typical frequency range of 0.1 to 200 Hz, encompassing oscillations such as (4–8 Hz) and gamma (30–100 Hz) bands, though higher frequencies up to several hundred Hz may contribute under certain conditions. In contrast to action potentials, which are brief, high-frequency transients (~1 ms duration) generated by individual neurons, LFPs arise from slower synaptic processes and are attenuated at higher frequencies due to the filtering properties of the extracellular medium. The spatial scale of LFPs typically extends over hundreds of micrometers to a few millimeters, sensitive to synchronized activity in neuronal populations within this volume, though contributions from more distant sources can occur via volume conduction; this distinguishes them from broader signals like (ECoG), which span millimeters to centimeters. Understanding LFPs requires familiarity with foundational neuronal : neurons maintain a resting of approximately –65 to –70 mV, established by selective ion permeability and across the . Synaptic transmission occurs when presynaptic neurons release neurotransmitters, opening ion channels in the postsynaptic membrane and generating transient depolarizations (excitatory postsynaptic potentials, or EPSPs) or hyperpolarizations (inhibitory postsynaptic potentials, or IPSPs) that alter the by a few millivolts. When these postsynaptic potentials occur synchronously across multiple neurons, their associated transmembrane currents produce measurable extracellular voltage changes, forming the basis of LFP signals. The abbreviation LFP has been in standard use since the mid-20th century to denote these localized extracellular potentials in .

Historical Development

The study of local field potentials (LFPs) originated in the early amid broader investigations into electrical activity using early electrophysiological techniques. In the 1920s and 1930s, pioneers such as Edgar Douglas Adrian and Bryan H.C. Matthews recorded slow potential waves from the exposed cortex during neurosurgical procedures in humans, identifying rhythmic fluctuations associated with sensory stimuli. Their seminal 1934 work demonstrated that these potentials, particularly in the occipital region, arose from synchronized neuronal responses to visual flicker, marking an initial distinction between fast action potentials and slower cortical waves. These observations laid foundational insights into collective neuronal signaling, though initially interpreted within the framework of surface (EEG). Advancements in the mid-20th century shifted focus toward more precise, intracellular and microelectrode-based recordings, enabling the conceptualization of LFPs as localized synaptic events. In 1951, John C. Eccles proposed that evoked cortical potentials, including what would later be termed LFPs, primarily reflect synchronized postsynaptic potentials in dendrites rather than axonal action potentials. This interpretation was bolstered by microelectrode studies in the 1950s and 1960s, notably by Vernon B. Mountcastle, whose 1957 experiments on cat somatosensory cortex used fine electrodes to map columnar organization while simultaneously capturing signals alongside single-unit activity. The term "local field potential" emerged during this period to describe these microelectrode-derived signals, distinguishing them from broader EEG by their restricted spatial scale and emphasis on subcortical or intracortical sources. Seminal intracellular recordings by Manfred R. Klee and colleagues in 1965, followed by Otto D. Creutzfeldt's group in 1966, further confirmed the synaptic origins of these potentials through direct correlations with dendritic membrane fluctuations. By the 1970s, neurophysiologists increasingly transitioned from surface EEG to intracortical LFP recordings, driven by refined electrode designs that improved signal localization and reduced artifacts. This era emphasized LFPs' utility in probing synaptic integration within specific cortical layers, as articulated in reviews synthesizing Eccles' earlier frameworks with new data from chronic implants. The digital in the and accelerated LFP research through the widespread adoption of multi-electrode arrays, which allowed high-density, simultaneous sampling across neural populations. The Utah array, developed by Richard A. Normann and colleagues at the starting in the late 1980s, exemplified this advance by enabling chronic recordings of LFPs and spikes from up to 100 sites, facilitating spatial mapping of oscillatory patterns and network dynamics. These innovations, detailed in early implementations like the silicon probe arrays, transformed LFPs into a cornerstone for studying population-level activity.

Biophysical Mechanisms

Synaptic Contributions

The local field potential (LFP) is predominantly generated by synaptic activity, where excitatory and inhibitory postsynaptic potentials (EPSPs and IPSPs) produce transmembrane currents that summate in the to create measurable voltage fluctuations. These currents arise from the collective action of synaptic inputs across neuronal populations, with the net extracellular voltage reflecting the imbalance of inward and outward flows following current cancellation within individual neurons. In cortical and hippocampal circuits, for instance, the synchronous activation of synapses on dendrites amplifies these signals, making synaptic sources the primary biophysical basis for LFPs. At the ionic level, excitatory synaptic currents primarily involve inward flows through and NMDA receptors, depolarizing the postsynaptic membrane and generating negative extracellular voltage deflections near the synaptic sites due to current sinks, while inhibitory currents mediated by GABA receptors often produce outward flows, resulting in positive potentials near the sites due to current sources, with the observed polarity depending on the location relative to the recording . These receptor-specific mechanisms ensure that LFPs capture the dynamic balance of excitation and inhibition; for example, in the hippocampus, /NMDA-driven EPSPs contribute to the negative phase of sharp waves, whereas IPSPs modulate the waveform's polarity through hyperpolarizing effects. The resulting transmembrane currents establish local voltage gradients that are essential for LFP generation, with the strength and timing of these ionic events directly influencing signal and content. Volume conduction plays a crucial role in propagating these synaptic currents as voltage fields through the extracellular medium, allowing LFPs to reflect activity from synaptic clefts within a radius of several hundred micrometers. The extracellular resistivity and of the tissue facilitate the spread of these fields, where current dipoles formed at synapses create detectable potentials that decay with but remain coherent over local scales due to the high conductivity of the brain's interstitial fluid. This propagation mechanism ensures that LFPs provide a spatially integrated view of synaptic dynamics, though the exact field shape is modulated by the orientation and distribution of synaptic sources. While synaptic mechanisms dominate, non-synaptic contributions such as those from gap junctions or glial cells are minor, becoming negligible compared to the robust synaptic inputs. Gap junctions may facilitate minor current shunts between neurons, and glial potassium buffering can subtly influence extracellular potentials, but experimental validations confirm that blocking synaptic transmission abolishes most LFP activity, underscoring the primacy of synaptic sources.

Role of Synchronized Neuronal Activity

Synchronized neuronal activity plays a pivotal role in generating prominent local field potential (LFP) signals by coordinating the timing of synaptic inputs across multiple neurons, resulting in phase-locking that produces coherent transmembrane currents and amplified . This phase-locking occurs when synaptic barrages arrive simultaneously at neuronal populations, aligning their fluctuations and enhancing the summation of postsynaptic currents in the . Such temporal coordination transforms weak, distributed synaptic events into detectable oscillatory patterns in the LFP, reflecting the collective dynamics of neural ensembles rather than isolated cellular activity. Prominent examples of this synchronization are seen in oscillatory rhythms within specific regions. In the hippocampus, oscillations (4-8 Hz) emerge from the phase-locked firing of s, driven by rhythmic inputs from the medial septum, which synchronize the population to produce coherent LFP waves during spatial navigation. Similarly, gamma oscillations (30-100 Hz) in the hippocampus arise from synchronized activity modulated by fast-spiking , where periodic inhibitory inputs align excitatory synaptic barrages to generate LFP peaks that facilitate information processing in CA1 networks. In the cortex, gamma rhythms reflect synchronized activity across local circuits, often linked to attentional states, where phase-locking enhances LFP amplitude during sensory integration. Several factors contribute to the promotion of this neuronal . Network connectivity, particularly through recurrent excitatory-inhibitory loops, enables the and of coherent activity across neuronal groups. Common afferent inputs from upstream regions, such as thalamic or entorhinal projections, provide synchronized drive that aligns firing phases in target populations. Additionally, neuromodulators like and norepinephrine modulate excitability and coupling strength, facilitating synchronization during by enhancing inhibitory activity and reducing asynchronous noise. Quantitatively, the degree of dramatically influences LFP amplitude: for uncorrelated neuronal activity, the signal scales with the of the number of contributing neurons (√N), reflecting random , whereas fully synchronized activity leads to linear scaling proportional to N, due to constructive interference of aligned currents. This enhancement underscores how temporal alignment amplifies LFP detectability, with synchronized ensembles producing signals orders of magnitude stronger than asynchronous ones.

Recording and Spatial Factors

Geometrical Arrangements in Recordings

Common electrode types for multi-site local field potential (LFP) recordings include probes, tetrodes, and arrays. probes consist of slender shanks with multiple recording sites arranged linearly or in a planar configuration, enabling high-density sampling along a single trajectory. Tetrodes, formed by bundling four fine microwires (typically 12-25 μm diameter), provide closely spaced sites for improved and are particularly useful in small animal models like for capturing both spiking activity and LFPs. arrays feature a three-dimensional grid of shanks, each tipped with a single , allowing simultaneous recordings from up to 100 sites across a broader cortical volume. Spatial considerations in LFP recordings emphasize geometry to balance locality and coverage. Recording site diameters typically range from 10-50 μm, with smaller tips (around 10-20 μm) favoring more localized signals and larger ones (up to 50 μm) capturing broader field potentials due to increased averaging over the surface. Inter-electrode spacing along shanks or between sites is commonly 50-200 μm, such as 100 μm vertical intervals on probes, to resolve laminar or columnar structures without excessive overlap in the spatial decay of LFP signals. Implantation depth varies by brain region—for instance, 1-2 mm into the or 2-3 mm for hippocampal targets—but must account for tissue trauma minimization and precise targeting via stereotaxic coordinates. Reference electrode placement is critical to reduce artifacts and common-mode noise. Distant monopolar referencing, often to a skull screw or distant cortical site, preserves the full LFP amplitude but can include volume-conducted signals, while local bipolar configurations—using adjacent electrodes on the same —enhance specificity by subtracting nearby activity, though at the cost of . Practical aspects of LFP setups involve optimizing impedance, (SNR), and recording duration. impedances are typically targeted at 100-500 kΩ at 1 kHz to minimize noise while maintaining , with mismatches addressed through preamplification calibration for uniform SNR across channels. Acute recordings, performed during short-term surgical sessions, allow immediate access but risk inflammation, whereas chronic implants, such as drivable hyperdrives or fixed arrays, enable weeks-to-months of stable data in behaving animals, though they require anti-inflammatory coatings or adjuncts to sustain SNR over time.

Properties of Extracellular Space

The brain's (ECS) is a complex milieu filled with interstitial fluid containing key s that facilitate neuronal signaling and current flow underlying local field potentials (LFPs). Typical concentrations include approximately 145 mM Na⁺, 3–5 mM K⁺, 1–1.5 mM Ca²⁺, and 110–130 mM Cl⁻, creating an environment with lower K⁺ and Ca²⁺ levels relative to intracellular compartments but optimized for maintaining resting potentials and synaptic transmission. The resistivity of the ECS, which governs the spread of extracellular currents contributing to LFPs, is approximately 300 Ω·cm, reflecting the conductive properties of this ion-rich fluid amid cellular structures. Additionally, the ECS exhibits values of 1.5–2.0, arising from the tortuous paths imposed by densely packed neurons, , and components that impede free diffusion and current propagation. The volume fraction of the ECS, representing the proportion of brain tissue occupied by this , is typically 15–20%, which significantly influences the and amplitude of LFP signals by constraining current spread to local domains. This limited volume promotes efficient signaling within neural circuits but also leads to higher local ion fluctuations during activity. The diffusive properties of the ECS, quantified by an effective diffusion coefficient reduced by the factor (D* = D / λ², where λ is ), contribute to spatial smoothing of electrical signals, attenuating high-frequency components in LFPs as ions redistribute over short distances. Furthermore, the inherent to cell membranes bordering the ECS introduces a low-pass filtering effect, rapid transients (e.g., action potential-associated currents above 100–500 Hz) while preserving slower synaptic potentials that dominate LFP waveforms. These biophysical attributes ensure that LFPs primarily reflect population-level synaptic activity rather than isolated spikes. Pathological alterations in the ECS profoundly impact LFP recordings by modifying its conductive properties. For instance, vasogenic can expand the and dilute ion concentrations, reducing resistivity, which broadens current spread and diminishes LFP amplitudes by 43% in simulations of acute swelling. In contrast, cytotoxic edema from ischemia typically shrinks the ECS . Conversely, —characterized by reactive proliferation—typically shrinks the to below 10% and elevates to around 1.8–2.0, increasing resistivity and restricting current flow; simulations show this can increase LFP signal strength by counteracting neuronal loss, though it alters the spatial profile. Such changes, observed in conditions like or , complicate LFP interpretation and highlight the ECS's dynamic role in modulating neural .

Theoretical Models and Interpretation

Basic Interpretations of LFP Signals

The local field potential (LFP) is theoretically modeled as the extracellular potential arising from the collective transmembrane currents of neural populations, under the in a homogeneous, isotropic conducting medium. The potential ϕ(r)\phi(\mathbf{r}) at a recording site r\mathbf{r} is approximated by the ϕ(r)≈14πσ∫Im(r′)∣r−r′∣ dV′\phi(\mathbf{r}) \approx \frac{1}{4\pi\sigma} \int \frac{I_m(\mathbf{r}')}{|\mathbf{r} - \mathbf{r}'|} \, dV', where σ\sigma is the conductivity of the , Im(r′)I_m(\mathbf{r}') is the transmembrane at source location r′\mathbf{r}', and the sums contributions over V′V' containing current sources. This formulation derives from solving ∇⋅(σ∇ϕ)=−Im\nabla \cdot (\sigma \nabla \phi) = -I_m in the low-frequency limit, where capacitive effects are negligible. Relatedly, the current source density (CSD), which localizes ImI_m, is obtained as Im≈−σ∇2ϕI_m \approx -\sigma \nabla^2 \phi, linking the second spatial derivative of the LFP potential directly to the underlying current distribution. For a single point-like current source, such as an isolated or current injection, the LFP simplifies to a monopole approximation ϕ(r)=I4πσ∣r−r0∣\phi(\mathbf{r}) = \frac{I}{4\pi\sigma |\mathbf{r} - \mathbf{r}_0|}, where II is the current and r0\mathbf{r}_0 is the source position; this yields a spatial decay proportional to 1/r1/r, with r=∣r−r0∣r = |\mathbf{r} - \mathbf{r}_0|. In neural tissue, however, LFPs emerge from distributed sources, and the of the underlying equations allows superposition: the total LFP is the vector sum of individual contributions. For a population of NN uncorrelated sources with randomly oriented dipoles, the expected LFP scales as N\sqrt{N}
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