Recording human cortical population spikes non-invasively – An EEG tutorial

2015 ◽  
Vol 250 ◽  
pp. 74-84 ◽  
Author(s):  
Gunnar Waterstraat ◽  
Tommaso Fedele ◽  
Martin Burghoff ◽  
Hans-Jürgen Scheer ◽  
Gabriel Curio
Keyword(s):  
Population Spikes

Effect of acute lead treatmant on in vivo hippocampal population spikes in rats

1995 ◽  
Vol 78 ◽  
pp. 64
Author(s):  
A. Papp ◽  
K. Györgyi ◽  
L. Nagymajtényi ◽  
I. Dési
Keyword(s):  
Population Spikes

scholarly journals KCNQ/Kv7 Channel Regulation of Hippocampal Gamma-Frequency Firing in the Absence of Synaptic Transmission

2006 ◽  
Vol 95 (5) ◽  
pp. 3105-3112 ◽  
Author(s):  
S. Piccinin ◽  
A. D. Randall ◽  
J. T. Brown
Keyword(s):  
Synaptic Transmission ◽  
High Frequency ◽  
Epileptiform Activity ◽  
Hippocampal Slices ◽  
Neuronal Firing ◽  
Population Spike ◽  
Channel Blockers ◽  
Kv7 Channels ◽  
Population Spikes ◽  
Gamma Frequency

Synchronous neuronal firing can be induced in hippocampal slices in the absence of synaptic transmission by lowering extracellular Ca2+ and raising extracellular K+. However, the ionic mechanisms underlying this nonsynaptic synchronous firing are not well understood. In this study we have investigated the role of KCNQ /Kv7 channels in regulating this form of nonsynaptic bursting activity. Incubation of rat hippocampal slices in reduced (<0.2 mM) [Ca2+]o and increased (6.3 mM) [K+]o, blocked synaptic transmission, increased neuronal firing, and led to the development of spontaneous periodic nonsynaptic epileptiform activity. This activity was recorded extracellularly as large (4.7 ± 1.9 mV) depolarizing envelopes with superimposed high-frequency synchronous population spikes. These intraburst population spikes initially occurred at a high frequency (about 120 Hz), which decayed throughout the burst stabilizing in the gamma-frequency band (30–80 Hz). Further increasing [K+]o resulted in an increase in the interburst frequency without altering the intraburst population spike frequency. Application of retigabine (10 μM), a Kv7 channel modulator, completely abolished the bursts, in an XE-991–sensitive manner. Furthermore, application of the Kv7 channel blockers, linopirdine (10 μM) or XE-991 (10 μM) alone, abolished the gamma frequency, but not the higher-frequency population spike firing observed during low Ca2+/high K+ bursts. These data suggest that Kv7 channels are likely to play a role in the regulation of synchronous population firing activity.

scholarly journals Investigation of the Neuronal Aggregate Generating Seizures in the Rat Tetanus Toxin Model of Epilepsy

2002 ◽  
Vol 88 (6) ◽  
pp. 2919-2927 ◽  
Author(s):  
G. T. Finnerty ◽  
J.G.R. Jefferys
Keyword(s):  
Phase Difference ◽  
Tetanus Toxin ◽  
Neuronal Networks ◽  
Dorsal Hippocampus ◽  
Interictal Spikes ◽  
Population Spikes ◽  
Spontaneous Seizures ◽  
Spatially Distributed ◽  
The Right

A key question in epilepsy is the organization and size of the neuronal networks necessary for generating seizures. Hypotheses include: a single focal neuronal network drives seizure discharges across the brain, which may or may not be identical with the circuits that generate interictal spikes; or multiple neuronal networks link together in re-entrant loops or other long-range networks. It remains unclear whether any of these hypotheses apply to spontaneous seizures in freely moving animals. We used the tetanus toxin chronic model of epilepsy to test the different predictions made by each hypothesis about the propagation and interaction of epileptic discharges during seizures. Seizures could start in either the injected or noninjected dorsal hippocampus, suggesting that seizures have multifocal onsets in the tetanus toxin model. During seizures, individual bursts propagated in either direction, both between the right and left dorsal hippocampi, and between CA3 and the dentate gyrus in the same hippocampus. These findings argue against one site “driving” seizures or seizures propagating around a limbic loop. Specifically, the side leading each burst switched a median of three times during the first 20 s of a seizure. Analysis of bursts during seizures suggested that the network at each recording site acted like a neuronal oscillator. Coupling of population spikes in right and left CA3 increased during the early part of seizures, but the cross-correlation of their whole-discharge waveforms changed little over the same period. Furthermore, the polarity of the phase difference between population spikes did not follow the phase difference for complete discharges. We concluded that the neuronal aggregate necessary for seizures in our animals comprises multiple spatially distributed neuronal networks and that the increased synchrony of the output (population spike firing) of these networks during the early part of seizures may contribute to seizure generation.

Tissue Resistance Changes and the Profile of Synchronized Neuronal Activity During Ictal Events in the Low-Calcium Model of Epilepsy

2004 ◽  
Vol 92 (1) ◽  
pp. 181-188 ◽  
Author(s):  
John E. Fox ◽  
Marom Bikson ◽  
John G. R. Jefferys
Keyword(s):  
High Amplitude ◽  
Spike Frequency ◽  
Population Spike ◽  
Spatial Synchronization ◽  
Population Spikes ◽  
Field Effects ◽  
Tissue Resistance ◽  
Pyramidal Layer ◽  
Population Spike Amplitude ◽  
Main Discharge

Population spikes vary in size during prolonged epileptic (“ictal”) discharges, indicating variations in neuronal synchronization. Here we investigate the role of changes in tissue electrical resistivity in this process. We used the rat hippocampal slice, low-Ca2+ model of epilepsy and measured changes in pyramidal layer extracellular resistance during the course of electrographic seizures. During each burst, population spike frequency decreased, whereas amplitude and spatial synchronization increased; after the main discharge, there could be brief secondary discharges that, in contrast with those in the primary discharge, started with high-amplitude population spikes. Mean resistivity increased from 1,231 Ω.cm immediately before the burst to a maximum of 1,507 Ω.cm during the burst. There was no significant increase during the first 0.5–1 s of the field burst, but resistance then increased (τ ∼ 5 s), reaching its peak at the end of the burst, and then decayed slowly (τ ∼ 10 s). In further experiments, we modulated the efficacy of electrical field effects by changing perfusate osmolarity. Reducing osmolarity by 40–70 mOsm increased preburst resistivity by 19%; it reduced minimum population spike frequency (×0.6–0.7) and increased both maximum population spike amplitude (×1.5–2.3) and spatial synchronization (×1.4–2.5, cross-correlation over 0.5 mm) during bursts. Increasing osmolarity by 20–40 mOsm had the opposite effects. These results suggest that, during each field burst, field effects between neurons gradually become more effective as cells swell, thereby modulating burst dynamics and facilitating the rapid synchronization of secondary discharges.

Heptanol But Not Fluoroacetate Prevents the Propagation of Spreading Depression in Rat Hippocampal Slices

1997 ◽  
Vol 77 (1) ◽  
pp. 9-16 ◽  
Author(s):  
Carlota Largo ◽  
Geoffrey C. Tombaugh ◽  
Peter G. Aitken ◽  
Oscar Herreras ◽  
George G. Somjen
Keyword(s):  
Synaptic Transmission ◽  
Gap Junctions ◽  
Spreading Depression ◽  
Pyramidal Neurons ◽  
Hippocampal Slices ◽  
Lipid Phase ◽  
Tissue Slices ◽  
Population Spikes ◽  
Afferent Volleys ◽  
Stimulation Of

Largo, Carlota, Geoffrey C. Tombaugh, Peter G. Aitken, Oscar Herreras, and George G. Somjen. Heptanol but not fluoroacetate prevents the propagation of spreading depression in rat hippocampal slices. J. Neurophysiol. 77: 9–16, 1997. We investigated whether heptanol and other long-chain alcohols that are known to block gap junctions interfere with the generation or the propagation of spreading depression (SD). Waves of SD were triggered by micro-injection of concentrated KCl solution in stratum (s.) radiatum of CA1 of rat hippocampal tissue slices. DC-coupled recordings of extracellular potential ( V o) were made at the injection and at a second site ∼1 mm distant in st. radiatum and sometimes also in st. pyramidale. Extracellular excitatory postsynaptic potentials (fEPSPs) were evoked by stimulation of the Schaffer collateral bundle; in some experiments, antidromic population spikes were evoked by stimulation of the alveus. Bath application of 3 mM heptanol or 5 mM hexanol completely and reversibly prevented the propagation of the SD-related potential shift (Δ V o) without abolishing the Δ V o at the injection site. Octanol (1 mM) had a similar but less reliably reversible effect. fEPSPs were depressed by ∼30% by heptanol and octanol, 65% by hexanol. Antidromic population spikes were depressed by 30%. In isolated, patch-clamped CA1 pyramidal neurons, heptanol partially and reversibly depressed voltage-dependent Na currents possibly explaining the slight depression of antidromic spikes and, by acting on presynaptic action potentials, also the depression of fEPSPs. Fluoroacetate (FAc), a putative selective blocker of glial metabolism, first induced multiple spike firing in response to single afferent volleys and then severely suppressed synaptic transmission (confirming earlier reports) without depressing the antidromic population spike. FAc did not inhibit SD propagation. The effect of alkyl alcohols is compatible with the idea that the opening of normally closed neuronal gap junctions is required for SD propagation. Alternative possible explanations include interference with the lipid phase of neuron membranes. The absence of SD inhibition by FAc confirms that synaptic transmission is not necessary for the propagation of SD, and it suggests that normally functioning glial cells are not essential for SD generation or propagation.

Persistent hyperexcitability in isolated hippocampal CA1 of kainate-lesioned rats

1992 ◽  
Vol 68 (6) ◽  
pp. 2120-2127 ◽  
Author(s):  
C. L. Meier ◽  
A. Obenaus ◽  
F. E. Dudek
Keyword(s):  
Pyramidal Neurons ◽  
Hippocampal Sclerosis ◽  
Mean Amplitude ◽  
Cell Loss ◽  
Stratum Radiatum ◽  
Excitatory Postsynaptic Potential ◽  
Population Spikes ◽  
Acute Seizures ◽  
Postsynaptic Potential ◽  
Area Ca1

1. Subcutaneous kainate injection in rats evoked acute seizures and led to cell loss in the hilus and areas CA1 and CA3, which resembled the pattern of hippocampal sclerosis often associated with temporal lobe epilepsy in humans. 2. Simultaneous intra- and extracellular recordings were performed in the stratum pyramidale of area CA1 while stimulating in the stratum radiatum close to the recording electrodes. Responses from control slices consisted of a brief excitatory postsynaptic potential (EPSP) with only one action potential, corresponding to a single extracellular population spike, followed by a clear biphasic inhibitory postsynaptic potential (IPSP). In slices from kainate-treated animals, however, stimulation evoked a prolonged EPSP, which often triggered multiple action potentials corresponding to multiple extracellular population spikes. 3. In slices from kainate-treated animals, the mean amplitude but not the duration of the stimulation-evoked IPSP was reduced. The extent of the kainate-induced loss of inhibition in area CA1 was highly variable. 4. Low concentrations of bicuculline in control slices led to a moderate hyperexcitability, which consisted of multiple population spikes and mirrored the responses observed in slices from kainate-treated animals in normal ACSF. Prolonged application of 10-30 microM bicuculline for > or = 30 min led to a much higher level of hyperexcitability, which was similar in slices from controls and kainate-treated rats. These findings are consistent with the hypothesis that the hyperexcitability of CA1 pyramidal neurons following kainate treatment is mainly due to decreased GABAA-receptor-mediated inhibition and that the loss of inhibition is only partial.(ABSTRACT TRUNCATED AT 250 WORDS)

Excitation of hippocampal pyramidal cells by an electrical field effect

1984 ◽  
Vol 52 (1) ◽  
pp. 126-142 ◽  
Author(s):  
C. P. Taylor ◽  
F. E. Dudek
Keyword(s):  
Cell Body ◽  
Pyramidal Cell ◽  
Action Potentials ◽  
Current Source ◽  
Extracellular Recording ◽  
Pyramidal Cells ◽  
Physiological Solution ◽  
Adjacent Cell ◽  
Electrical Field ◽  
Population Spikes

The effects of electrical fields from antidromic stimulation of CA1 pyramidal cells were studied in slices of rat hippocampus in which chemical synaptic transmission had been blocked by superfusion with physiological solution containing Mn2+ and lowered concentration of Ca2+. Differential voltage recordings were made between two microelectrode positions, on intracellular to a pyramidal cell and the other in the adjacent extracellular space. This technique revealed brief transmembrane depolarizations that occurred synchronously with negative-going extracellular population spikes in the adjacent cell body layer. Glial cells in this region did not exhibit these depolarizations. In some pyramidal cells, alvear stimulation that was too weak to excite the axon of the impaled cell elicited action potentials, which appeared to arise from transmembrane depolarizations at the soma. When subthreshold transmembrane depolarizations were superimposed on subthreshold depolarizing current pulses, somatic action potentials were generated synchronously with the antidromic population spikes. The depolarizations of pyramidal somata were finely graded with stimulus intensity, were unaffected by polarization of the membrane, and were not occluded by preceding action potentials. The laminar profile of extracellular field potentials perpendicular to the cell body layer was obtained with an array of extracellular recording locations. Numerical techniques of current source-density analysis indicated that at the peak of the somatic population spike, there was an extracellular current sink near pyramidal somata and sources in distal dendritic regions. It is concluded that during population spikes an extracellular electrical field causes currents to flow passively across inactive pyramidal cell membranes, thus depolarizing their somata. The transmembrane depolarizations associated with population spikes would tend to excite and synchronize the population of pyramidal cells.

Serotonin blocks the facilitatory action of muscarinic and nicotinic agents in the hippocampus in vivo

1989 ◽  
Vol 67 (1) ◽  
pp. 47-53 ◽  
Author(s):  
Y. Hong ◽  
K. Krnjević
Keyword(s):  
Inhibitory Action ◽  
Pyramidal Cells ◽  
Inhibitory Effect ◽  
Population Spike ◽  
Rat Hippocampus ◽  
Population Spikes ◽  
Ca1 Region ◽  
Facilitatory Action ◽  
Hippocampal Pyramidal Cells

The inhibitory effect of serotonin, released iontophoretically, on acetylcholine-induced facilitation of population spikes evoked by fimbria–commissural stimulation was studied in the CA1 region of rat hippocampus in vivo. After serotonin was applied for 2.6 ± 0.8 min, acetylcholine's action was inhibited in 39 cases out of 57 (68.4%), by 68.9 ± 23.1%, irrespective of whether serotonin alone increased or reduced the population spike. Spiperone, used as a 5-hydroxytryptamine1A (5-HT1A) antagonist, suppressed the inhibitory action of serotonin in 14 of 21 tests. Serotonin had similar effects on population spike facilitations induced by acetyl-β-methylcholine and dimethylphenylpiperazinium. Thus serotonin, probably acting on 5-HT1A receptors, blocks effectively but indiscriminately all cholinergic facilitations, whether mediated by nicotinic or muscarinic receptors.Key words: serotonin, cholinergic facilitation, hippocampal pyramidal cells, spiperone, muscarinic and nicotinic actions.

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