Neocortical Very Fast Oscillations (Ripples, 80–200 Hz) During Seizures: Intracellular Correlates

2003 ◽  
Vol 89 (2) ◽  
pp. 841-852 ◽  
Author(s):  
François Grenier ◽  
Igor Timofeev ◽  
Mircea Steriade
Keyword(s):  
Action Potentials ◽  
Field Potential ◽  
Network Activity ◽  
Intracellular Recordings ◽  
Field Potentials ◽  
Neocortical Neurons ◽  
Electrographic Seizures ◽  
Threshold Amplitude ◽  
Site Field ◽  
Fast Oscillations

Multi-site field potential and intracellular recordings from various neocortical areas were used to study very fast oscillations or ripples (80–200 Hz) during electrographic seizures in cats under ketamine-xylazine anesthesia. The animals displayed spontaneously occurring and electrically induced seizures comprising spike-wave complexes (2–3 Hz) and fast runs (10–20 Hz). Neocortical ripples had much higher amplitudes during seizures than during the slow oscillation preceding the onset of seizures. A series of experimental data from the present study supports the hypothesis that ripples are implicated in seizure initiation. Ripples were particularly strong at the onset of seizures and halothane, which antagonizes the occurrence of ripples, also blocked seizures. The firing of electrophysiologically defined cellular types was phase-locked with ripples in simultaneously recorded field potentials. This indicates that ripples during paroxysmal events are associated with a coordination of firing in a majority of neocortical neurons. This was confirmed with dual intracellular recordings. Based on the amplitude that neocortical ripples reach during paroxysmal events, we propose a mechanism by which neocortical ripples during normal network activity could actively participate in the initiation of seizures on reaching a certain threshold amplitude. This mechanism involves a vicious feedback loop in which very fast oscillations in field potentials are a reflection of synchronous action potentials, and in turn these oscillations help generate and synchronize action potentials in adjacent neurons through electrical interactions.

Dynamic coupling among neocortical neurons during evoked and spontaneous spike-wave seizure activity

1994 ◽  
Vol 72 (5) ◽  
pp. 2051-2069 ◽  
Author(s):  
M. Steriade ◽  
F. Amzica
Keyword(s):  
Cortical Neurons ◽  
Time Course ◽  
Early Stage ◽  
Field Potential ◽  
Time Lags ◽  
Temporal Relations ◽  
Intracellular Recordings ◽  
Field Potentials ◽  
Thalamic Nuclei ◽  
Spike Wave

1. We investigated the development from patterns of electroencephalogram (EEG) synchronization to paroxysms consisting of spike-wave (SW) complexes at 2–4 Hz or to seizures at higher frequencies (7–15 Hz). We used multisite, simultaneous EEG, extracellular, and intracellular recordings from various neocortical areas and thalamic nuclei of anesthetized cats. 2. The seizures were observed in 25% of experimental animals, all maintained under ketamine and xylazine anesthesia, and were either induced by thalamocortical volleys and photic stimulation or occurred spontaneously. Out of unit and field potential recordings within 370 cortical and 65 thalamic sites, paroxysmal events occurred in 70 cortical and 8 thalamic sites (approximately 18% and 12%, respectively), within which a total of 181 neurons (143 extracellular and 38 intracellular) were simultaneously recorded in various combinations of cell groups. 3. Stimulus-elicited and spontaneous SW seizures at 2–4 Hz lasted for 15–35 s and consisted of barrages of action potentials related to the spiky depth-negative (surface-positive) field potentials, followed by neuronal silence during the depth-positive wave component of SW complexes. The duration of inhibitory periods progressively increased during the seizure, at the expense of the phasic excitatory phases. 4. Intracellular recordings showed that, during such paroxysms, cortical neurons displayed a tonic depolarization (approximately 10–20 mV), sculptured by rhythmic hyperpolarizations. 5. In all cases, measures of synchrony demonstrated time lags between discharges of simultaneously recorded cortical neurons, from as short as 3–10 ms up to 50 ms or even longer intervals. Synchrony was assessed by cross-correlograms, by a method termed first-spike-analysis designed to detect dynamic temporal relations between neurons and relying on the detection of the first action potential in a spike train, and by a method termed sequential-field-correlation that analyzed the time course of field potentials simultaneously recorded from different cortical areas. 6. The degree of synchrony progressively increased from preseizure sleep patterns to the early stage of the SW seizure and, further, to its late stage. In some cases the time relation between neurons during the early stages of seizures was inversed during late stages. 7. These data show that, although the common definition of SW seizures, regarded as suddenly generalized and bilaterally synchronous activities, may be valid at the macroscopic EEG level, cortical neurons display time lags between their rhythmic spike trains, progressively increased synchrony, and changes in the temporal relations between their discharges during the paroxysms.(ABSTRACT TRUNCATED AT 400 WORDS)

Epileptiform activity induced by low chloride medium in the CA1 subfield of the hippocampal slice

1990 ◽  
Vol 64 (6) ◽  
pp. 1747-1757 ◽  
Author(s):  
M. Avoli ◽  
C. Drapeau ◽  
P. Perreault ◽  
J. Louvel ◽  
R. Pumain
Keyword(s):  
Membrane Potential ◽  
Large Amplitude ◽  
Action Potentials ◽  
Hippocampal Slice ◽  
Epileptiform Activity ◽  
Field Potential ◽  
Pyramidal Cells ◽  
Input Resistance ◽  
Field Potentials ◽  
Maximal Amplitude

1. Extracellular and intracellular recordings and measurements of the extracellular concentration of free K+ ([K+]o) were performed in the CA1 subfield of the rat hippocampal slice during perfusion with artificial cerebrospinal fluid (ACSF) in which NaCl had been replaced with equimolar Na-isethionate or Na-methylsulfate (hereafter called low Cl- ACSF). 2. CAl pyramidal cells perfused with low Cl- ACSF generated intracellular epileptiform potentials in response to orthodromic, single-shock stimuli delivered in stratum (S.) radiatum. Low-intensity stimuli evoked a short-lasting epileptiform burst (SB) of action potentials that lasted 40–150 ms and was followed by a prolonged hyperpolarization. When the stimulus strength was increased, a long-lasting epileptiform burst (LB) appeared; it had a duration of 4–15 s and consisted of an early discharge of action potentials similar to the SB, followed by a prolonged, large-amplitude depolarizing plateau. The refractory period of the LB was longer than 20 s. SB and LB were also seen after stimulation of the alveus. 3. Variations of the membrane potential with injection of steady. DC current modified the shape of SB and LB. When microelectrodes filled with the lidocaine derivative QX-314 were used, the amplitudes of both SB and LB increased in a linear fashion during changes of the baseline membrane potential in the hyperpolarizing direction. The membrane input resistance, as measured by injecting brief square pulses of hyperpolarizing current, decreased by 65-80% during the long-lasting depolarizing plateau of LB. 4. A synchronous field potential and a transient increase in [K+]o accompanied the epileptiform responses. The extracellular counterpart of the SB was a burst of three to six population spikes and a small increase in [K+]o (less than or equal to 2 mM from a resting value of approximately 2.5 mM). The LB was associated with a large-amplitude, biphasic, negative field potential and a large increase in [K+]o (up to 12.4 mM above the resting value). Changes in [K+]o during the LB were largest at the border between S. oriens and S. pyramidale. This was also the site where the field potentials measured 2–5 s after the stimulus attained their maximal amplitude. Conversely, field potentials associated with the early component of the LB or with the SB displayed a maximal amplitude in the S. radiatum. 5. Spontaneous SBs and LBs were at times recorded in the CA1 and in the CA3 subfield.(ABSTRACT TRUNCATED AT 400 WORDS)

scholarly journals A Method to Estimate Synaptic Conductances From Membrane Potential Fluctuations

2004 ◽  
Vol 91 (6) ◽  
pp. 2884-2896 ◽  
Author(s):  
Michael Rudolph ◽  
Zuzanna Piwkowska ◽  
Mathilde Badoual ◽  
Thierry Bal ◽  
Alain Destexhe
Keyword(s):  
Membrane Potential ◽  
Computational Models ◽  
Network Activity ◽  
Intracellular Recordings ◽  
Neocortical Neurons ◽  
Underlying Network ◽  
Analytic Expression ◽  
Synaptic Conductances

In neocortical neurons, network activity can activate a large number of synaptic inputs, resulting in highly irregular subthreshold membrane potential ( Vm) fluctuations, commonly called “synaptic noise.” This activity contains information about the underlying network dynamics, but it is not easy to extract network properties from such complex and irregular activity. Here, we propose a method to estimate properties of network activity from intracellular recordings and test this method using theoretical and experimental approaches. The method is based on the analytic expression of the subthreshold Vm distribution at steady state in conductance-based models. Fitting this analytic expression to Vm distributions obtained from intracellular recordings provides estimates of the mean and variance of excitatory and inhibitory conductances. We test the accuracy of these estimates against computational models of increasing complexity. We also test the method using dynamic-clamp recordings of neocortical neurons in vitro. By using an on-line analysis procedure, we show that the measured conductances from spontaneous network activity can be used to re-create artificial states equivalent to real network activity. This approach should be applicable to intracellular recordings during different network states in vivo, providing a characterization of the global properties of synaptic conductances and possible insight into the underlying network mechanisms.

Focal Synchronization of Ripples (80–200 Hz) in Neocortex and Their Neuronal Correlates

2001 ◽  
Vol 86 (4) ◽  
pp. 1884-1898 ◽  
Author(s):  
François Grenier ◽  
Igor Timofeev ◽  
Mircea Steriade
Keyword(s):  
Slow Wave ◽  
Slow Wave Sleep ◽  
Spiking Neurons ◽  
Slow Oscillation ◽  
Field Potentials ◽  
Firing Rates ◽  
Neuronal Excitation ◽  
Neocortical Neurons ◽  
Fast Spiking ◽  
Fast Oscillations

Field potentials from different neocortical areas and intracellular recordings from areas 5 and 7 in acutely prepared cats under ketamine-xylazine anesthesia and during natural states of vigilance in chronic experiments, revealed the presence of fast oscillations (80–200 Hz), termed ripples. During anesthesia and slow-wave sleep, these oscillations were selectively related to the depth-negative (depolarizing) component of the field slow oscillation (0.5–1 Hz) and could be synchronized over ∼10 mm. The dependence of ripples on neuronal depolarization was also shown by their increased amplitude in field potentials in parallel with progressively more depolarized values of the membrane potential of neurons. The origin of ripples was intracortical as they were also detected in small isolated slabs from the suprasylvian gyrus. Of all types of electrophysiologically identified neocortical neurons, fast-rhythmic-bursting and fast-spiking cells displayed the highest firing rates during ripples. Although linked with neuronal excitation, ripples also comprised an important inhibitory component. Indeed, when regular-spiking neurons were recorded with chloride-filled pipettes, their firing rates increased and their phase relation with ripples was modified. Thus besides excitatory connections, inhibitory processes probably play a major role in the generation of ripples. During natural states of vigilance, ripples were generally more prominent during the depolarizing component of the slow oscillation in slow-wave sleep than during the states of waking and rapid-eye movement (REM) sleep. The mechanisms of generation and synchronization, and the possible functions of neocortical ripples in plasticity processes are discussed.

Dendritic Initiation and Propagation of Spikes and Spike Bursts in a Multimodal Sensory Interneuron: The Crustacean Parasol Cell

2003 ◽  
Vol 90 (4) ◽  
pp. 2465-2477 ◽  
Author(s):  
DeForest Mellon
Keyword(s):  
Action Potentials ◽  
Procambarus Clarkii ◽  
Critical Role ◽  
Field Potential ◽  
Dendritic Arbor ◽  
Freshwater Crayfish ◽  
Intracellular Recordings ◽  
Antidromic Activation ◽  
Initiation Point ◽  
Spike Bursts

Invasion of dendrites by spikes and spike bursts can play a critical role in regulating the output of central neurons by modifying their dynamic input-output relationships. Back-propagating bursts can modulate voltage-gated channels in the short term and can also modify long-term responses to synaptic input. Determining the morphological site of spike initiation and the mode of propagation through the dendritic arbor is therefore crucial to an understanding of a neuron's functional properties. I used electrophysiological methods to study parasol cells in isolated, perfused head preparations of the freshwater crayfish Procambarus clarkii to determine the compartment of origin of orthodromically activated action potentials and bursts that propagate within the dendritic arbor and to examine the identity of low-amplitude, electrotonically recorded spike events that are present in more than one-half of the intracellular recordings obtained from dendrites in these neurons. Experiments using antidromic activation of parasol cell axons indicated that electrotonically recorded spikes probably are generated in neighboring parasol cells, to which the impaled neurons are electrically coupled. Both paired intracellular recordings and extracellular field potential measurements were used to compare arrival times of antidromic and orthodromic spikes at loci in the vicinity of the trunk and the basal branch compartments of parasol cell dendrites. These methods provided consistent results, indicating that synaptically evoked action potentials are initiated at a site on the trunk, from which point they back-propagate into the basal branches within the hemiellipsoid body, and presumably, also orthodromically to the axon. Data are presented suggesting that bursts also arise at a trunk locus, but one that is different from the initiation point of single spikes evoked by excitatory postsynaptic potentials (EPSPs). Morphological specializations between the dendritic trunk and basal branches may facilitate back-propagation of spikes and spike bursts into the basal branches.

Fast oscillations trigger bursts of action potentials in neocortical neurons in vitro: A quasi-white-noise analysis study

2006 ◽  
Vol 1110 (1) ◽  
pp. 201-210 ◽  
Author(s):  
Kaspar A. Schindler ◽  
Philip H. Goodman ◽  
Heinz G. Wieser ◽  
Rodney J. Douglas
Keyword(s):  
White Noise ◽  
Action Potentials ◽  
Noise Analysis ◽  
White Noise Analysis ◽  
Analysis Study ◽  
Neocortical Neurons ◽  
Fast Oscillations

scholarly journals Measurements of Subthreshold and Fast Population Neuronal Activity with Genetically Encoded Calcium Indicator GCaMP-6f

2018 ◽  
Author(s):  
Pinggan Li ◽  
Xinling Geng ◽  
Huiyi Jiang ◽  
Adam Caccavano ◽  
Stefano Vicini ◽  
...  
Keyword(s):  
Neuronal Activity ◽  
Local Field ◽  
Local Field Potential ◽  
Action Potentials ◽  
Neuronal Response ◽  
Field Potential ◽  
Network Activity ◽  
Population Activity ◽  
Calcium Indicators ◽  
Local Field Potential Lfp

GCaMP-6f is among the best calcium indicators and has been widely used for monitoring neuronal activity in the brain. Applications are at cellular level (calcium transients of action potentials) or population activity (fluorimetry) during network events. Two important issues remain less explored: 1) Is GCaMP-6f signal sensitive enough for detecting subthreshold activity, similar to the sensitivity of local field potential (LFP)? 2) Is the GCaMP-6f signal fast enough for detecting network oscillations seen in LFP? Here the two issues are explored in a number of network events including hippocampus sharp waves (SWs), carbachol induced theta oscillations, interictal-like spikes and neuronal response evoked by high frequency stimuli. SWs are a typical network event with the majority of neurons receiving subthreshold excitatory or inhibitory synaptic input without firing action potentials. The excitatory/inhibitory post synaptic potentials (EPSP/IPSP) in the neuropil become detectable in local field potential (LFP) signals. We compare simultaneously recorded LFP and optical recording of GCaMP-6f fluorescent signals in Thy1-GCaMP-6f mice hippocampal slices. We found that the occurrence of SWs produces a clear population GCaMP-6f signal of 0.3% dF/F. This population GCaMP-6f signal correlated well with the LFP, albeit a delay of ~50 ms was observed. The population GCaMP-6f signal follows well with the 20 Hz population activity evoked by electric stimuli, while activity up to 40 Hz was detected with reduced amplitude. GCaMP-6f and LFP signals showed a large amplitude discrepancy. The amplitude of GCaMP increased ~1000 times from SW to carbachol induced theta burst, while the LFP changed less than 10 times. Our results suggested that population GCaMP-6f signals may become a sensitive tool for detecting network activity, especially for that with low LFP amplitude during elevated spiking rate but asynchronized events. GCaMP signal is fast enough for monitoring theta and beta oscillations (<25Hz) in the neuronal population. Faster calcium indicators (e.g., GCaMP-7) may improve the frequency response property for detecting gamma band oscillations. In addition, population GCaMP recordings are non-contact and free from stimulation artifacts. These features may be useful for high throughput recordings and applications sensitive to stimulus artifact, e.g., monitoring response during continuous stimulations.

scholarly journals Chloride-Cotransport Blockade Desynchronizes Neuronal Discharge in the “Epileptic” Hippocampal Slice

2000 ◽  
Vol 83 (1) ◽  
pp. 406-417 ◽  
Author(s):  
Daryl W. Hochman ◽  
Philip A. Schwartzkroin
Keyword(s):  
Action Potential ◽  
Action Potentials ◽  
Hippocampal Slices ◽  
Field Potential ◽  
Pyramidal Cells ◽  
Extracellular Potassium ◽  
Intracellular Recordings ◽  
Population Activity ◽  
Ca1 Pyramidal Cells ◽  
Epileptiform Discharges

Antagonism of the chloride-cotransport system in hippocampal slices has been shown to block spontaneous epileptiform (i.e., hypersynchronized) discharges without diminishing excitatory synaptic transmission. Here we test the hypotheses that chloride-cotransport blockade, with furosemide or low-chloride (low-[Cl−]o) medium, desynchronizes the firing activity of neuronal populations and that this desynchronization is mediated through nonsynaptic mechanisms. Spontaneous epileptiform discharges were recorded from the CA1 and CA3 cell body layers of hippocampal slices. Treatment with low-[Cl−]o medium led to cessation of spontaneous synchronized bursting in CA1 ≥5–10 min before its disappearance from CA3. During the time that CA3 continued to burst spontaneously but CA1 was silent, electrical stimulation of the Schaffer collaterals showed that hyperexcited CA1 synaptic responses were maintained. Paired intracellular recordings from CA1 pyramidal cells showed that during low-[Cl−]otreatment, the timing of action potential discharges became desynchronized; desynchronization was identified with phase lags in firing times of action potentials between pairs of neurons as well as a with a broadening and diminution of the CA1 field amplitude. Continued exposure to low-[Cl−]o medium increased the degree of the firing-time phase shifts between pairs of CA1 pyramidal cells until the epileptiform CA1 field potential was abolished completely. Intracellular recordings during 4-aminopyridine (4-AP) treatment showed that prolonged low-[Cl−]oexposure did not diminish the frequency or amplitude of spontaneous postsynaptic potentials. CA3 antidromic responses to Schaffer collateral stimulation were not significantly affected by prolonged low-[Cl−]o exposure. In contrast to CA1, paired intracellular recordings from CA3 pyramidal cells showed that chloride-cotransport blockade did not cause a significant desynchronization of action potential firing times in the CA3 subregion at the time that CA1 synchronous discharge was blocked but did reduce the number of action potentials associated with CA3 burst discharges. These data support our hypothesis that the anti-epileptic effects of chloride-cotransport antagonism in CA1 are mediated through the desynchronization of population activity. We hypothesize that interference with Na+,K+,2Cl−cotransport results in an increase in extracellular potassium ([K+]o) that reduces the number of action potentials that are able to invade axonal arborizations and varicosities in all hippocampal subregions. This reduced efficacy of presynaptic action potential propagation ultimately leads to a reduction of synaptic drive and a desynchronization of the firing of CA1 pyramidal cells.

Contribution of Intrinsic Neuronal Factors in the Generation of Cortically Driven Electrographic Seizures

2004 ◽  
Vol 92 (2) ◽  
pp. 1133-1143 ◽  
Author(s):  
Igor Timofeev ◽  
François Grenier ◽  
Mircea Steriade
Keyword(s):  
High Threshold ◽  
Intracellular Recordings ◽  
Control Solution ◽  
Paroxysmal Activity ◽  
Neocortical Neurons ◽  
Spontaneous Seizures ◽  
Cellular Factors ◽  
Electrographic Seizures ◽  
High Degree ◽  
Spike Wave

Some electrographic seizures are generated intracortically. The cellular and ionic bases of cortically generated spontaneous seizures are not fully understood. Here we investigated spontaneously occurring seizures consisting of spike-wave complexes intermingled with fast runs in ketamine-xylazine anesthetized cats, using dual intracellular recordings in which one pipette contained a control solution and another pipette contained blockers of K+, Na+, or Ca2+ currents. We show that closely located neocortical neurons display virtually identical fluctuations of the membrane potential during electrographic seizures, thus directly demonstrating a high degree of focal synchrony during paroxysmal activity. In addition to synaptic drives, the persistent Na+ current [ INa(p)] and probably the high-threshold Ca2+ current contributed to the generation of paroxysmal depolarizing shifts (PDSs) during cortically driven seizures. Ca2+-activated K+ current [ IK(Ca)] took also part in the control of the amplitude and duration of PDSs. The hyperpolarizing components of seizures largely depended on Cs+-sensitive K+ currents. IK(Ca) played a significant, while not exclusive, role in the mediation of hyperpolarizing potentials related to EEG “waves” during spike-wave seizures. We conclude that intrinsic cellular factors have significant role in the generation of depolarizing and hyperpolarizing components of seizures.

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