Dentate EEG spikes and associated interneuronal population bursts in the hippocampal hilar region of the rat

1995 ◽  
Vol 73 (4) ◽  
pp. 1691-1705 ◽  
Author(s):  
A. Bragin ◽  
G. Jando ◽  
Z. Nadasdy ◽  
M. van Landeghem ◽  
G. Buzsaki

1. This paper describes two novel population patterns in the dentate gyrus of the awake rat, termed type 1 and type 2 dentate spikes (DS1, DS2). Their cellular generation and spatial distribution were examined by simultaneous recording of field potentials and unit activity using multiple-site silicon probes and wire electrode arrays. 2. Dentate spikes were large amplitude (2-4 mV), short duration (< 30 ms) field potentials that occurred sparsely during behavioral immobility and slow-wave sleep. Current-source density analysis revealed large sinks in the outer (DS1) and middle (DS2) thirds of the dentate molecular layer, respectively. DS1 and DS2 had similar longitudinal, lateral, and interhemispheric synchrony. 3. Dentate spikes invariably were coupled to synchronous population bursts of putative hilar interneurons. CA3 pyramidal cells, on the other hand were suppressed during dentate spikes. 4. After bilateral removal of the entorhinal cortex, dentate spikes disappeared, whereas sharp wave-associated bursts, reflecting synchronous discharge of the CA3-CA1 network, increased several fold. 5. These physiological characteristics of the dentate spikes suggest that they are triggered by a population burst of layer II stellate cells of the lateral (DS1) and medial (DS2) entorhinal cortex. 6. We suggest that dentate spike-associated synchronized bursts of hilar-region interneurons provide a suppressive effect on the excitability of the CA3-CA1 network in the intact brain.

1996 ◽  
Vol 76 (5) ◽  
pp. 2986-3001 ◽  
Author(s):  
H. E. Scharfman

1. Injection of aminooxyacetic acid (AOAA) into the entorhinal cortex in vivo produces acute seizures and cell loss in medial entorhinal cortex. To understand these effects, AOAA was applied directly to the medial entorhinal cortex in slices containing both the entorhinal cortex and hippocampus. Extracellular and intracellular recordings were made in both the entorhinal cortex and hippocampus to study responses to angular bundle stimulation and spontaneous activity. 2. AOAA was applied focally by leak from a micropipette or by pressure ejection. Evoked potentials increased gradually within 5 min of application, particularly the late, negative components. Evoked potentials continued to increase for up to 1 h, and these changes persisted for the remainder of the experiment (up to 5 h after drug application). 3. Paired pulse facilitation (100-ms interval) was also enhanced after AOAA application. Increasing stimulus frequency to 1-10 Hz increased evoked potentials further, and after several seconds of such stimulation multiple field potentials occurred. When stimulation was stopped at this point, repetitive field potentials occurred spontaneously for 1-2 min. These recordings, and simultaneous extracellular recordings in different layers, indicated that spontaneous synchronous activity occurred in entorhinal neurons. Intracellularly labeled cortical pyramidal cells depolarized and discharged during spontaneous and evoked field potentials. 4. The effects of AOAA were blocked reversibly by bath application of the N-methyl-D-aspartate (NMDA) receptor antagonist D-amino-5-phosphonovalerate (D-APV; 25 microM) or focal application of D-APV to the medial entorhinal cortex. 5. Simultaneous extracellular recordings from the entorhinal cortex and hippocampus demonstrated that spontaneous synchronous activity in layer III was often followed within several milliseconds by negative field potentials in the terminal zones of the perforant path (stratum moleculare of the dentate gyrus and stratum lacunosum-moleculare of area CA1). The extracellular potentials recorded in the dentate gyrus corresponded to excitatory postsynaptic potentials and action potentials in dentate granule cells. However, extracellular potentials in area CA1 were small and rarely correlated with discharge in CA1 pyramidal cells. 6. The results demonstrate that AOAA application leads to an NMDA-receptor-dependent enhancement of evoked potentials in medial entorhinal cortical neurons, which appears to be irreversible. The potentials can be facilitated by repetitive stimulation, and lead to synchronized discharges of entorhinal neurons. The discharges invade other areas such as the hippocampus, indicating how seizure activity may spread after AOAA injection in vivo. These data suggest that AOAA may be a useful tool to study longlasting changes in NMDA receptor function that lead to epileptiform activity and neurodegeneration.


2005 ◽  
Vol 94 (1) ◽  
pp. 896-900 ◽  
Author(s):  
Paul S. Buckmaster

The predominant excitatory synaptic input to the hippocampus arises from entorhinal cortical axons that synapse with dentate granule cells, which in turn synapse with CA3 pyramidal cells.Thus two highly excitable brain areas—the entorhinal cortex and the CA3 field—are separated by dentate granule cells, which have been proposed to function as a gate or filter. However, unlike rats, primates have “dentate” CA3 pyramidal cells with an apical dendrite that extends into the molecular layer of the dentate gyrus, where they could receive strong, monosynaptic, excitatory synaptic input from the entorhinal cortex. To test this possibility, the dentate gyrus molecular layer was stimulated while intracellular recordings were obtained from CA3 pyramidal cells in hippocampal slices from neurologically normal macaque monkeys. Stimulus intensity of the outer molecular layer of the dentate gyrus was standardized by the threshold intensity for evoking a dentate gyrus field potential population spike. Recorded proximal CA3 pyramidal cells were labeled with biocytin, processed with diaminobenzidine for visualization, and classified according to their dendritic morphology. In response to stimulation of the dentate gyrus molecular layer, action potential thresholds were similar in proximal CA3 pyramidal cells with different dendritic morphologies. These findings do not support the hypothesis that dentate CA3 pyramidal cells receive stronger synaptic input from the entorhinal cortex than do other proximal CA3 pyramidal cells.


2017 ◽  
Author(s):  
Yevgenij Yanovsky ◽  
Jurij Brankačk

summaryThe relative electrical conductivity gradient with depth was estimated in the frontal cortex of anaesthetized rats. Current source density (CSD) approximations of field potentials evoked by ventromedial thalamic stimulations with an assumed homogeneous electrical conductivity of the neocortical tissue were compared to those with correction for the estimated conductivity gradient. In spite of the cellular heterogeneity the electrical conductivity of the frontal cortical tissue was found to be fairly homogeneous inside the superficial (layers I through IV) or deep layers (V- VI). The relative conductivity increased twofold at the transition between superficial and deep layers. Regardless of this changes CSD analysis of the field potentials evoked by ventromedial thalamic stimulation revealed negligible differences between estimations ignoring the conductivity and those taking the conductivity into account. No sinks or sources appeared or disappeared. Both CSD approximations revealed: 1) a strong sink in layer I representing most likely summed monosynaptic EPSPs of the ventromedial thalamic afferents; 2) a strong sink in layer VI, probably representing summed disynaptic EPSPs on dendrites of layer VI pyramidal cells, generated by axons of upper layer pyramidal cells; and 3) a sink in lower layer V representing probably threesynaptic summed EPSPs on dendrites of layer V pyramidal cells.


1990 ◽  
Vol 63 (4) ◽  
pp. 832-840 ◽  
Author(s):  
S. Di ◽  
C. Baumgartner ◽  
D. S. Barth

1. A 16-channel electrode array was used to record simultaneously extracellular laminar field potentials evoked by displacement of contralateral vibrissa from vibrissa/barrel cortex in five rats. Current source-density (CSD) analysis combined with principal component analysis (PCA) was used to determine the time course of laminar-specific transmembrane currents during the evoked response. 2. The potential complex consisted of biphasic fast components followed by long-lasting slow waves. It began with activity in supragranular cells consisting of a source in layers I-II and a sink in layers IV-V; this was followed by activation of the infragranular cells with a paired sink and source in layers I-IV and V-VI, respectively. The slow-wave sequences also began in the supragranular cells followed by infragranular neurons. 3. We propose that the fast components reflect sequential intralaminar depolarization processes, and the slow waves, hyper- or repolarization processes. These results suggest that a basic neuronal circuit, consisting of sequential activation of the supragranular and then the infragranular pyramidal cells, gives rise to the field potentials evoked by physiological stimulation. This is consistent with our previous studies of direct cortical responses (DCR) and pathological discharges of the penicillin focus.


2004 ◽  
Vol 91 (6) ◽  
pp. 2649-2657 ◽  
Author(s):  
Beata Jarosiewicz ◽  
William E. Skaggs

The sleeping rat cycles between two well-characterized hippocampal physiological states, large irregular activity (LIA) during slow-wave sleep (SWS) and theta activity during rapid-eye-movement sleep (REM). A third, less well-characterized electroencephalographic (EEG) state, termed “small irregular activity” (SIA), has been reported to occur when an animal is startled out of sleep without moving and during active waking when it abruptly freezes. We recently found that the hippocampal population activity of a spontaneous sleep state whose EEG resembles SIA reflects the rat's current location in space, suggesting that it is also a state of heightened arousal. To test whether this spontaneous SIA state corresponds to the SIA state reported in the literature and to compare the level of arousal during SIA to the other well-characterized physiological states, we recorded unit activity from ensembles of hippocampal CA1 pyramidal cells, EEG from the hippocampus and the neocortex, and electromyography (EMG) from the dorsal neck musculature in rats presented with auditory stimuli while foraging for randomly scattered food pellets and while sleeping. Auditory stimuli presented during sleep reliably induced SIA episodes very similar to spontaneous SIA in hippocampal and neocortical EEG amplitudes and power spectra, EMG amplitude, and CA1 population activity. Both spontaneous and elicited SIA exhibited neocortical desynchronization, and both had EMG amplitude comparable to that of waking LIA. We conclude based on this and other evidence that spontaneous SIA and elicited SIA correspond to a single state and that the level of arousal in SIA is higher than in the well-characterized sleep states but lower than the active theta state.


2020 ◽  
Vol V (3) ◽  
pp. 167-169
Author(s):  
A. E. Smirnov

The author's research refers to the anterior cerebral cortex of a newborn dog. The author studies in detail the so-called tiny pyramidal cells, lying between the pluripolar cells of the molecular layer and the small (true) pyramidal cells. Already R. y Cajal drew attention to polygonal or core-shaped cells, the cells that lie behind the layer of the outermost cells (pluripolare Nervenzellen von R. y Cajal), but did not separate them into a special group, believing that these cells were gradually changing vid, go into the small pyramids, to which he numbered them. Schaffer separates these cells into a special group, calling it the layer of surface polymorphic cells. These cells have a dark variety of shapes (fusiform, oval, roundish, pear-shaped, polygonal) and lie in approximately four (4) rows. Dendrites go then, mainly, in two opposite directions (for fusiform cells), then they move radially in all directions (for round and polygonal cells). The number of dendrites is sometimes strikingly abundant. Dendrites going to the surface of the brain reach it, while dendrites of the opposite direction sometimes go down to the ammonium formations of the cerebral cortex. Special attention should be paid to the axial cylinder of the disassembled cells; on the basis of the features of this appendix, the author distinguishes 3 types of disassembled cells.


2020 ◽  
Author(s):  
Corrinne Dunbar ◽  
Junzhan Jing ◽  
Alina Sonesra ◽  
Suhyeorn Park ◽  
Heun Soh ◽  
...  

AbstractMost anti-seizure drugs (ASDs) achieve their effects by suppressing neuronal excitability through various drug targets. However, these drug targets are widely expressed in both excitatory and inhibitory neurons. Here, we investigate whether the efficacy of the ASD retigabine (RTG) is altered after removal of the potassium channel subunit KCNQ2, one of its drug targets, from parvalbumin-expressing interneurons (PV-INs). Parvalbumin-Cre (PV-Cre) mice were crossed with Kcnq2-floxed (Kcnq2fl/fl) mice to conditionally delete Kcnq2, the gene encoding KCNQ2, from PV-INs. The efficacy of RTG (10 mg/kg, i.p.) in preventing seizures induced by picrotoxin (PTX, 10 mg/kg, i.p.) and kainic acid (KA, 30mg/kg, i.p.) in conditional knockout mice (cKO, PV-Kcnq2fl/fl) was tested. Immunostaining for KCNQ2 and KCNQ3 and in vitro pharmacological studies with whole-cell recordings were also performed. The cKO mice had no significant change in appearance, body mass, balance, heat sensitivity, depressive behavior, mortality, or EEG spectral power. RTG significantly delayed the onset of PTX- and KA-induced convulsive seizures in cKO mice, but not in wild-type littermates (WT). The expression of both KCNQ2 and KCNQ3 subunits was specifically enriched at the distal axon initial segments (AISs) of hippocampal CA1 PV-INs. In cKO mice, this specific expression and the potassium currents mediated by these subunits were greatly reduced in PV-INs, while their expression in CA1 pyramidal cells (CA1-PCs) remained unchanged. Accordingly, while the ability of RTG to suppress CA1-PC spike activity was unchanged in cKO mice, its suppressive effect on high-frequency spike activity of CA1 PV-INs (elicited by >540pA depolarizing currents) was significantly reduced compared with WT mice. In addition, the RTG-induced suppressive effect on intrinsic membrane excitability of PV-INs in WT mice became absent or decreased in cKO mice. These findings suggest that reducing the suppression of PV-INs by RTG improves its anticonvulsant effect.Key Points(3-5 bullets, no longer than 85 characters each)RTG was effective for seizures only after Kcnq2 was removed from PV-INs.KCNQ2/KCNQ3 was enriched at PV-IN AISs, sites of AP initiation.Kcnq2 removal greatly reduced KCNQ2/KCNQ3 expression and function in CA1 PV-INs.The suppressive effect of RTG on hippocampal PV-INs was blunted in cKO mice.Therefore, the efficacy of RTG may improve with partial sparing of interneurons.


2022 ◽  
Vol 13 (1) ◽  
Author(s):  
Hua Tang ◽  
Mitchell R. Riley ◽  
Balbir Singh ◽  
Xue-Lian Qi ◽  
David T. Blake ◽  
...  

AbstractTraining in working memory tasks is associated with lasting changes in prefrontal cortical activity. To assess the neural activity changes induced by training, we recorded single units, multi-unit activity (MUA) and local field potentials (LFP) with chronic electrode arrays implanted in the prefrontal cortex of two monkeys, throughout the period they were trained to perform cognitive tasks. Mastering different task phases was associated with distinct changes in neural activity, which included recruitment of larger numbers of neurons, increases or decreases of their firing rate, changes in the correlation structure between neurons, and redistribution of power across LFP frequency bands. In every training phase, changes induced by the actively learned task were also observed in a control task, which remained the same across the training period. Our results reveal how learning to perform cognitive tasks induces plasticity of prefrontal cortical activity, and how activity changes may generalize between tasks.


1990 ◽  
Vol 64 (6) ◽  
pp. 1747-1757 ◽  
Author(s):  
M. Avoli ◽  
C. Drapeau ◽  
P. Perreault ◽  
J. Louvel ◽  
R. Pumain

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)


1988 ◽  
Vol 59 (5) ◽  
pp. 1476-1496 ◽  
Author(s):  
R. S. Jones ◽  
U. Heinemann

1. Extracellular recordings were made from slices of hippocampus plus parahippocampal regions maintained in vitro. Field potentials, recorded in the entorhinal cortex after stimulation in the subiculum, resembled those observed in vivo. 2. Washout of magnesium from the slices resulted in paroxysmal events which resembled those occurring during sustained seizures in vivo. These events were greatest in amplitude and duration in layers IV/V of the medial entorhinal cortex and could occur both spontaneously and in response to subicular stimulation. Spontaneous seizure-like events were not prevented by severing the connections between the hippocampus and entorhinal cortex, but much smaller and shorter events occurring in the dentate gyrus were stopped by this manipulation. Both spontaneous and evoked paroxysmal events were blocked by perfusion with the N-methyl-D-aspartate (NMDA) receptor antagonist, DL-2-amino-5-phosphonovalerate (2-AP5). 3. Neurons in layers IV/V were characterized by intracellular recording. Injection of depolarizing current in most cells evoked a train of nondecrementing action potentials with only weak spike frequency accommodation and little or no posttrain after hyperpolarization. 4. A small number of cells displayed burst response when depolarized by positive current. The burst consisted of a slow depolarization with superimposed action potentials which decreased in amplitude and increased in duration during the discharge. The burst was terminated by a strong after hyperpolarization and thereafter, during prolonged current pulses a train of nondecrementing spikes occurred. The burst response remained if the cell was held at hyperpolarized levels but was inactivated by holding the cell at a depolarized level. 5. Depolarizing synaptic potentials could be evoked by stimulation in the subiculum. A delayed and prolonged depolarization clearly decremented with membrane hyperpolarization and, occasionally, increased with depolarization. 6. Washout of magnesium from the slices resulted in an enhancement of the late depolarization and a reversal of its voltage dependence. Eventually a single shock to the subiculum evoked a large all-or-none paroxysmal depolarization associated with a massive increase in membrane conductance. Similar events occurred spontaneously in all cells tested. The paroxysmal depolarizations, both spontaneous and evoked, were rapidly blocked by 2-AP5. 7. It is concluded that medial entorhinal cortical cells possess several intrinsic and synaptic properties which confer an extreme susceptibility to generation of sustained seizure activity.(ABSTRACT TRUNCATED AT 400 WORDS)


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