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E H Bertram

Publications and source records attributed to E H Bertram.

At least 37 records · Page 2Linked to original sources
PubMed1998

Responses of deep entorhinal cortex are epileptiform in an electrogenic rat model of chronic temporal lobe epilepsy.

We investigated whether entorhinal cortex (EC) layer IV neurons are hyperexcitable in the post-selfsustaining limbic status epilepticus (post-SSLSE) animal model of temporal lobe epilepsy. We studied naive rats (n = 44), epileptic rats that had experienced SSLSE resulting in spontaneous seizures (n = 45), and electrode controls (n = 7). There were no differences between electrode control and naive groups, which were pooled into a single control group. Intracellular and extracellular recordings were made from deep layers of EC, targeting layer IV, which was activated by stimulation of the superficial layers of EC or the angular bundle. There were no differences between epileptic and control neurons in basic cellular characteristics, and all neurons were quiescent under resting conditions. In control tissue, 77% of evoked intracellular responses consisted of a short-duration [8.6 +/- 1.3 (SE) ms] excitatory postsynaptic potential and a single action potential followed by gamma-aminobutyric acid-A (GABAA) and GABAB inhibitory post synaptic potentials (IPSPs). Ten percent of controls did not contain IPSPs. In chronically epileptic tissue, evoked intracellular responses demonstrated prolonged depolarizing potentials (256 +/- 39 ms), multiple action potentials (13 +/- 4), and no IPSPs. Ten percent of epileptic responses were followed by rhythmic "clonic" depolarizations. Epileptic responses exhibited an all-or-none response to progressive increases in stimulus intensity and required less stimulation to elicit action potentials. In both epileptic and control animals, intracellular responses correlated precisely in morphology and duration with extracellular field potentials. Severing the hippocampus from the EC did not alter the responses. Duration of intracellular epileptic responses was reduced 22% by the N-methyl--aspartate (NMDA) antagonist (-)-2-amino-5-phosphonovaleric acid (APV), but they did not return to normal and IPSPs were not restored. Epileptic and control responses were abolished by the non-NMDA antagonist 6, 7-dinitroquinoxaline-2-3-dione (DNQX). A monosynaptic IPSP protocol was used to test connectivity of inhibitory interneurons to primary cells by direct activation of interneurons with a stimulating electrode placed near the recording electrode in the presence of APV and DNQX. Using this protocol, IPSPs similar to control (P > 0.05) were seen in epileptic cells. The findings demonstrate that deep layer EC cells are hyperexcitable or "epileptiform" in this model. Hyperexcitability is not due to interactions with the hippocampus. It is due partially to augmented NMDA-mediated excitation. The lack of IPSPs in epileptic neurons may suggest inhibition is impaired, but we found evidence that inhibitory interneurons are connected to their target cells and are capable of inducing IPSPs.

Action Potentials↗
PubMed1997

Design and construction of a long-term continuous video-EEG monitoring unit for simultaneous recording of multiple small animals.

In recent years several new rat models of human limbic/mesial temporal lobe epilepsy have been described [1,2,4-7,11,15-17]. Unlike earlier models such as kindling in which the seizures are induced by an exogenous stimulus, these new models are characterized by seizures that occur spontaneously at random intervals. Although the spontaneity of the seizures makes these models more like human epilepsy, documentation of these seizures by direct observation is highly inefficient, and sub-behavioral electrographic seizures could be missed. Continuous paper EEG and video recording have been used [5-7,15], but these techniques are resource intensive. The slow paper speed required by long-term paper recordings limits the ability to differentiate between true seizure activity and electrical artifact. Subtle behavioral seizures are likely to be missed during rapid review of video recordings alone [16]. Ambulatory cassette EEG recordings have been used [3], but the systems require expensive proprietary hardware, and the systems have limited channels for recording (8-16). To improve the utility of the models, we developed a long-term EEG/video monitoring system to detect the electrographic seizures and document their behavioral accompaniment. The system is based on commercially available components, including a computerized EEG seizure detection system that was initially developed for human seizure monitoring [8,9,13]. Seizures are reliably detected and the data are reduced so that 24 h of recording can be reviewed in 30-90 min. Although the computer program is accurate, special care must be taken in system design and construction to reduce sources of electrical artifact that can cause false detections when multiple animals are recorded simultaneously on a single EEG machine. During data review it is necessary to differentiate between electrical artifact induced by animal activity from true seizure activity by key EEG patterns. Certain seizure patterns (less than 3 hz. low amplitude) will not be detected by the seizure detection program, but the system is highly effective for typical limbic seizures and may be useful for the animal models of absence epilepsy [12,14]. It can also be used as a continuous or intermittent EEG/physiological recording device for experiments that examine animals' spontaneous behavior and the EEG correlate (e.g. sleep/wake cycles, learning and memory tasks).

Animals↗
PubMed1997

Histological and 1H magnetic resonance spectroscopic imaging analysis of quinolinic acid-induced damage to the rat striatum.

NAA has been described as a neuron-specific compound. NAA levels as determined by magnetic resonance spectroscopic imaging (MRSI) have been used to determine degree of neuronal loss in several neurological diseases, but there has been limited work to document the accuracy and reliability of this technique. This study addresses this question quantitatively with histological analysis of cell viability and tissue shrinkage in quinolinic acid (QA)-induced damage of the rat striatum compared with 1H MRSI measurement of N-acetyl aspartate (NAA) as a noninvasive measure of neuronal loss. Both 1H MRSI and histology detect damage to the lesioned striatum; however, there are differences in the degree of damage as assessed by the two methods. Although partial-volume effects and tissue shrinkage may decrease the sensitivity of MR to such damage, the sparing of axons by QA may be another important factor in the differences in assessment. These results indicate that further studies of NAA metabolism and its distribution within neurons are warranted.

Animals↗
PubMed1997

In contrast to kindled seizures, the frequency of spontaneous epilepsy in the limbic status model correlates with greater aberrant fascia dentata excitatory and inhibitory axon sprouting, and increased staining for N-methyl-D-aspartate, AMPA and GABA(A) receptors.

This study determined whether there were differences in hippocampal neuron loss and synaptic plasticity by comparing rats with spontaneous epilepsy after limbic status epilepticus and animals with a similar frequency of kindled seizures. At the University of Virginia, Sprague-Dawley rats were implanted with bilateral ventral hippocampal electrodes and treated as follows; no stimulation (electrode controls; n=5): hippocampal stimulation without status (stimulation controls; n=5); and limbic status from continuous hippocampal stimulation (n=12). The limbic status group were electrographically monitored for a minimum of four weeks. Four rats had no recorded chronic seizures (status controls), and all three control groups showed no differences in hippocampal pathology and were therefore incorporated into a single group (controls). Eight limbic status animals eventually developed chronic epilepsy (spontaneous seizures) and an additional eight rats were kindled to a similar number and frequency of stage 5 seizures (kindled) as the spontaneous seizures group. At the University of California (UCLA) the hippocampi were processed for: (i) Niss1 stain for densitometric neuron counts; (ii) neo-Timm's histochemistry for mossy fiber sprouting; and (iii) immunocytochemical staining for glutamate decarboxylase, N-methyl-D-aspartate receptor subunit 2, AMPA receptor subunit 1 and the GABA(A) receptor. In the fascia dentata inner and outer molecular layers the neo-Timm's stain and immunoreactivity was quantified as gray values using computer image analysis techniques. Statistically significant results (P<0.05) showed the following. Compared to controls and kindled animals, rats with spontaneous seizures had: (i) lower neuron counts for the fascia dentata hilus, CA3 and CA1 stratum pyramidale; (ii) greater supragranular inner molecular layer mossy fiber staining; and (iii) greater glutamate decarboxylase immunoreactivity in both molecular layers. Greater supragranular excitatory mossy fiber and GABAergic axon sprouting correlated with: (i) increases in N-methyl-D-aspartate receptor subunit 2 inner molecular layer staining; (ii) more AMPA receptor subunit 1 immunoreactivity in both molecular layers; and (iii) greater outer than inner molecular layer GABA(A) immunoreactivity. Furthermore, in contrast to kindled animals, rats with spontaneous seizures showed that increasing seizure frequency per week and the total number of natural seizures positively correlated with greater Timm's and GABAergic axon sprouting, and with increases in N-methyl-D-aspartate receptor subunit 2 and AMPA receptor subunit 1 receptor staining. In this rat limbic status model these findings indicate that chronic seizures are associated with hippocampal neuron loss, reactive axon sprouting and increases in excitatory receptor plasticity that differ from rats with an equal frequency of kindled seizures and controls. The hippocampal pathological findings in the limbic status model are similar to those in humans with hippocampal sclerosis and mesial temporal lobe epilepsy, and support the hypothesis that synaptic reorganization of both excitatory and inhibitory systems in the fascia dentata is an important pathophysiological mechanism that probably contributes to or generates chronic limbic seizures.

Animals↗
PubMed1997

Shortened-duration GABA(A) receptor-mediated synaptic potentials underlie enhanced CA1 excitability in a chronic model of temporal lobe epilepsy.

Intracellular recording techniques were used to examine GABA(A) receptor-mediated synaptic inhibition in pyramidal cells of the CA1 region of the rat hippocampus in the post-self sustaining limbic status epilepticus model of temporal lobe epilepsy. Orthodromically evoked, monosynaptic inhibitory postsynaptic potentials were recorded in vitro following pharmacological blockade of ionotropic glutamate and GABA(B) receptors. Inhibitory postsynaptic potentials from epileptic tissue were kinetically altered relative to controls; both the 10-90% rise-time and width (measured at half-maximum amplitude) were reduced by approximately 50% resulting in significant shortening of duration. The degree of pyramidal cell hyperexcitability, assessed before pharmacological treatment as the number of action potentials evoked by maximum intensity afferent stimulation, correlated significantly with the magnitude of synaptic potential duration reduction determined following blockade of glutamatergic neurotransmission. Bath application of the benzodiazepine type 1 receptor agonist zolpidem reduced post-self sustaining limbic status epilepticus CA1 pyramidal cell hyperexcitability substantially (but not completely) via a marked increase in inhibitory postsynaptic potential area. Post-self-sustaining limbic status epilepticus inhibitory postsynaptic potentials which exhibited the most pronounced shortening were augmented by zolpidem to a greater degree than longer duration synaptic potentials. In contrast, zolpidem-induced augmentation of control inhibitor, postsynaptic potential area was much less robust. It is suggested that a deficiency in post-self-sustaining limbic status epilepticus GABA(A) receptor-mediated synaptic inhibition contributes to a state of partial disinhibition which is a major factor in enhanced CA1 excitability in chronic limbic epilepsy. Possible mechanisms underlying post-self-sustaining limbic status epilepticus kinetic abnormalities are discussed.

2-Amino-5-phosphonovalerate↗
PubMed1997

Longitudinal distribution of hippocampal atrophy in mesial temporal lobe epilepsy.

Patients with mesial temporal lobe epilepsy (MTLE) have asymmetric hippocampal volumes with atrophy that sometimes by visual inspection appears to favor different regions along the longitudinal axis of the affected hippocampus. Histological studies suggest that cell loss may affect the anterior hippocampus preferentially, and that hippocampal sclerosis (HS) limited to the anterior of the hippocampus may indicate better surgical outcome. We used volumetric magnetic resonance imaging (MRI): (1) to objectively describe the distribution of volume loss in HS; and (2) to relate this distribution to outcome of temporal lobectomy. Hippocampal volumes and anterior and posterior subvolumes (AHV, PHV) were measured from MP-RAGE MRI in 43 temporal lobectomy patients with MTLE determined by pathological findings of HS and compared to 23 age-matched controls. Atrophy was defined as 'anterior', 'diffuse', 'posterior', or 'normal' depending on position of AHV and PHV relative to the mean +/- 2 S.D. of regional volumes of control hippocampi. Anterior to posterior ratios (APR = AHV/PHV) were also calculated. Mean APR of hippocampi ipsilateral to lobectomy cannot be distinguished from hippocampi contralateral to lobectomy or from controls. AHV and PHV from hippocampi contralateral to temporal lobectomy were smaller than controls but larger than hippocampi ipsilateral to lobectomy. Surgical outcome was independent of longitudinal distribution of atrophy. We determined that overall volume loss in HS is diffuse, neither clearly favoring the head nor body-tail. Surgical outcome for MTLE is not related to the longitudinal distribution of atrophy revealed by volumetric MRI.

Adult↗
PubMed1997

Functional anatomy of spontaneous seizures in a rat model of limbic epilepsy.

PURPOSE: The substrate of seizure initiation in partial epilepsy is not well understood. Although many studies imply a focus that is will localized to a single structure, some information suggests that seizures arise regionally with simultaneous or near-simultaneous onset at several separate sites. To determine the physiological pattern of seizure onset, recordings were made of spontaneous seizures from multiple limbic structures in a rat model of limbic epilepsy. METHODS: Seventeen rats with chronic spontaneous limbic seizures that occurred after an episode of electrical hippocampal stimulation-induced status epilepticus (SE) underwent chronic recording of seizures with a minimum of four electrodes placed bilaterally in the midventral hippocampus and either the amygdala or piriform cortex. As many as 15 of the first recorded spontaneous seizures (mean of 12 seizures, range 2-15) was evaluated for each animal with regard to pattern of seizure onset (focal hippocampal, focal nonhippocampal, or diffuse). The results were evaluated for number of seizure patterns displayed by each animal and the potential change in the pattern of onset with successive seizures (from the first to the fifteenth). RESULTS: In all, 210 seizures were evaluated beginning 1 week after SE and with monitoring lasting < or = 18 weeks (mean recording duration 6 weeks) to record a maximum of 15 seizures for each animal. Overall, 54% of the seizures were of diffuse onset, 25% were of nonhippocampal onset, and 21% were of hippocampal onset. Eight of the 17 (47%) animals had seizures with all three patterns of onset. Evaluation of the evolution of the pattern of onset from the first to the fifteenth seizure recorded for the animals showed a clear tendency for the later seizures to have diffuse onsets (regression analysis r = 0.737, p < 0.002). Qualitative histologic analysis demonstrated neuronal loss in the recorded regions. CONCLUSIONS: These findings indicate that the epileptogenic zone is broad in this model of limbic "focal" epilepsy and suggest that the substrate for seizure generation is distributed over several structures.

Animals↗
PubMed1997

Volumetric magnetic resonance imaging evidence of bilateral hippocampal atrophy in mesial temporal lobe epilepsy.

PURPOSE: We measured absolute volumes and volume differences of hippocampi in patients with mesial temporal lobe epilepsy (MTLE) using volumetric magnetic resonance imaging (MRI) to determine the extent of bilateral atrophy in MTLE and to relate hippocampal volumes (HV) to outcome of temporal lobectomy. METHODS: HV and hippocampal differences (HD) were measured in 40 patients with MTLE determined by pathology of hippocampal sclerosis (HS) and compared with those of age-matched controls. Results were matched with surgical outcome. RESULTS: Hippocampi contralateral to lobectomy (right hippocampi 2.96 +/- 0.49 cm3, left 3.14 +/- 0.51 cm3) were significantly smaller than those of controls (right hippocampi 3.73 +/- 0.52 cm3, left 3.60 +/- 0.51 cm3) but were significantly larger than hippocampi ipsilateral to lobectomy (right hippocampi 2.63 +/- 0.61 cm3, 2.18 cm3) as compared across groups by analysis of variance (ANOVA: F = 27.2, p < 0.0001). The smaller hippocampus was ipsilateral to lobectomy in 39 of 40 cases. Seven of 40 MTLE patients (18%) had bilateral atrophy, defined by volumes of each hippocampi 2 SD lower than control means. Surgical outcome was independent of hippocampal asymmetry and bilateral atrophy measured by chi-square and Fisher's exact tests. CONCLUSIONS: We determined that most patients with MTLE have some degree of bilateral, asymmetric hippocampal pathology. However, asymmetry and bilateral atrophy have no clear relation to surgical outcome.

Adult↗
PubMed1997

Interneurons in area CA1 stratum radiatum and stratum oriens remain functionally connected to excitatory synaptic input in chronically epileptic animals.

Past work has demonstrated a reduction of stimulus-evoked inhibitory input to hippocampal CA1 pyramidal cells in chronic models of temporal lobe epilepsy (TLE). It has been postulated that this reduction in inhibition results from impaired excitation of inhibitory interneurons. In this report, we evaluate the connectivity of area CA1 interneurons to their excitatory afferents in hippocampal-parahippocampal slices obtained from a rat model of chronic TLE. Rats were made chronically epileptic by a period of continuous electrical stimulation of the hippocampus, which establishes an acute condition of self-sustained limbic status epilepticus (SSLSE). This period of SSLSE is followed by a development of chronic recurrent spontaneous limbic seizures that are associated with chronic neuropathological changes reminiscent of those encountered in human TLE. Under visual control, whole cell patch-clamp recordings of interneurons and pyramidal cells were obtained in area CA1 of slices taken from adult, chronically epileptic post-SSLSE rats. Neurons were activated by means of electrodes positioned in stratum radiatum. Intrinsic membrane properties, including resting membrane potential, action potential (AP) threshold, AP half-height width, and membrane impedance, were unchanged in interneurons from chronically epileptic (post-SSLSE) tissue compared with control tissue. Single stimuli delivered to stratum radiatum evoked depolarizing excitatory postsynaptic potentials and APs in interneurons, whereas paired-pulse stimulation evoked facilitation of the postsynaptic current (PSC) in both control and post-SSLSE tissue. No differences between interneurons in control versus post-SSLSE tissue could be found with respect to the mean stimulus intensity or mean stimulus duration needed to evoke an AP. A multiple linear regression analysis over a range of stimulus intensities demonstrated that a greater number of APs could be evoked in interneurons in post-SSLSE tissue compared with control tissue. Spontaneous PSCs were observed in area CA1 interneurons in both control and post-SSLSE tissue and were markedly attenuated by glutamatergic antagonists. In conclusion, our data suggest that stimulus-evoked and spontaneous excitatory synaptic input to area CA1 interneurons remains functional in an animal model of chronic temporal lobe epilepsy. These findings suggest, therefore, that the apparent decrease of polysynaptic inhibitory PSPs in CA1 pyramidal cells in epileptic tissue is not due to a deficit in excitatory transmission from Schaffer collaterals to interneurons in stratum radiatum and straum oriens.

Animals↗
PubMed1996

Epilepsy surgery in children and adolescents.

There has been a considerable increase in interest in the surgical management of intractable epilepsy in children. Better methods of diagnosis and improved knowledge of natural history and results of surgery have been major factors in this phenomenon. The results of surgery in 76 patients who were 19 years of age or younger are reported. Success rates, defined as no postoperative seizures with loss of consciousness (Engel Grades I and II) were 78% in 52 patients treated by temporal lobectomy, 75% in eight patients who had extratemporal resections, 80% in 10 children treated by hemispherectomy, and 33% in three patients treated by corpus callosotomy.

Journal Article↗
PubMed1994

The evolution of a rat model of chronic spontaneous limbic seizures.

The evolution of untreated partial epilepsy is unknown. This study uses a newly developed model of chronic limbic epilepsy to determine whether seizures inexorably worsen in duration, frequency and behavioral accompaniment. The seizures begin following an episode of limbic status epilepticus induced by continuous electrical stimulation of the hippocampus, and they persist for more than a year (longest duration followed). We monitored 10 rats continuously with combined EEG and closed circuit television for 24 weeks following the first recorded spontaneous seizure. Seizure duration, behavioral accompaniment and frequency all intensified during the early stages, but the last 12-16 weeks of the study were characterized by a plateau for all measures. The results showed significant increases that occurred over the first 12 weeks only (P < 0.01 for duration and behavioral accompaniment, P < 0.05 for seizure frequency). These findings suggest that untreated epilepsy will undergo an early maturation process, but that once the seizures mature they remain stable over a prolonged period. It was also noted that 67% (P < 0.00001) of the seizures occurred during the day, suggesting that the sleep-wake cycle has a strong influence on the occurrence of seizures in this model of limbic epilepsy.

Analysis of Variance↗
PubMed1993

The ontogeny of seizures in a rat model of limbic epilepsy: evidence for a kindling process in the development of chronic spontaneous seizures.

Kindling is an experimental model for epilepsy in which repeated stimuli induce longer electrographic seizures and eventually cause behavioral convulsions. Although kindling has some features that are similar to chronic human epilepsy, it is not known whether this process plays a role in the development of chronic seizure disorders. We have recently described a rat model of chronic spontaneous limbic seizures that has a number of similarities to human limbic epilepsy. To determine whether a kindling process is involved in the ontogeny of the seizures in this animal model, we continuously monitored 16 rats with EEG and closed circuit television until they had experienced a minimum of 5 and as many as 10 seizures following the first motor seizure. All animals had at least one non-motor seizure before the first motor event (mean 5.1 +/- 0.9 S.E.M. initial non-motor seizures, range 1-12). In addition the seizures significantly lengthened in duration with succeeding events (mean 90 s for the first motor seizure to mean 110 s for the tenth subsequent seizure). These data demonstrate that there is a kindling process involved in the early development of chronic limbic seizures.

Animals↗
PubMed1993

Morphometric effects of intermittent kindled seizures and limbic status epilepticus in the dentate gyrus of the rat.

The effect of recurrent seizures on the hippocampus has been controversial for many years. To determine the effect different seizure paradigms had on the structure of the dentate gyrus, we conducted histological studies on the dentate gyrus (DG) from three groups of rats: (1) those that had experienced 1500 intermittent kindled seizures; (2) those that had experienced a single episode of limbic status epilepticus (SE); and (3) control rats that had been implanted with electrodes. When compared to controls the DG of SE rats was overall slightly, but non-significantly, smaller, but the DG of rats with 1500 kindled seizures was significantly larger. The decrease of size following SE was attributable to a significant atrophy of the molecular layer. The increase in area associated with kindling was the result of an enlargement of the molecular layer and the hilus. Absolute neuronal counts showed a decrease in the hilus after SE but no change following kindling, but both groups had decreased neuronal densities in the hilus when compared to controls. The decreased density after SE was secondary to neuronal loss, but the decrease in neuronal density following kindling was the result of the expansion of the hilar neuropil without change in the number of neurons. This study extends our previous findings in Ammon's horn and indicates that SE induces significant neuronal loss, but numerous intermittent kindled seizures have no effect on neuronal numbers in the DG.

Animals↗
PubMed1993

Epileptogenic effects of status epilepticus.

Determining whether and under what conditions status epilepticus (SE) leads to undesirable long-term sequelae has major clinical ramifications. In addition to structural brain damage and enduring neurological deficits following SE, it has been suggested that SE can establish a chronic condition of active epilepsy. These three residua (epileptic brain damage, neurological deficits, and epilepsy) have been especially linked to protracted SE. The older clinical literature indicates that these sequelae are especially likely if SE occurs in an immature brain, but this point has been challenged in recent studies. Clinical and animal model work that examines the issue of chronic nervous system deficits arising as a consequence of SE is reviewed, with particular attention to the question of the epileptogenic effect of SE. Because of the inherent problem of not being able to exclude occult neurological disease antecedent to SE in brain, animal model work promises to be especially relevant to the issues at hand. Work done on adult rats has shown that a previously normal brain can be "converted" after a bout of SE to an epileptic brain, as manifest both by epileptic brain damage resembling that found in the hippocampus of patients with intractable temporal lobe epilepsy and by spontaneous recurrent seizures registered in the hippocampus. A two-step model is proposed: morphological brain injury takes place first and this change, in turn, promotes seizures. This model is offered as one way in which chronic active epilepsy can be established by a transient episode of SE. Although some findings from work with animal models have been interpreted as not supporting the idea that the immature brain is sensitive to a chronic epileptogenic influence initiated by SE, the majority of such work is consistent with this idea. On the other hand, a considerable amount of animal work indicates that the brains of immature animals are quite resistant to SE-induced brain damage, in contrast to those of adults. Thus, under these circumstances, a different process of epileptogenesis than the two-step model may be operational. It is concluded that, under appropriate conditions, SE does exert an epileptogenic effect that persists.

Animals↗
PubMed1992

The dentate gyrus as a control point for seizures in the hippocampus and beyond.

Considerable in vitro work has pointed to a resistance of dentate gyrus granule cells for expressing epileptiform paroxysms. However, in vivo work has shown that these neurons, under appropriate conditions, support and sustain seizure discharges. This range of activity of granule cells, along with their location in the middle of a pathway that connects hippocampal regions with high propensities for generating seizures, allows the dentate gyrus to act as a critical regulator of seizures. In the following report we review experiments on a stereotyped, robust paroxysmal discharge, maximal dentate activation (MDA), that occurs in granule cells, and we examine the role of MDA in reinforcing seizures in hippocampal circuits. In addition, work is presented that indicates MDA regulates seizures at sites beyond the hippocampus and its connections. Other studies that examine morphological and functional changes in the local circuits of granule cells and other neurons in the dentate gyrus in different models of epilepsy are discussed. We conclude that the dentate gyrus functions in several modes during seizures, even in the naive brain, and that in chronic epilepsy alterations take place that provide an even greater diversity of functional capabilities. Explicating these heterogeneous conditions will provide important insight into basic mechanisms of seizures and epileptogenesis.

Afferent Pathways↗
PubMed1991

Ambulatory EEG cassette recorders for prolonged electroencephalographic monitoring in animals.

We describe the use of ambulatory cassette EEG recorders for monitoring in vivo neurophysiologic signals from multiple animals over prolonged periods of time. This technique centers around a simple interface device that attenuates the intracerebral signals to the input range of the recording device and around a common indifferent input for all animals. The resulting analog recordings have the advantage of good signal resolution and rapid review of 24 h of recorded data.

Animals↗