Temporal Lobe Volumetric Cell Densities in Temporal Lobe Epilepsy

Babb, Thomas L.; Brown, W. J.; Pretorius, James K.; Davenport, Cynthia J.; Lieb, Jeffrey P.; Crandall, Paul H.

doi:10.1111/j.1528-1157.1984.tb03484.x

Cited by 453 publications

(253 citation statements)

References 19 publications

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“…However, it is the CA1 pyramidal neurons along with those in CA3 and the dentate hilus that have been shown by previous quantitative stereological studies to be decreased to the greatest extent in rats having undergone amygdala kindling (Cavazos et al, 1994). Importantly, it is these same cell types that are maximally lost in patients with chronic MTLE (Babb and Brown, 1987;Babb et al, 1984). Additionally, it was in the CA1 pyramidal neurons, in the study of Karst et al (1999), that significant neurophysiological changes (ie increased amplitude of population spike and of voltage-gated Ca 2 þ currents) were detected in brain slices taken from kindled rats treated with high-dose CS vs control kindled rats.…”

Section: Discussionmentioning

confidence: 94%

Chronic Low-Dose Corticosterone Supplementation Enhances Acquired Epileptogenesis in the Rat Amygdala Kindling Model of TLE

Taher

Salzberg

Morris

et al. 2005

Neuropsychopharmacol

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Mesial temporal lobe epilepsy (MTLE) is associated with high rates of depression and anxiety. A bidirectional causal relationship has been suggested, with these psychiatric comorbidities themselves enhancing epileptogenesis, possibly via hypercortisolemia. We examined the effects on epileptogenesis of chronic supplementation with low-dose corticosterone (CS) in the electrical amygdala kindling rat model. Adult Wistar rats were ovariectomized and implanted with bipolar electrodes into the left amygdala. After 1 week recovery, one group (n ¼ 7) had CS (3 mg/100 mlFapprox. 4.5 mg/kg/day) and a control group saline (n ¼ 7) added to their drinking water, and both groups underwent twice daily electrical stimulations. Rats were culled 2 weeks after reaching the fully kindled state. A stereological optical fractionator technique was used to estimate the number of CA1 pyramidal cells in the hippocampus ipsilateral to the stimulations. Fewer stimulations were required in the CS-supplemented rats than in controls to reach the fully kindled state (32 vs 81, po0.03, Student's t-test) and the first Class V seizure (14 vs 57, po0.05). The mean after-discharge length was greater in the CS group (p ¼ 0.03, repeated measures analysis of variance). There was no difference in the mean number of CA1 neurons (1.05 Â 10 5 vs 1.04 Â 10 5 , p ¼ 0.98). These data demonstrate that low-dose CS enhances epileptogenesis in this model of MTLE. This provides support for the hypothesis that chronic hypercortisolemia, as a result of stress, anxiety, and/or depression, may facilitate the development and progression of epilepsy in patients with MTLE. The lack of difference in hippocampal CA1 neurons indicates that the mechanism does not primarily involve pyramidal cell loss.

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Section: Discussionmentioning

confidence: 94%

Chronic Low-Dose Corticosterone Supplementation Enhances Acquired Epileptogenesis in the Rat Amygdala Kindling Model of TLE

Taher

Salzberg

Morris

et al. 2005

Neuropsychopharmacol

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“…81 In the sclerotic hippocampus significant neuronal loss is reported in both the dentate gyrus and hippocampus proper (Ammon's horn). 9,82 Area CA1 neurons are the most susceptible to injury and was so noted more than a decade ago by Sommer. 83 The region is filled with reactive astrocytes, resulting in the hardening or sclerotic nature of the hippocampus.…”

Section: What Role Do Astrocytes Play In the Hippocampal Seizure Focus?mentioning

confidence: 94%

Astrocytes and Epilepsy

2010

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Summary: Astrocytes form a significant constituent of seizure foci in the human brain. For a long time it was believed that astrocytes play a significant role in the causation of seizures. With the increase in our understanding of the unique biology of these cells, their precise role in seizure foci is receiving renewed attention. This article reviews the information now available on the role of astrocytes in the hippocampal seizure focus in patients with temporal lobe epilepsy with hippocampal sclerosis. Our intent is to try to integrate the available data. Astrocytes at seizure foci seem to not be a homogeneous population of cells, and in addition to typical glial fibrillary acidic protein, positive reactive astrocytes also include a population of neuron glia-2-like cells The astrocytes in sclerotic hippocampi differ from those in nonsclerotic hippocampi in their membrane physiology, having elevated Naϩ channels and reduced inwardly rectifying potassium ion channels, and some having the capacity to generate action potentials. They also have reduced glutamine synthetase and increased glutamate dehydrogenase activity. The molecular interface between the astrocyte and microvasculature is also changed. The astrocytes are also associated with increased expression of many molecules normally concerned with immune and inflammatory functions. A speculative mechanism postulates that neuron glia-2-like cells may be involved in creating a high glutamate environment, whereas the function of more typical reactive astrocytes contribute to maintain high extracellular Kϩ levels; both factors contributing to the hyperexcitability of subicular neurons to generate epileptiform activity. The functions of the astrocyte vascular interface may be more critical to the processes involved in epileptogenesis.

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“…The relationship of these physiological differences to variations in anatomical organization along the septotemporal axis is unclear, but could influence the development of epilepsy, as the temporal pole is more vulnerable than the septal pole to the development of kindling (Racine et al, 1977). The observation of greater vulnerability to seizure-induced neuronal loss in the temporal poles of the hilus of the DG and CAlc in rodents is also of interest, as the anterior pole of the human hippocampus (which corresponds to the rodent temporal pole) is frequently involved in human temporal lobe epilepsy, and may be more prominently involved in the lesion of hippocampal sclerosis (Babb et al, 1984).…”

Section: Septotemporal Variation Of Neuronal Densities In Normal Ratsmentioning

confidence: 99%

Neuronal loss induced in limbic pathways by kindling: evidence for induction of hippocampal sclerosis by repeated brief seizures

Cavazos

Das

Sutula³

1994

J. Neurosci.

432

228

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Repeated kindled seizures induce long-lasting physiological and morphological alterations in the hippocampal formation. In the dentate gyrus (DG), the morphological alterations induced by kindled seizures include loss of polymorphic neurons in the hilus, mossy fiber axon sprouting, and synaptic reorganization of the mossy fiber pathway. In this study, quantitative stereological methods were used to determine the distribution and time course of neuronal loss induced by 3, 30, or 150 kindled generalized tonic-clonic seizures in hippocampal, limbic, and neocortical pathways. Neuronal loss was observed in the hilus of the DG and CA1 after three generalized tonic-clonic seizures, and progressed in these sites to 49% and 44% of controls after 150 seizures. Neuronal loss was also observed in CA3, entorhinal cortex, and the rostral endopyriform nucleus after 30 seizures, and was detected in the granule cell layer and CA2 after 150 seizures. There was no evidence of neuronal loss in the somatosensory cortex after 150 seizures. The time course of the neuronal loss demonstrated selective vulnerability of hippocampal neuronal populations to seizure-induced injury, and suggests that even brief seizures may induce excitotoxic injury in vulnerable neuronal populations. Repeated brief seizures induced neuronal loss in a distribution that resembled hippocampal sclerosis, the most common lesion observed in human epilepsy. The results demonstrated that kindling induces alterations in neural circuitry in a variety of locations in the limbic system, and suggest that hippocampal sclerosis may be acquired in human epilepsy as a consequence of repeated seizures.

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Temporal Lobe Volumetric Cell Densities in Temporal Lobe Epilepsy

Cited by 453 publications

References 19 publications

Chronic Low-Dose Corticosterone Supplementation Enhances Acquired Epileptogenesis in the Rat Amygdala Kindling Model of TLE

Chronic Low-Dose Corticosterone Supplementation Enhances Acquired Epileptogenesis in the Rat Amygdala Kindling Model of TLE

Astrocytes and Epilepsy

Neuronal loss induced in limbic pathways by kindling: evidence for induction of hippocampal sclerosis by repeated brief seizures

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