“Epileptic” brain damage in rats induced by sustained electrical stimulation of the perforant path. I. Acute electrophysiological and light microscopic studies
References (99)
- et al.
Control of hippocampal output by afferent volley frequency
Prog Brain Res
(1967) - et al.
Electrographic, clinical and pathological alterations following systemic administration of kainic acid, bicuculline or pentetrazole; metabolic mapping using the deoxyglucose method with special reference to the pathology of epilepsy
Neuroscience
(1981) - et al.
The role of epileptic activity in hippocampal and “remote” cerebral lesions induced by kainic acid
Brain Res
(1980) - et al.
Evidence suggesting secondary epileptogenic lesions after kainic acid: pretreatment with diazepam reduces distant but not local brain damage
Brain Res
(1979) - et al.
Hippocampal polymorph neurons are the cells of origin for ipsilateral association and commissural afferents to the dentate gyrus
Brain Res
(1981) - et al.
Single seizures cause no ultrastructural changes in brain
Brain Res
(1972) - et al.
Cerebral metabolic response to systemic kainic acid: 14C-deoxyglucose studies
Life Sci
(1980) - et al.
The number of hippocampal neurons in rats after electrically-induced generalized seizures
Brain Res
(1980) - et al.
Is aspartic acid the neurotransmitter of the perforant path?
Brain Res
(1981) - et al.
A permanent change in brain function resulting from daily electrical stimulation
Exp Neurol
(1969)
Anatomical evidence for a projection from the entorhinal cortex to the contralateral dentate gyrus of the rat
Exp Neurol
Kainic acid neurotoxicity; effect of systemic injection on neurotransmitter markers in different brain regions
Brain Res
Regional cerebral blood flow in the rat during prolonged seizure activity
Brain Res
Delayed neuronal death in the gerbil hippocampus following ischemia
Brain Res
Monosodium glutamate: increased neurotoxicity after removal of neuronal re-uptake sites
Brain Res
Perforant path transections protect hippocampal granule cells from kainate lesion
Neurosci Lett
Associational and commissural collaterals of neurons in the hippocampal formation (hilus fasciae dentatae and subfield CA3)
Brain Res
Kainic acid induced limbic seizures: metabolic, behavioral, electroencephalographic and neuropathological correlates
Brain Res
Synaptic enhancement in fascia dentata: cooperativity among coactive afferents
Brain Res
“Epileptic” brain damage in rats induced by sustained electrical stimulation of the perforant path. II. Ultrastructural analysis of acute hippocampal pathology
Brain Res Bull
Systemic dipiperidinoethane mimics the convulsant and neurotoxic actions of kainic acid
Brain Res
Acute dendrotoxic changes in the hippocampus of kainate treated rats
Brain Res
Kainic acid: a powerful neurotoxic analogue of glutamate
Brain Res
Epilepsy and antiepileptic drugs: a speculative synthesis
Widespread patterns of neuronal damage following systemic or intracerebral injections of kainic acid: a histological study
Neuroscience
A metabolic basis for the selective vulnerability of neurons in status epilepticus
Acta Physiol Scand
Sustained electrical stimulation of the perforant path duplicates kainate-induced electrophysiological effects and hippocampal damage in rats
Neurosci Lett
On the relationship between kainic acid-induced epileptiform activity and hippocampal neuronal damage
Neuropharmacology
Erkrankung des Ammonshorns als Actiologisches Moment der Epilepsie
Arch Psychiat Nerven
Localization of transmitter amino acids: application to hippocampus and septum
Morphology of the experimental epileptic focus
J Neurosurg
A Golgi study of cell types in the hilar region of the hippocampus in the rat
J Comp Neurol
Entorhinal activation of dentate granule cells
Acta Physiol Scand
Science and art in preparing tissues embedded in plastic for light microscopy, with special reference to glycol methacrylate, glass knives and simple stains
Stain Technol
Commissural connections of the hippocampal region in the rat, with special reference to their mode of termination
J Comp Neurol
On the termination of some afferents to the hippocampus and fascia dentate
Acta Anat
Epileptic brain damage. The role of systemic factors that modify cerebral energy metabolism
Brain
Long-lasting potentiation of synaptic transmission in the dentate area of the anesthetized rabbit following stimulation of the perforant path
J Physiol (Lond)
Epileptogenic effects of small hippocampal lesions: relevance of iron deposition
Soc Neurosci Abst
Glutamate and aspartate as hippocampal transmitters: biochemical and pharmacological evidence
Localization and release of glutamic acid in relation to the hippocampal mossy fiber pathway
Nature
Epilepsy and neuron loss in the hippocampus
Epilepsia
The Understanding of the Brain
Early changes in the rat hippocampus following seizures induced by bicuculline or L-allylglycine: a light and electron microscope study
Neuropathol Appl Neurobiol
Kainic acid stimulates excitatory amino acid neurotransmitter release at presynaptic receptors
Nature
Long-lasting morphological changes in dendritic spines of dentate granule cells following stimulation of the entorhinal area
J Neurocytol
Perforant path afférents to the hippocampus: Hippocampal pyramidal cell firing and regional metabolism demonstrated by the 2-deoxyglucose autoradiographic technique
Soc Neurosci Abstr
Only certain anticonvulsants protect against kainate neurotoxicity
Neurobehav Toxicol Teratol
Localization of enkephalin-like immunoreactivity to identified axonal and neuronal populations of the rat hippocampus
J Comp Neurol
Cited by (459)
Brain pathology in focal status epilepticus: evidence from experimental models
2021, Neuroscience and Biobehavioral ReviewsCitation Excerpt :Since stimulation can be timely stopped, the severity of the FSE is often better controlled in these models in comparison to the pharmacological models. The stimulation protocol that is commonly utilized is a high frequency (>20 Hz) tetanic stimulation for max 60−90 min with or without low frequency (<2 Hz) prolonged stimulation, leading to a self-sustained SE (Bertram and Lothman, 1993; Gorter and Van Vliet, 2017; Sloviter, 1983). As for the intracerebral convulsant application models, these procedures lead to either FbcSE or FncSE.
Life and death in the hippocampus: What's bad?
2021, Epilepsy and BehaviorElectrical Stimulation Seizure Models
2017, Models of Seizures and Epilepsy: Second EditionKindling: A Model and Phenomenon of Epilepsy
2017, Models of Seizures and Epilepsy: Second EditionHippocampal Area CA2: An Overlooked but Promising Therapeutic Target
2016, Trends in Molecular MedicineCitation Excerpt :Hippocampal sclerosis comprising neuronal loss is consistently observed during temporal lobe epilepsy (TLE). Surprisingly, while a large degree of neuronal loss occurs in CA1 and CA3, there seems to be little or no neuronal death either in the DG or CA2 of humans [54] or in rodent models of epilepsy [55]. However, despite moderate cell loss in CA2, there is evidence that reorganization of the local circuitry occurs during TLE.
- 1
Present position: Neurology Center, Helen Hayes Hospital, Route 9W, West Haverstraw. NY 10993 and Departments of Pharmacology and Neurology, College of Physicians and Surgeons, Columbia University, New York, NY 10032.