Interaction between superficial layers of the entorhinal cortex and the hippocampus in normal and epileptic temporal lobe

The entorhinal cortex (EC) is a major gateway for sensory information into the hippocampal formation. The information flow from layer II and III of the medial EC to the hippocampus is regulated in a frequency dependent manner. Spread of low Mg 2+-induced epileptiform activity from EC to hippocampus...

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Bibliographic Details
Published in:Epilepsy research 1998-09, Vol.32 (1), p.183-193
Main Authors: Gloveli, Tengis, Schmitz, Dietmar, Heinemann, Uwe
Format: Article
Language:English
Subjects:
Action Potentials
Animals
Biological and medical sciences
Cell Communication
Disease Models, Animal
Entorhinal cortex
Entorhinal Cortex - physiology
Entorhinal Cortex - physiopathology
Epilepsy, Temporal Lobe - physiopathology
Epileptiform activity
Excitatory Postsynaptic Potentials
Headache. Facial pains. Syncopes. Epilepsia. Intracranial hypertension. Brain oedema. Cerebral palsy
Hippocampus
Hippocampus - physiology
Hippocampus - physiopathology
In Vitro Techniques
Kindling, Neurologic
Low magnesium
Magnesium - pharmacology
Medical sciences
Nervous system (semeiology, syndromes)
Neurology
Neurons - drug effects
Neurons - physiology
Rat
Rats
Reference Values
Synapses - physiology
Temporal Lobe - physiology
Temporal Lobe - physiopathology
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Summary:The entorhinal cortex (EC) is a major gateway for sensory information into the hippocampal formation. The information flow from layer II and III of the medial EC to the hippocampus is regulated in a frequency dependent manner. Spread of low Mg 2+-induced epileptiform activity from EC to hippocampus differs in slices obtained from normal and kindled rats, and in adult versus juvenile rats. In slices from normal rats, low Mg 2+-induced epileptiform activity in the EC had only moderate effects on the areas CA3 and CA1, apparently gated by powerful inhibition in the dentate gyrus. In slices from kindled rats, and from juvenile rats, there is facilitated propagation of the seizure-like events and late recurrent discharges through the EC-hippocampal slice. Temporal lobe epilepsy is associated with selective lesions in layer III of the medial EC. Such loss of layer III cells of the medial EC during epilepsy may contribute to the disturbance of frequency dependent information flow from the EC to the hippocampus, and, therefore, to the cognitive impairments associated with these disorders.
ISSN:0920-1211
1872-6844
DOI:10.1016/S0920-1211(98)00050-3