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Ibotenate Injections into the Pre‐ and Parasubiculum Provide Partial Protection against Kainate‐Induced Epileptic Damage in Layer III of Rat Entorhinal Cortex
Author(s) -
Eid Tore,
Du Fu,
Schwarcz Robert
Publication year - 2001
Publication title -
epilepsia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.687
H-Index - 191
eISSN - 1528-1167
pISSN - 0013-9580
DOI - 10.1046/j.1528-1157.2001.042007817.x
Subject(s) - ibotenic acid , subiculum , entorhinal cortex , neuroscience , epileptogenesis , kainate receptor , kainic acid , status epilepticus , lesion , hippocampus , epilepsy , chemistry , temporal lobe , medicine , pathology , biology , glutamate receptor , central nervous system , biochemistry , ampa receptor , dentate gyrus , receptor
Summary: Purpose: A loss of neurons in layer III of the entorhinal cortex (EC) is often observed in patients with temporal lobe epilepsy and in animal models of the disorder. We hypothesized that the susceptibility of layer III of the EC to prolonged seizure activity might be mediated by excitatory afferents originating in the presubiculum. Methods: Experiments were designed to ablate the presubiculum unilaterally by focal ibotenate injections and to evaluate the effect of this deafferentation on the vulnerability of EC layer III neurons to the chemoconvulsant kainate (injected systemically 5 days later). Results: After treatment with kainate, 11 of the 15 rats preinjected with ibotenate showed clear‐cut, partial neuroprotection in layer III of the EC ipsilateral to the ibotenate lesion. Serial reconstruction of the ibotenate‐induced primary lesion revealed that entorhinal neurons were protected only in animals that had lesions in the pre‐ and parasubiculum, especially in the deep layers (IV–VI). Conclusions: The deep layers of the pre‐ and parasubiculum appear to control the seizure‐induced damage of EC layer III. This phenomenon may be of relevance for epileptogenesis and for the pathogenesis of temporal lobe epilepsy.