Altered Interaction Between the Entorhinal Cortex and Hippocampus in Amygdala Kindled Rats

Abstract

The entorhinal cortex is the main input and output region for the hippocampus. Perirhinal and postrhinal cells send their axons into superficial layers of the EC where they interact with projection cells in layer II and III of the entorhinal cortex but also with apical dendrites of the deep layer entorhinal cortex cells.1 These receive input from olfactory cortex and subiculum and cholinergic input from the basal ganglia and the nucleus basalis Meynert as well as from the septum. Layer II stellate cells form the major portion of the perforant path, which projects to the dentate gyrus, while layer III cells project to the subiculum and in addition to the stratum moleculare of the CA1 area and perhaps also to area CA3.2 Studies on the normal interaction between the entorhinal cortex and hippocampus from adult rats have revealed that seizure susceptibility is larger in the EC than in the hippocampus, which tends to develop only interictal discharges and short ictal events.3,4 In adult rats seizure like events spread from the EC to the subiculum, but rarely fully recruit area CA1 and the DG. This limitation of spread seems to relate to the extensive feedforward and feedback inhibitory network in the DG and the prominent activation of inhibitory interneurons in area CA1.5 The DG was therefore assumed to play a gating role in transfer of information from layer II of the EC to the DG.6 We asked the question whether the properties of EC layer II stellate cells also contribute to the limitation of seizure spread from the EC through the DG to area CA3. Indeed layer II stellate cells express a flat input output curve when stimulated at low frequencies.