| Abstrakt: |
Temporal lobe epilepsy (TE) is characterized by loss of hippocampal cells, often leading to hippocampal sclerosis, subsequent reorganization of the hippocampal network, and deficits in declarative memory. Despite a huge amount of experimental, preclinical, and clinical research, there is still limited understanding of the mechanisms underlying the development of TE. The dentate gyrus (DG) has been suggested to play a decisive role in the mechanisms of the development of this disease. The protective function of the DG, which is based on the low excitability of granule neurons and protects hippocampal pyramidal cells from hyperactivation under strong excitatory influences, is believed to be impaired in TE. Loss of mossy cells has been found in the hilus of the DG in patients with temporal lobe epilepsy. Some authors consider mossy cell vulnerability a critical factor in the development of TE: these neurons normally behave as circuit breakers, and their death breaks the natural neural network, leading to pathological activity. The present paper discusses changes in the morphological and functional properties of the DG in the epileptic brain, the roles of mossy fiber sprouting and neurogenesis in the development of TE, and impairments to the cognitive functions of the hippocampus when the dentate gyrus loses its protective role in conditions of hyperactivation. [ABSTRACT FROM AUTHOR] |
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