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- Etay Aloni, Antonella Ruggiero, Atan Gross, and Menahem Segal.
- Department of Neurobiology, The Weizmann Institute, Rehovot 76100, Israel.
- Neuroscience. 2018 Dec 1; 394: 156-163.
AbstractMitochondrial Carrier Homolog 2 (MTCH2) acts as a receptor for the BH3 interacting-domain death agonist (BID) in the mitochondrial outer membrane. Loss of MTCH2 affects mitochondria energy metabolism and function. MTCH2 forebrain conditional KO (MTCH2 BKO) display a deficit in hippocampus-dependent cognitive functions. Here we study age-related MTCH2 BKO behavioral and electrophysiological aspects of hippocampal functions. MTCH2 BKO exhibit impaired spatial but not motor learning and an impairment in long-term potentiation (LTP) in hippocampal slices. Moreover, MTCH2 BKO express an increase in activated microglia, in addition to a reduction in neuron density in the hippocampus, but do not express amyloid-β plaques or neurofibrillary tangles. These results highlight the role of mitochondria in the normal hippocampus-dependent memory formation.Copyright © 2018 IBRO. Published by Elsevier Ltd. All rights reserved.
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