Learning Deficits in Adult Mitochondria Carrier Homolog 2 Forebrain Knockout Mouse. (1st December 2018)

• Record Type: Journal Article
• Authors: Aloni, Etay; Ruggiero, Antonella; Gross, Atan; Segal, Menahem
• Is Part Of: Neuroscience. Volume 394(2018)
• Page Start: 156
• Page End: 163
• Publication Date: 2018-12-01
• Subjects: AD Alzheimer's disease -- DG dentate gyrus -- EPSP excitatory postsynaptic potential -- LTP long-term potentiation -- MTCH2 BKO mitochondrial carrier homolog forebrain conditional KO 2; MTCH2 -- hippocampus -- spatial learning -- LTP; Neurochemistry -- Periodicals; Neurophysiology -- Periodicals; Neurology -- Periodicals; Neurochimie -- Périodiques; Neurophysiologie -- Périodiques; Neurochemistry; Neurophysiology; Electronic journals; Periodicals; Electronic journals; 612.8
• DOI: 10.1016/j.neuroscience.2018.10.035
• Languages: English
• ISSNs: 0306-4522

Abstract

Highlights: MTCH2 BKO results in loss of spatial learning but not motor skills in middle aged mice. This is associated with an age-dependent loss of long-term potentiation in CA1 region of the hippocampus. These experiments highlight the role of mitochondria malfunction in hippocampus-dependent memory. Abstract: Mitochondrial 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.