期刊
JOURNALS OF GERONTOLOGY SERIES A-BIOLOGICAL SCIENCES AND MEDICAL SCIENCES
卷 78, 期 6, 页码 930-937出版社
OXFORD UNIV PRESS INC
DOI: 10.1093/gerona/glac137
关键词
Aging-related cognitive decline; Contextual fear memory; Infralimbic prefrontal cortex; Memory extinction; Synaptic plasticity
This study reveals that the extinction of Pavlovian contextual fear memory is impaired in aged mice, which is associated with a reduction in the efficacy of excitatory synaptic transmission onto the pyramidal neurons of the infralimbic prefrontal cortex (ilPFC). Restoring the reduced excitation can restore contextual fear memory extinction. This finding may potentially contribute to the development of therapeutic approaches for cognitive decline in aging.
Human beings are living longer than ever before and the cognitive decline experienced by aged adults, such as compromise in cognitive flexibility, has been attracting more and more attention. One such example is the aging-related impairment of memory extinction. However, its underlying neural basis, especially its functional basis at the synapse level, is largely unknown. This study verifies that Pavlovian contextual fear memory extinction is impaired in aged mice. A large body of previous studies has shown that the infralimbic prefrontal cortex (ilPFC) plays a pivotal role in memory extinction. Correspondingly, this study reveals an aging-related reduction in the efficacy of excitatory synaptic transmission onto the ilPFC pyramidal neurons via electrophysiology recordings. This study further suggests that this reduced excitation potentially contributes to the aging-related impairment of contextual fear memory extinction: chemogenetically suppressing the activity of the ilPFC pyramidal neurons in young mice impairs contextual fear memory extinction, whereas chemogenetically compensating for the reduced excitation of the ilPFC pyramidal neurons in aged mice restores contextual fear memory extinction. This study identifies a functional synaptic plasticity in the ilPFC pyramidal neurons that potentially contributes to the aging-related impairment of contextual fear memory extinction, which would potentially help to develop a therapy to treat related cognitive decline in aged human adults.
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