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Exercise Prevents Memory Consolidation Defects Via Enhancing Prolactin Responsiveness of CA1 Neurons in Mice Under Chronic Stress

Title
Exercise Prevents Memory Consolidation Defects Via Enhancing Prolactin Responsiveness of CA1 Neurons in Mice Under Chronic Stress
Authors
Leem, Yea-HyunPark, Jin-SunChang, HyukkiPark, JonghoonKim, Hee-Sun
Ewha Authors
김희선박진선임예현
SCOPUS Author ID
김희선scopus; 박진선scopus; 임예현scopus
Issue Date
2019
Journal Title
MOLECULAR NEUROBIOLOGY
ISSN
0893-7648JCR Link

1559-1182JCR Link
Citation
MOLECULAR NEUROBIOLOGY vol. 56, no. 9, pp. 6609 - 6625
Keywords
Chronic stressRegular exerciseMemory consolidationProlactinCalcium-permeable AMPA receptorHippocampus
Publisher
SPRINGER
Indexed
SCI; SCIE; SCOPUS WOS
Document Type
Article
Abstract
We investigated the effects of regular exercise on chronic stress-induced memory consolidation impairment and its underlying mechanism. We focused on prolactin (PRL)-modulated calcium-permeable (CP)-alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors (AMPARs) in neurons in the CA1 stratum lacunosum-moleculare (SLM) area of the dorsal hippocampus. Regular exercise protected against memory retention defects and prevented dendritic retraction in apical distal segments of hippocampal CA1 neurons, as indicated by enhanced dendritic ramification, dendritic length, spine density, and synaptic protein levels following chronic stress. Regular exercise normalized synaptic CP-AMPAR assembly in the hippocampal CA1 SLM area, as evidenced by an enhanced ratio of GluR1 to GluR2 during chronic stress. This alteration in AMPARs was critical to memory retention, whereby memory retention was blunted by local blockage of CP-AMPARs in the SLM of naive and exercised mice. Regular exercise improved PRL responsiveness in the hippocampal CA1 region during chronic stress, which led to increased binding of PRL to its receptor (PRLR) and PRL-dependent enhancement in phosphorylated signal transducer and activator of transcription 5 levels. The improvement in PRL responsiveness contributed to memory retention during chronic stress, as the protective action of exercise on memory persistence during stress was abolished by PRLR knockdown in the hippocampal CA1 area. Finally, in primary hippocampal cultures, repeated treatment with corticosterone led to decreased AMPAR-mediated Ca2+ influx, which was restored by PRL treatment. The above findings suggest a protective role for exercise against chronic stress-evoked defects in memory consolidation via PRL-modulated incorporation of CP-AMPARs into hippocampal CA1 synapses.
DOI
10.1007/s12035-019-1560-z
Appears in Collections:
의과대학 > 의학과 > Journal papers
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