Enriched environment modulates behavior, myelination and augments molecules governing the plasticity in the forebrain region of rats exposed to chronic immobilization stress.
Behavioral plasticity
Corticosterone
Enriched environment
Immobilization stress
Myelin basic protein
Myelination
Neurotrophic growth factor
Journal
Metabolic brain disease
ISSN: 1573-7365
Titre abrégé: Metab Brain Dis
Pays: United States
ID NLM: 8610370
Informations de publication
Date de publication:
06 2019
06 2019
Historique:
received:
15
09
2018
accepted:
11
12
2018
pubmed:
4
1
2019
medline:
12
5
2020
entrez:
4
1
2019
Statut:
ppublish
Résumé
Recently, several reports on chronic stress have shown that prolonged exposure to stress contributes to psychological and neurological complications. However, the impact of stress-induced alterations in myelination remains to be unexplored. Therefore, in the current study, the rats were subjected to immobilization stress (IS) followed by enriched environment (EE) and the behavioral, neurochemical changes pertaining to neuronal survival pathway, in addition, to the ultrastructural changes in myelin in forebrain (FB) region of rats were analyzed. Immobilization stress-exposed rats (4 h/day IS, for 28 days) exhibited increased anhedonia, anxiety, immobility, and reduced social interaction, which could be reflected in increased levels of corticosterone. In contrast, exposure to EE (4 h IS+2 h EE/day, for 28 days) was found to minimize anhedonic state, supress the depressive-like features, enhance social interaction and also reduce the levels of corticosterone. The ultrastructural changes in the FB region of the brain revealed that IS group showed enhanced g-ratio indicating decreased myelin thickness, while EE group exhibited reduced g-ratio manifesting increased myelination. Further, the study revealed that IS exposed group showed decreased levels of NGF, TrkA, PI3K, AKT, ERK, CREB, and MBP in FB regions whereas EE group could preserve normal protein and mRNA levels of these neuronal survival molecules. The results from this study suggest that EE exerts a positive impact by improving myelination in rats exposed to chronic immobilization stress.
Identifiants
pubmed: 30604029
doi: 10.1007/s11011-018-0370-8
pii: 10.1007/s11011-018-0370-8
doi:
Substances chimiques
Corticosterone
W980KJ009P
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
875-887Références
PLoS One. 2013;8(1):e53888
pubmed: 23342033
Cell Mol Life Sci. 2001 Jul;58(8):1054-60
pubmed: 11529498
J Neurosci. 2008 Jul 9;28(28):7174-83
pubmed: 18614687
Arch Gen Psychiatry. 1999 Jun;56(6):527-33
pubmed: 10359467
Anat Rec. 1961 Jun;140:83-90
pubmed: 13989706
Neurotox Res. 2002 Jun;4(4):281-96
pubmed: 12829419
Biochim Biophys Acta. 2007 Aug;1773(8):1161-76
pubmed: 17306385
Nat Neurosci. 2009 Nov;12(11):1370-1
pubmed: 19820707
Eur J Neurosci. 2003 Dec;18(12):3367-74
pubmed: 14686910
PLoS One. 2011;6(6):e20678
pubmed: 21701690
Anat Rec (Hoboken). 2012 Jun;295(6):999-1005
pubmed: 22431229
Neuropsychiatr Dis Treat. 2015 Mar 06;11:597-607
pubmed: 25834438
Front Behav Neurosci. 2014 Mar 07;8:74
pubmed: 24639637
Cell Mol Life Sci. 2016 Feb;73(4):723-35
pubmed: 26514731
Cochrane Database Syst Rev. 2017 Jan 24;1:CD011464
pubmed: 28116752
PLoS One. 2010 Nov 15;5(11):e13993
pubmed: 21085588
Neurosci Lett. 2016 Jun 15;624:34-41
pubmed: 27132084
Integr Comp Biol. 2009 Oct;49(4):423-40
pubmed: 21665831
Science. 2014 Oct 17;346(6207):318-22
pubmed: 25324381
Nat Neurosci. 2008 Dec;11(12):1392-401
pubmed: 18849983
PLoS One. 2009 Nov 13;4(11):e7754
pubmed: 19915661
Nat Neurosci. 2016 Sep;19(9):1210-1217
pubmed: 27455109
J Neurosci. 2013 Dec 11;33(50):19499-503
pubmed: 24336716
Science. 2012 Sep 14;337(6100):1357-60
pubmed: 22984073
Anal Biochem. 1976 May 7;72:248-54
pubmed: 942051
J Neurosci. 2010 Jun 30;30(26):8953-64
pubmed: 20592216
Psychopharmacology (Berl). 2011 Mar;214(2):477-94
pubmed: 21052984
J Neurosci. 2012 Jun 27;32(26):8855-64
pubmed: 22745486
Nat Rev Neurosci. 2015 Dec;16(12):756-67
pubmed: 26585800
J Neurosci Res. 2001 Oct 1;66(1):37-45
pubmed: 11599000
Sci Rep. 2016 Mar 15;6:23084
pubmed: 26976207
Nat Neurosci. 2012 Dec;15(12):1621-3
pubmed: 23143512
Dialogues Clin Neurosci. 2013 Mar;15(1):45-52
pubmed: 23576888
Science. 2014 May 2;344(6183):1252304
pubmed: 24727982
Physiol Behav. 2001 Jun;73(3):313-20
pubmed: 11438356
J Neurosci Res. 2017 Aug;95(8):1602-1610
pubmed: 27862185
Behav Neurosci. 2008 Apr;122(2):282-92
pubmed: 18410168
J Neuroendocrinol. 2004 May;16(5):423-31
pubmed: 15117335
Glia. 2014 Feb;62(2):284-99
pubmed: 24339157
Neurobiol Aging. 2013 Jan;34(1):263-74
pubmed: 22795793
J Neurosci. 2016 Aug 31;36(35):9186-200
pubmed: 27581459
J Vis Exp. 2012 Jan 29;(59):e3638
pubmed: 22314943
FEBS Lett. 1985 Sep 9;189(1):37-41
pubmed: 3839757
Proc Natl Acad Sci U S A. 1989 Nov;86(21):8555-9
pubmed: 2813412
Neurochem Res. 2018 Feb;43(2):407-419
pubmed: 29143164
Curr Biol. 2007 Jan 9;17(1):R29-35
pubmed: 17208176
Front Aging Neurosci. 2017 Jul 26;9:245
pubmed: 28798684
EMBO J. 2000 Oct 16;19(20):5429-39
pubmed: 11032810
J Can Acad Child Adolesc Psychiatry. 2011 Nov;20(4):265-76
pubmed: 22114608
Neuroscience. 2004;128(4):667-73
pubmed: 15464275
Neurosci Biobehav Rev. 2015 Nov;58:79-91
pubmed: 26116544
Neurobiol Stress. 2016 Aug 24;6:78-93
pubmed: 28229111
J Neural Transm (Vienna). 2008;115(1):35-42
pubmed: 18087670
PLoS One. 2017 Sep 25;12(9):e0185061
pubmed: 28945761
J Neurosci. 2002 Aug 1;22(15):6810-8
pubmed: 12151561
Biochemistry (Mosc). 2017 Mar;82(3):291-300
pubmed: 28320270
Eur J Pharmacol. 1978 Feb 15;47(4):379-91
pubmed: 204499
Mol Psychiatry. 2010 Dec;15(12):1152-63
pubmed: 20308988
Ann Neurol. 2010 Nov;68(5):703-16
pubmed: 20853437
Naturwissenschaften. 1984 Jun;71(6):309-15
pubmed: 6472480
J Vis Exp. 2011 Feb 25;(48):
pubmed: 21403628