Disarranged neuroplastin environment upon aging and chronic stress recovery in female Sprague Dawley rats

  1. Gaspar, Robert 1
  2. Ivić, Vedrana 2
  3. Canerina‐Amaro, Ana 3
  4. Balog, Marta 2
  5. Pablo, Daniel Pereda 3
  6. Szűcs, Kálmán Ferenc 1
  7. Marin, Raquel 3
  8. Vari, Sandor G. 4
  9. Heffer, Marija 2
  10. Labak, Irena 5
  11. Krajnik, Bartosz 6
  12. Bardak, Ana 2
  13. Blažetić, Senka 5
  1. 1 Department of Pharmacology and Pharmacotherapy Faculty of Medicine Interdisciplinary Excellence Centre University of Szeged Szeged Hungary
  2. 2 Department of Medical Biology and Genetics Faculty of Medicine J. J. Strossmayer University of Osijek Osijek Croatia
  3. 3 Laboratory of Cellular Neurobiology Department of Basic Medical Sciences School of Health SciencesUniversidad de La Laguna La Laguna Spain
  4. 4 Cedars‐Sinai Medical CenterInternational Research and Innovation in Medicine Program Los Angeles CA USA
  5. 5 Department of Biology J. J. Strossmayer University of Osijek Osijek Croatia
  6. 6 Department of Experimental Physics Wroclaw University of Science and Technology Wroclaw Poland
Revue:
European Journal of Neuroscience

ISSN: 0953-816X 1460-9568

Année de publication: 2021

Type: Article

DOI: 10.1111/EJN.15256 GOOGLE SCHOLAR lock_openAccès ouvert editor

D'autres publications dans: European Journal of Neuroscience

Résumé

Chronic stress produces long-term metabolic changes throughout the superfamily ofnuclear receptors, potentially causing various pathologies. Sex hormones modulatethe stress response and generate a sex-specific age-dependent metabolic imprint, especially distinct in the reproductive senescence of females. We monitored chronicstress recovery in two age groups of female Sprague Dawley rats to determinewhether stress and/or aging structurally changed the glycolipid microenvironment,a milieu playing an important role in cognitive functions. Old females experiencedmemory impairment even at basal conditions, which was additionally amplified bystress. On the other hand, the memory of young females was not disrupted. Stressrecovery was followed by a microglial decrease and an increase in astrocyte countin the hippocampal immune system. Since dysfunction of the brain immune systemcould contribute to disturbed synaptogenesis, we analyzed neuroplastin expressionand the lipid environment. Neuroplastin microenvironments were explored by analyzing immunofluorescent stainings using a newly developed Python script method.Stress reorganized glycolipid microenvironment in the Cornu Ammonis 1 (CA1)and dentate gyrus (DG) hippocampal regions of old females but in a very differentfashion, thus affecting neuroplasticity. The postulation of four possible neuroplastin environments pointed to the GD1a ganglioside enrichment during reproductive senescence of stressed females, as well as its high dispersion in both regions and toGD1a and GM1 loss in the CA1 region. A specific lipid environment might influenceneuroplastin functionality and underlie synaptic dysfunction triggered by a combination of aging and chronic stress.

Références bibliographiques

  • 10.1212/WNL.54.3.588
  • Ali S. A., (2018), The Malaysian Journal of Medical Sciences, 25, pp. 31, 10.21315/mjms2018.25.4.3
  • An G. H., (2020), BioMed Research International, 2020, pp. 4701563
  • Balog M., (2015), Croatian Medical Journal, 56, pp. 104, 10.3325/cmj.2015.56.104
  • 10.1016/j.celrep.2018.04.021
  • 10.1111/jnc.12816
  • Belarbi K., (2020), Molecular Neurodegeneration, 15, pp. 59, 10.1186/s13024-020-00408-1
  • 10.1016/j.biopsych.2016.03.2107
  • Blennow K., (1991), Archives of Neurology, 48, pp. 1032, 10.1001/archneur.1991.00530220048018
  • 10.1038/s41586-018-0543-y
  • 10.1016/j.expneurol.2003.12.010
  • 10.1073/pnas.0507313103
  • 10.3390/ijms21030868
  • 10.1037/0735-7044.113.5.902
  • 10.1016/j.physbeh.2016.11.017
  • 10.1530/REP-16-0117
  • 10.1016/j.neurobiolaging.2018.02.022
  • 10.1097/JGP.0b013e31825c0a14
  • 10.1097/GME.0000000000000579
  • 10.1016/j.bbalip.2004.10.002
  • Hou Q., (2008), Molecular and Cellular Neurosciences, 38, pp. 213, 10.1016/j.mcn.2008.02.010
  • Hung C. W., (2010), Ageing Research Reviews, 9, pp. S36, 10.1016/j.arr.2010.08.006
  • Ilic K., (2019), Frontiers in Cell and Developmental Biology, 7, pp. 27, 10.3389/fcell.2019.00027
  • 10.1111/j.1460-9568.1997.tb01427.x
  • 10.1093/brain/awg089
  • 10.1523/JNEUROSCI.2588-13.2013
  • 10.1038/nrn849
  • 10.18097/PBMC20166201093
  • 10.1046/j.1471-4159.2003.01770.x
  • 10.1196/annals.1329.035
  • 10.1590/S0100-879X2012007500044
  • 10.1016/0006-8993(94)91778-7
  • 10.1016/j.neubiorev.2020.05.010
  • 10.3389/fnins.2018.00128
  • 10.1002/cne.10719
  • 10.3390/ijms20153810
  • 10.1093/glycob/cws057
  • 10.1111/j.1471-4159.2011.07269.x
  • 10.3389/fnmol.2019.00258
  • 10.1073/pnas.2004259117
  • Prendergast J., (2014), The Journal of Neuroscience, 34, pp. 13246, 10.1523/JNEUROSCI.1149-14.2014
  • 10.1016/j.brainresbull.2009.07.012
  • 10.1096/fj.03-1378fje
  • 10.1038/nrn1555
  • 10.1038/nmeth.2019
  • 10.1152/physrev.00033.2013
  • 10.1038/35036052
  • 10.1073/pnas.080389297
  • 10.1007/978-1-4419-7877-6_14
  • 10.1007/s11357-010-9145-9
  • 10.1016/S0079-6123(08)61965-2
  • 10.1016/0005-2760(89)90175-6
  • 10.1371/journal.pone.0075720
  • 10.2174/13894501113149990208
  • Wang Y., (2011), Endocrinology, 152, pp. 2704, 10.1210/en.2011-0145
  • 10.3389/fncel.2018.00424
  • 10.1186/s13041-018-0381-8
  • 10.3389/fnagi.2017.00430
  • 10.1038/s41593-019-0372-9
  • 10.3233/JAD-170879