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Research Article | Open Access

Effects of chronic stress on nectin1 levels in the mouse primary somatosensory cortex

Department of Neurobiology and Department of Psychiatryof Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, Hangzhou 310058, China
NHC and CAMS Key Laboratory of Medical Neurobiology, MOE Frontier Science Center for Brain Research and Brain-Machine Integration, School of Brain Science and Brain Medicine, Zhejiang University, Hangzhou 310058, China
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Abstract

Chronic exposure to stressful experiences impairs synaptic plasticity. Previous studies have shown that the spine densities of pyramidal neurons, the turnover of mushroom-type spines, and the excitatory–inhibitory balance in the primary somatosensory cortex (S1) are modulated by stress. Trans-synaptic cell adhesion molecules (CAMs) are implicated in stress-induced synaptic deficits. However, it remains unknown whether stress dysregulates CAMs in S1 and thereby impairs synaptic plasticity. In this study, we applied the early-life stress (ELS), chronic social defeat stress (CSDS), and chronic restraint stress paradigms and measured the mRNA levels of nectin1 in S1 of wild-type and conditional forebrain corticotropin-releasing hormone receptor 1 type (CRHR1) conditional knockout mice. We found that ELS increased nectin1 mRNA levels in S1 in adult but not adolescent mice. Moreover, CSDS increased the nectin1 mRNA levels in S1 in adult mice via the CRH-CRHR1 system. Our findings suggest that S1 is vulnerable to repeated stress exposures at some life stages, and dysregulated nectin1 expression may underlie stress-induced structural and functional abnormalities in S1.

Keywords

stressnectin1primary somatosensory cortexcorticotropin-releasing hormone

References

[1]

Krishnan, V., Han, M. H., Graham, D. L., Berton, O., Renthal, W., Russo, S. J., Laplant, Q., Graham, A., Lutter, M., Lagace, D. C. et al. Molecular adaptations underlying susceptibility and resistance to social defeat in brain reward regions. Cell, 2007, 131(2): 391–404.
Crossref Google Scholar
[2]

Chen, Y., Rex, C. S., Rice, C. J., Dubé, C. M., Gall, C. M., Lynch, G., Baram, T. Z. Correlated memory defects and hippocampal dendritic spine loss after acute stress involve corticotropin-releasing hormone signaling. Proceedings of the National Academy of Sciences USA, 2010, 107(29): 13123–13128.
Crossref Google Scholar
[3]

Ma, M., Chang, X., Wu, H. Animal models of stress and stress-related neurocircuits: A comprehensive review. Stress and Brain, 2021, 1(2): 108–127.
Crossref Google Scholar
[4]

Christoffel, D. J., Golden, S. A., Russo, S. J. Structural and synaptic plasticity in stress-related disorders. Reviews in the Neurosciences, 2011, 22(5): 535–549.
Crossref Google Scholar
[5]

Cruz-Martín, A., Crespo, M., Portera-Cailliau, C. Delayed stabilization of dendritic spines in fragile X mice. The Journal of Neuroscience, 2010, 30(23): 7793–7803.
Crossref Google Scholar
[6]

Hayashi-Takagi, A., Tataki, M., Graziane, N., Seshadri, S., Murdoch, H., Dunlop, A. J., Makino, Y., Seshadri, A. J., Ishizuka, K., Srivastava, D. P. et al. Disrupted-in-Schizophrenia 1 (DISC1) regulates spines of the glutamate synapse via Rac1. Nature Neuroscience, 2010, 13(3): 327–323.
Crossref Google Scholar
[7]

Penzes, P., Woolfrey, K. M., Srivastava, D. P. Epac2-mediated dendritic spine remodeling: Implications for disease. Molecular and Cellular Neurosciences, 2011, 46(2): 368–380.
Crossref Google Scholar
[8]

Akram, A., Christoffel, D., Rocher, A. B., Bouras, C., Kövari, E., Perl, D. P., Morrison, J. H., Herrmann, F. R., Haroutunian, V., Giannakopoulos, P. et al. Stereologic estimates of total spinophilin-immunoreactive spine number in area 9 and the CA1 field: Relationship with the progression of Alzheimer's disease. Neurobiology of Aging, 2008, 29(9): 1296–1307.
Crossref Google Scholar
[9]

Dumitriu, D., Hao, J., Hara, Y., Kaufmann, J., Janssen, W. G., Lou, W., Rapp, P. R., Morrison, J. H. Selective changes in thin spine density and morphology in monkey prefrontal cortex correlate with aging-related cognitive impairment. The Journal of Neuroscience, 2010, 30(22): 7507–7515.
Crossref Google Scholar
[10]

McEwen, B. S. Stress and hippocampal plasticity. Annual Review of Neuroscience, 1999, 22: 105–122.
Crossref Google Scholar
[11]

McEwen, B. S., Morrison, J. H. The brain on stress: Vulnerability and plasticity of the prefrontal cortex over the life course. Neuron, 2013, 79(1): 16–29.
Crossref Google Scholar
[12]

Radley, J. J., Sisti, H. M., Hao, J., Rocher, A. B., McCall, T., McEwen B. S., Morrison, J. H. Chronic behavioral stress induces apical dendritic reorganization in pyramidal neurons of the medial prefrontal cortex. Neuroscience, 2004, 125(1): 1–6.
Crossref Google Scholar
[13]

Akirav, I., Maroun, M. The role of the medial prefrontal cortex-amygdala circuit in stress effects on the extinction of fear. Neural Plasticity, 2007, 2007: 30873.
Crossref Google Scholar
[14]

Tottenham, N., Galván, A. Stress and the adolescent brain: Amygdala-prefrontal cortex circuitry and ventral striatum as developmental targets. Neuroscience and Biobehavioral Reviews, 2016, 70: 217–227.
Crossref Google Scholar
[15]

López, J. F., Akil, H., Watson, S. J. Neural circuits mediating stress. Biological Psychiatry, 1999, 46(11): 1461–1471.
Crossref Google Scholar
[16]

Chen, C. C., Lu, J., Yang, R., Ding, J. B., Zuo, Y. Selective activation of parvalbumin interneurons prevents stress-induced synapse loss and perceptual defects. Molecular Psychiatry, 2018, 23(7): 1614–1625.
Crossref Google Scholar
[17]

Chen, K., Zhang, L., Tan, M., Lai, C. S., Li, A., Ren, C., So, K. F. Treadmill exercise suppressed stress-induced dendritic spine elimination in mouse barrel cortex and improved working memory via BDNF/TrkB pathway. Translational Psychiatry, 2017, 7(3): e1069.
Crossref Google Scholar
[18]

Wang, C., Liu, H., Li, K., Wu, Z. Z., Wu, C., Yu, J. Y., Gong, Q., Fang, P., Wang, X. X., Duan, S. M. et al. Tactile modulation of memory and anxiety requires dentate granule cells along the dorsoventral axis. Nature Communications, 2020, 11(1): 6045.
Crossref Google Scholar
[19]

Dalva, M. B., McClelland, A. C., Kayser, M. S. Cell adhesion molecules: signalling functions at the synapse. Nature Review Neuroscience, 2007, 8(3): 206–220.
Crossref Google Scholar
[20]

Gong, Q., Su, Y. A., Wu, C., Si, T. M., Deussing, J. M., Schmidt, M. V., Wang, X. D. Chronic stress reduces nectin-1 mRNA levels and disrupts dendritic spine plasticity in the adult mouse perirhinal cortex. Frontiers in Cellular Neuroscience, 2018, 12: 67.
Crossref Google Scholar
[21]

Takai, Y., Ikeda, W., Ogita, H., Rikitake, Y. The immunoglobulin-like cell adhesion molecule nectin and its associated protein afadin. Annual Review of Cell and Developmental Biology, 2008, 24: 309–342.
Crossref Google Scholar
[22]

van der Kooij, M. A., Fantin, M., Rejmak, E., Grosse, J., Zanoletti, O., Fournier, C., Ganguly, K., Kalita, K., Kaczmarek, L., Sandi, C. Role for MMP-9 in stress-induced downregulation of nectin-3 in hippocampal CA1 and associated behavioural alterations. Nature Communications, 2014, 5: 4995.
Crossref Google Scholar
[23]

Wang, X. D., Chen, Y., Wolf, M., Wagner, K. V., Liebl, C., Scharf, S. H., Harbich, D., Mayer, B., Wurst, W., Holsboer, F. et al. Forebrain CRHR1 deficiency attenuates chronic stress-induced cognitive deficits and dendritic remodeling. Neurobiology of Disease, 2011, 42(3): 300–310.
Crossref Google Scholar
[24]

Liao, X. M., Yang, X. D., Jia, J., Li, J. T., Xie, X. M., Su, Y. A., Schmidt, M. V., Si, T. M., Wang, X. D. Blockade of corticotropin-releasing hormone receptor 1 attenuates early-life stress-induced synaptic abnormalities in the neonatal hippocampus. Hippocampus, 2014, 24(5): 528–540.
Crossref Google Scholar
[25]

Müller, M. B., Zimmermann, S., Sillaber, I., Hagemeyer, T. P., Deussing, J. M., Timpl, P., Kormann, M. S., Droste, S. K., Kühn, R., Reul, J. M. et al. Limbic corticotropin-releasing hormone receptor 1 mediates anxiety-related behavior and hormonal adaptation to stress. Nature Neuroscience, 2003, 6(10): 1100–1107.
Crossref Google Scholar
[26]

Lu, A., Steiner, M. A., Whittle, N., Vogl, A. M., Walser, S. M., Ableitner, M., Refojo, D., Ekker, M., Rubenstein, J. L., Stalla, G. K. et al. Conditional mouse mutants highlight mechanisms of corticotropin-releasing hormone effects on stress-coping behavior. Molecular Psychiatry, 2008, 13(11): 1028–1042.
Crossref Google Scholar
[27]

Wang, X. D., Su, Y. A., Avrabos, C., Wagner, K. V., Liebl, C., Wolf, M., Scharf, S. H., Hartmann, J., Wurst, W., Holsboer, F. et al. Nectin-3 links CRHR1 signaling to stress-induced memory deficits and spine loss. Nature Neuroscience, 2013, 16: 706–713.
Crossref Google Scholar
[28]

Rice, C. J., Sandman, C. A., Lenjavi, M. R., Baram, T. Z. A novel mouse model for acute and long-lasting consequences of early life stress. Endocrinology, 2008, 149(10): 4892–4900.
Crossref Google Scholar
[29]

Wang, X. D., Rammes, G., Igor, K., Wolf, M., Liebl, C., Scharf, S. H., Rice, C. J., Wurst, W., Holsboer, F., Deussing, J. M. et al. Forebrain CRF1 modulates early-life stress-programmed cognitive deficits. The Journal of Neuroscience, 2011, 31(38): 13625–13634.
Crossref Google Scholar
[30]

Wagner, K. V., Hartmann, J., Labermaier, C., Häusl, A. S., Zhao, G., Harbich, D., Schmid, B., Wang, X. D., Santarelli, S., Kohl, C. et al. Homer1/mGluR5 activity moderates vulnerability to chronic social stress. Neuropsychopharmacology, 2015, 40(5): 1222–1233.
Crossref Google Scholar
[31]

Schmidt, M. V., Sterlemann, V., Ganea, K., Liebl, C., Alam, S., Harbich, D., Greetfeld, M., Uhr, M., Holsboer, F., Müller, M. B. Persistent neuroendocrine and behavioral effects of a novel, etiologically relevant mouse paradigm for chronic social stress during adolescence. Psychoneuroendocrinology, 2007, 32(5): 417–429.
Crossref Google Scholar
[32]

Maurin, H., Seymour, C. M., Lechat, B., Borghgraef, P., Devijver, H., Jaworski, T., Schmidt, M. V., Kuegler, S., Van Leuven, F. Tauopathy differentially affects cell adhesion molecules in mouse brain: Early down-regulation of nectin-3 in stratum lacunosum moleculare. PLoS One, 2013, 8(5): e63589.
Crossref Google Scholar
[33]

Schmidt, M. V., Oitzl, M. S., Levine, S., de Kloet, E. R. The HPA system during the postnatal development of CD1 mice and the effects of maternal deprivation. Developmental Brain Research, 2002, 139(1): 39–49.
Crossref Google Scholar
[34]

Lupien, S. J., McEwen, B. S., Gunnar, M. R., Heim, C. Effects of stress throughout the lifespan on the brain, behaviour and cognition. Nature Reviews Neuroscience, 2009, 10(6): 434–445.
Crossref Google Scholar
[35]

McEwen, B. S. Protective and damaging effects of stress mediators: Central role of the brain. Dialogues in Clinical Neuroscience, 2006, 8(4): 367–381.
Crossref Google Scholar
[36]

Wang, C., Liu, H., Li, K., Wu, Z. Z., Wu, C., Yu, J. Y., Gong, Q., Fang, P., Wang, X. X., Duan, S. M. et al. Tactile modulation of memory and anxiety requires dentate granule cells along the dorsoventral axis. Nature Communications, 2020, 11(1): 6045.
Crossref Google Scholar
[37]

Bock, J., Gruss, M., Becker, S., Braun, K. Experience-induced changes of dendritic spine densities in the prefrontal and sensory cortex: Correlation with developmental time windows. Cerebral Cortex, 2004, 15(6): 802–808.
Crossref Google Scholar
[38]

Takatsuru, Y., Yoshitomo, M., Nemoto, T., Eto, K., Nabekura, J. Maternal separation decreases the stability of mushroom spines in adult mice somatosensory cortex. Brain Research, 2009, 1294: 45–51.
Crossref Google Scholar
[39]

Chen, C. C., Lu, J., Yang, R., Ding, J. B., Zuo, Y. Selective activation of parvalbumin interneurons prevents stress-induced synapse loss and perceptual defects. Molecular Psychiatry, 2018, 23(7): 1614–1625.
Crossref Google Scholar
[40]

Sandi, C. Stress, cognitive impairment and cell adhesion molecules. Nature Reviews Neuroscience, 2004, 5(12): 917–930.
Crossref Google Scholar
[41]

Chen, Y., Andres, A. L., Frotscher, M., Baram, T. Z. Tuning synaptic transmission in the hippocampus by stress: The CRH system. Frontiers in Cellular Neuroscience, 2012, 6: 13.
Crossref Google Scholar
[42]

Maras, P. M., Baram, T. Z. Sculpting the hippocampus from within: Stress, spines, and CRH. Trends in Neurosciences, 2012, 35(5): 315–324.
Crossref Google Scholar
[43]

de Kloet, E. R., Vreugdenhil, E., Oitzl, M. S., Joëls, M. Brain corticosteroid receptor balance in health and disease. Endocrine Reviews, 1998, 19(3): 269–301.
Crossref Google Scholar
[44]

Meijer, O. C., Koorneef, L. L., Kroon, J. Glucocorticoid receptor modulators. Annales d'Endocrinologie, 2018, 79(3): 107–111.
Crossref Google Scholar
[45]

Van Looveren, K., Van Boxelaere, M., Callaerts-Vegh, Z., Libert, C. Cognitive dysfunction in mice lacking proper glucocorticoid receptor dimerization. PLoS One, 2019, 14(12): e0226753.
Crossref Google Scholar
[46]

Bale, T. L., Picetti, R., Contarino, A., Koob, G. F., Vale, W. W., Lee, K. F. Mice deficient for both corticotropin-releasing factor receptor 1 (CRFR1) and CRFR2 have an impaired stress response and display sexually dichotomous anxiety-like behavior. The Journal of Neuroscience, 2002, 22(1): 193–199.
Crossref Google Scholar
Stress and Brain
Volume 2 Issue 3,
September 2022
Pages 100-110
DOI: 10.26599/SAB.2022.9060013
Cite this article:
Xu X, Wang X-D. Effects of chronic stress on nectin1 levels in the mouse primary somatosensory cortex. Stress and Brain, 2022, 2(3): 100-110. https://doi.org/10.26599/SAB.2022.9060013

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Received: 30 March 2022
Revised: 30 July 2022
Accepted: 02 September 2022
Published: 22 September 2022
© The Author(s) 2022

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