Structural Plasticity and Molecular Markers in Hippocampus of Male Rats after Acute Stress

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Structural Plasticity and Molecular Markers in Hippocampus of Male Rats after Acute Stress. / Chen, Fenghua; Polsinelli, Benedetta; Nava, Nicoletta; Treccani, Giulia; Elfving, Betina; Müller, Heidi K.; Musazzi, Laura; Popoli, Maurizio; Nyengaard, Jens R.; Wegener, Gregers.

I: Neuroscience, Bind 438, 07.2020, s. 100-115.

Publikation: Bidrag til tidsskrift/Konferencebidrag i tidsskrift /Bidrag til avisTidsskriftartikelForskningpeer review

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@article{5e193ebdd5444577925128bf6c98dc01,
title = "Structural Plasticity and Molecular Markers in Hippocampus of Male Rats after Acute Stress",
abstract = "Stress plays a crucial role in the pathogenesis of psychiatric disorders and affects neuronal plasticity in different brain regions. We have previously found that acute foot-shock (FS) stress elicits fast and long-lasting functional and morphological remodeling of excitatory neurons in the prefrontal cortex (PFC), which were partly prevented by the pretreatment with antidepressants. Here we investigated, whether acute stress and pretreatment with desipramine (DMI) interfere in hippocampal dendritic remodeling. Male Sprague-Dawley rats were subjected to acute FS-stress, followed by measurement of time-dependent (1, 7 and 14 days) structural plasticity (dendritic arborization, spine number and morphology) in hippocampal CA1 pyramidal neurons and expression patterns of molecular markers implicated in neuronal plasticity. We found that acute stress significantly decreased spine number, dendritic length, and altered spine morphometric parameters at all time points evaluated after stress. This was paralleled by changes in the gene expression of Spinophilin and Cdc42, and protein expression of homer1. Pretreatment with DMI prevented the stress-induced dendritic atrophy and spine loss 14 days after acute FS. However, DMI treatment without stress differentially affected the expression patterns of spine-related genes and proteins. In conclusion, acute FS-stress and pretreatment with DMI significantly changed dendritic morphology, including number and morphology of spines, and the length of dendrites in hippocampal CA1 pyramidal cells as early as 1 day, and sustained up to 14 days after acute FS. The findings were paralleled by changes in gene and protein expression of actin binding and cytoskeletal proteins, Rho GTPases, and postsynaptic scaffolding proteins.",
keywords = "acute stress, antidepressant, dendrite, foot-shock, Golgi staining, spine",
author = "Fenghua Chen and Benedetta Polsinelli and Nicoletta Nava and Giulia Treccani and Betina Elfving and M{\"u}ller, {Heidi K.} and Laura Musazzi and Maurizio Popoli and Nyengaard, {Jens R.} and Gregers Wegener",
year = "2020",
month = jul,
doi = "10.1016/j.neuroscience.2020.05.001",
language = "English",
volume = "438",
pages = "100--115",
journal = "Neuroscience",
issn = "0306-4522",
publisher = "Pergamon Press",

}

RIS

TY - JOUR

T1 - Structural Plasticity and Molecular Markers in Hippocampus of Male Rats after Acute Stress

AU - Chen, Fenghua

AU - Polsinelli, Benedetta

AU - Nava, Nicoletta

AU - Treccani, Giulia

AU - Elfving, Betina

AU - Müller, Heidi K.

AU - Musazzi, Laura

AU - Popoli, Maurizio

AU - Nyengaard, Jens R.

AU - Wegener, Gregers

PY - 2020/7

Y1 - 2020/7

N2 - Stress plays a crucial role in the pathogenesis of psychiatric disorders and affects neuronal plasticity in different brain regions. We have previously found that acute foot-shock (FS) stress elicits fast and long-lasting functional and morphological remodeling of excitatory neurons in the prefrontal cortex (PFC), which were partly prevented by the pretreatment with antidepressants. Here we investigated, whether acute stress and pretreatment with desipramine (DMI) interfere in hippocampal dendritic remodeling. Male Sprague-Dawley rats were subjected to acute FS-stress, followed by measurement of time-dependent (1, 7 and 14 days) structural plasticity (dendritic arborization, spine number and morphology) in hippocampal CA1 pyramidal neurons and expression patterns of molecular markers implicated in neuronal plasticity. We found that acute stress significantly decreased spine number, dendritic length, and altered spine morphometric parameters at all time points evaluated after stress. This was paralleled by changes in the gene expression of Spinophilin and Cdc42, and protein expression of homer1. Pretreatment with DMI prevented the stress-induced dendritic atrophy and spine loss 14 days after acute FS. However, DMI treatment without stress differentially affected the expression patterns of spine-related genes and proteins. In conclusion, acute FS-stress and pretreatment with DMI significantly changed dendritic morphology, including number and morphology of spines, and the length of dendrites in hippocampal CA1 pyramidal cells as early as 1 day, and sustained up to 14 days after acute FS. The findings were paralleled by changes in gene and protein expression of actin binding and cytoskeletal proteins, Rho GTPases, and postsynaptic scaffolding proteins.

AB - Stress plays a crucial role in the pathogenesis of psychiatric disorders and affects neuronal plasticity in different brain regions. We have previously found that acute foot-shock (FS) stress elicits fast and long-lasting functional and morphological remodeling of excitatory neurons in the prefrontal cortex (PFC), which were partly prevented by the pretreatment with antidepressants. Here we investigated, whether acute stress and pretreatment with desipramine (DMI) interfere in hippocampal dendritic remodeling. Male Sprague-Dawley rats were subjected to acute FS-stress, followed by measurement of time-dependent (1, 7 and 14 days) structural plasticity (dendritic arborization, spine number and morphology) in hippocampal CA1 pyramidal neurons and expression patterns of molecular markers implicated in neuronal plasticity. We found that acute stress significantly decreased spine number, dendritic length, and altered spine morphometric parameters at all time points evaluated after stress. This was paralleled by changes in the gene expression of Spinophilin and Cdc42, and protein expression of homer1. Pretreatment with DMI prevented the stress-induced dendritic atrophy and spine loss 14 days after acute FS. However, DMI treatment without stress differentially affected the expression patterns of spine-related genes and proteins. In conclusion, acute FS-stress and pretreatment with DMI significantly changed dendritic morphology, including number and morphology of spines, and the length of dendrites in hippocampal CA1 pyramidal cells as early as 1 day, and sustained up to 14 days after acute FS. The findings were paralleled by changes in gene and protein expression of actin binding and cytoskeletal proteins, Rho GTPases, and postsynaptic scaffolding proteins.

KW - acute stress

KW - antidepressant

KW - dendrite

KW - foot-shock

KW - Golgi staining

KW - spine

UR - http://www.scopus.com/inward/record.url?scp=85084972931&partnerID=8YFLogxK

U2 - 10.1016/j.neuroscience.2020.05.001

DO - 10.1016/j.neuroscience.2020.05.001

M3 - Journal article

C2 - 32407976

AN - SCOPUS:85084972931

VL - 438

SP - 100

EP - 115

JO - Neuroscience

JF - Neuroscience

SN - 0306-4522

ER -