Proteomic investigation of the ventral rat hippocampus links DRP-2 to escitalopram treatment resistance and SNAP to stress resilience in the chronic mild stress model of depression.

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Proteomic investigation of the ventral rat hippocampus links DRP-2 to escitalopram treatment resistance and SNAP to stress resilience in the chronic mild stress model of depression. / Bisgaard, Christina; Jayatissa, Magdalena N; Enghild, Jan J et al.

In: Journal of Molecular Neuroscience, Vol. 32, No. 2, 2007, p. 132-44.

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@article{7ee24be0cff111dcabe4000ea68e967b,
title = "Proteomic investigation of the ventral rat hippocampus links DRP-2 to escitalopram treatment resistance and SNAP to stress resilience in the chronic mild stress model of depression.",
abstract = "The development of depression as well as recovery from depression is most likely accompanied by a change in protein expression profiles. The purpose of the present study was to quantitatively investigate global protein expression differences independent of any hypothesis describing depression etiology and recovery. Thus two-dimensional differential in-gel electrophoresis was employed to compare the ventral hippocampal proteomes between different treatment groups in the chronic mild stress (CMS) model of depression. The CMS paradigm induces anhedonic behaviour, which is a major symptom of depression, by exposing rats to a series of mild stressors for 7 weeks, with antidepressant treatment during the last 4 weeks. In the CMS model, animals were split into six different groups at the end of treatment; unchallenged control escitalopram (n = 12), unchallenged control vehicle (n = 12), CMS vehicle (n = 12), CMS escitalopram responders (n = 11), CMS escitalopram non-responders (n = 13) and CMS resilient (stress resistant) (n = 12). Protein levels in the ventral rat hippocampus were compared between the groups to provide putative markers of anhedonia, escitalopram resistance, and stress resilience. Twenty-eight candidate protein spots were selected, of which 13 were successfully identified using tandem mass spectrometry. DRP-2 (dihydropyrimidinase-related protein-2) was a potential marker for escitalopram resistance, whereas alpha-SNAP and beta-SNAP were associated with stress resilience. Furthermore, several molecular chaperones and cytoskeleton organisers were identified as being differentially expressed. Our data indicate that neuronal adaptation is an essential element of depression etiology and recovery, suggesting the involvement of cellular plasticity in the underlying molecular mechanism. Udgivelsesdato: 2007-null",
keywords = "Animal Feed, Animals, Citalopram, Cytoskeletal Proteins, Depression, Disease Models, Animal, Drug Resistance, Feeding Behavior, Hippocampus, Male, Membrane Proteins, Muscle Proteins, Nerve Tissue Proteins, Nitric Oxide Donors, Proteome, Rats, Rats, Wistar, S-Nitroso-N-Acetylpenicillamine, Serotonin Uptake Inhibitors, Stress, Psychological, Sucrose",
author = "Christina Bisgaard and Jayatissa, {Magdalena N} and Enghild, {Jan J} and Connie Sanch{\'e}z and Roman Artemychyn and Ove Wiborg",
year = "2007",
language = "English",
volume = "32",
pages = "132--44",
journal = "Journal of Molecular Neuroscience",
issn = "0895-8696",
publisher = "Humana Press, Inc.",
number = "2",

}

RIS

TY - JOUR

T1 - Proteomic investigation of the ventral rat hippocampus links DRP-2 to escitalopram treatment resistance and SNAP to stress resilience in the chronic mild stress model of depression.

AU - Bisgaard, Christina

AU - Jayatissa, Magdalena N

AU - Enghild, Jan J

AU - Sanchéz, Connie

AU - Artemychyn, Roman

AU - Wiborg, Ove

PY - 2007

Y1 - 2007

N2 - The development of depression as well as recovery from depression is most likely accompanied by a change in protein expression profiles. The purpose of the present study was to quantitatively investigate global protein expression differences independent of any hypothesis describing depression etiology and recovery. Thus two-dimensional differential in-gel electrophoresis was employed to compare the ventral hippocampal proteomes between different treatment groups in the chronic mild stress (CMS) model of depression. The CMS paradigm induces anhedonic behaviour, which is a major symptom of depression, by exposing rats to a series of mild stressors for 7 weeks, with antidepressant treatment during the last 4 weeks. In the CMS model, animals were split into six different groups at the end of treatment; unchallenged control escitalopram (n = 12), unchallenged control vehicle (n = 12), CMS vehicle (n = 12), CMS escitalopram responders (n = 11), CMS escitalopram non-responders (n = 13) and CMS resilient (stress resistant) (n = 12). Protein levels in the ventral rat hippocampus were compared between the groups to provide putative markers of anhedonia, escitalopram resistance, and stress resilience. Twenty-eight candidate protein spots were selected, of which 13 were successfully identified using tandem mass spectrometry. DRP-2 (dihydropyrimidinase-related protein-2) was a potential marker for escitalopram resistance, whereas alpha-SNAP and beta-SNAP were associated with stress resilience. Furthermore, several molecular chaperones and cytoskeleton organisers were identified as being differentially expressed. Our data indicate that neuronal adaptation is an essential element of depression etiology and recovery, suggesting the involvement of cellular plasticity in the underlying molecular mechanism. Udgivelsesdato: 2007-null

AB - The development of depression as well as recovery from depression is most likely accompanied by a change in protein expression profiles. The purpose of the present study was to quantitatively investigate global protein expression differences independent of any hypothesis describing depression etiology and recovery. Thus two-dimensional differential in-gel electrophoresis was employed to compare the ventral hippocampal proteomes between different treatment groups in the chronic mild stress (CMS) model of depression. The CMS paradigm induces anhedonic behaviour, which is a major symptom of depression, by exposing rats to a series of mild stressors for 7 weeks, with antidepressant treatment during the last 4 weeks. In the CMS model, animals were split into six different groups at the end of treatment; unchallenged control escitalopram (n = 12), unchallenged control vehicle (n = 12), CMS vehicle (n = 12), CMS escitalopram responders (n = 11), CMS escitalopram non-responders (n = 13) and CMS resilient (stress resistant) (n = 12). Protein levels in the ventral rat hippocampus were compared between the groups to provide putative markers of anhedonia, escitalopram resistance, and stress resilience. Twenty-eight candidate protein spots were selected, of which 13 were successfully identified using tandem mass spectrometry. DRP-2 (dihydropyrimidinase-related protein-2) was a potential marker for escitalopram resistance, whereas alpha-SNAP and beta-SNAP were associated with stress resilience. Furthermore, several molecular chaperones and cytoskeleton organisers were identified as being differentially expressed. Our data indicate that neuronal adaptation is an essential element of depression etiology and recovery, suggesting the involvement of cellular plasticity in the underlying molecular mechanism. Udgivelsesdato: 2007-null

KW - Animal Feed

KW - Animals

KW - Citalopram

KW - Cytoskeletal Proteins

KW - Depression

KW - Disease Models, Animal

KW - Drug Resistance

KW - Feeding Behavior

KW - Hippocampus

KW - Male

KW - Membrane Proteins

KW - Muscle Proteins

KW - Nerve Tissue Proteins

KW - Nitric Oxide Donors

KW - Proteome

KW - Rats

KW - Rats, Wistar

KW - S-Nitroso-N-Acetylpenicillamine

KW - Serotonin Uptake Inhibitors

KW - Stress, Psychological

KW - Sucrose

M3 - Journal article

C2 - 17873297

VL - 32

SP - 132

EP - 144

JO - Journal of Molecular Neuroscience

JF - Journal of Molecular Neuroscience

SN - 0895-8696

IS - 2

ER -