Jens Randel Nyengaard

Imipramine treatment increases the number of hippocampal synapses and neurons in a genetic animal model of depression

Research output: Contribution to journal/Conference contribution in journal/Contribution to newspaperJournal articleResearchpeer-review

Standard

Imipramine treatment increases the number of hippocampal synapses and neurons in a genetic animal model of depression. / Chen, Fenghua; Madsen, Torsten M; Wegener, Gregers et al.

In: The Hippocampus, Vol. 20, No. 12, 20.12.2010, p. 1376-84.

Research output: Contribution to journal/Conference contribution in journal/Contribution to newspaperJournal articleResearchpeer-review

Harvard

APA

CBE

MLA

Vancouver

Author

Bibtex

@article{a6c5d430d8d511de9e3b000ea68e967b,
title = "Imipramine treatment increases the number of hippocampal synapses and neurons in a genetic animal model of depression",
abstract = "The aim was to investigate treatment effects of the antidepressant imipramine on the markers of neuronal plasticity. We investigated changes in neuron and synapse numbers in a rat strain that displays a genetic susceptibility to depressive behavior, the Flinders Sensitive and Resistant Lines (FSL/FRL). All rats were treated with imipramine (15 mg/kg) or saline (i.p) once daily for 25 days. The volume, neuron and synapse numbers in the hippocampus were estimated using design-based stereological methods. Under untreated conditions, the volume and the number of neurons and synapses were significantly smaller in the FSL saline group (untreated {"}depressed{"} rats) compared with the FRL saline group (normal rats), showing correlation to the observed decreased immobility in the forced swim test. Imipramine treatment significantly increased the number of neurons in the granule cell layer (GCL) and spine synapses in the CA1 in the FSL imipramine group (treated {"}depressed{"} rats) compared with the FSL saline group. The neuron numbers in the GCL and Hilus showed no differences in the FSL imipramine group compared to the FRL saline group. In conclusion, baseline levels of the volume and the number of neurons and spine synapses in hippocampus were significantly smaller in the untreated FSL rats. Our findings indicate that chronic imipramine treatment reverses the suppression of neurogenesis and synaptogenesis in the hippocampus of the {"}depressed{"} FSL rats, and this occurs in correlation with behavioral effects. Our results support the neuronal plasticity hypothesis that depressive disorders may be related to impairments of structural plasticity and neuronal viability in hippocampus, furthermore, antidepressant treatment counteracts the structural impairments. (c) 2009 Wiley-Liss, Inc.",
author = "Fenghua Chen and Madsen, {Torsten M} and Gregers Wegener and Nyengaard, {Jens R}",
year = "2010",
month = dec,
day = "20",
doi = "10.1002/hipo.20718",
language = "English",
volume = "20",
pages = "1376--84",
journal = "The Hippocampus",
issn = "1050-9631",
publisher = "JohnWiley & Sons, Inc.",
number = "12",

}

RIS

TY - JOUR

T1 - Imipramine treatment increases the number of hippocampal synapses and neurons in a genetic animal model of depression

AU - Chen, Fenghua

AU - Madsen, Torsten M

AU - Wegener, Gregers

AU - Nyengaard, Jens R

PY - 2010/12/20

Y1 - 2010/12/20

N2 - The aim was to investigate treatment effects of the antidepressant imipramine on the markers of neuronal plasticity. We investigated changes in neuron and synapse numbers in a rat strain that displays a genetic susceptibility to depressive behavior, the Flinders Sensitive and Resistant Lines (FSL/FRL). All rats were treated with imipramine (15 mg/kg) or saline (i.p) once daily for 25 days. The volume, neuron and synapse numbers in the hippocampus were estimated using design-based stereological methods. Under untreated conditions, the volume and the number of neurons and synapses were significantly smaller in the FSL saline group (untreated "depressed" rats) compared with the FRL saline group (normal rats), showing correlation to the observed decreased immobility in the forced swim test. Imipramine treatment significantly increased the number of neurons in the granule cell layer (GCL) and spine synapses in the CA1 in the FSL imipramine group (treated "depressed" rats) compared with the FSL saline group. The neuron numbers in the GCL and Hilus showed no differences in the FSL imipramine group compared to the FRL saline group. In conclusion, baseline levels of the volume and the number of neurons and spine synapses in hippocampus were significantly smaller in the untreated FSL rats. Our findings indicate that chronic imipramine treatment reverses the suppression of neurogenesis and synaptogenesis in the hippocampus of the "depressed" FSL rats, and this occurs in correlation with behavioral effects. Our results support the neuronal plasticity hypothesis that depressive disorders may be related to impairments of structural plasticity and neuronal viability in hippocampus, furthermore, antidepressant treatment counteracts the structural impairments. (c) 2009 Wiley-Liss, Inc.

AB - The aim was to investigate treatment effects of the antidepressant imipramine on the markers of neuronal plasticity. We investigated changes in neuron and synapse numbers in a rat strain that displays a genetic susceptibility to depressive behavior, the Flinders Sensitive and Resistant Lines (FSL/FRL). All rats were treated with imipramine (15 mg/kg) or saline (i.p) once daily for 25 days. The volume, neuron and synapse numbers in the hippocampus were estimated using design-based stereological methods. Under untreated conditions, the volume and the number of neurons and synapses were significantly smaller in the FSL saline group (untreated "depressed" rats) compared with the FRL saline group (normal rats), showing correlation to the observed decreased immobility in the forced swim test. Imipramine treatment significantly increased the number of neurons in the granule cell layer (GCL) and spine synapses in the CA1 in the FSL imipramine group (treated "depressed" rats) compared with the FSL saline group. The neuron numbers in the GCL and Hilus showed no differences in the FSL imipramine group compared to the FRL saline group. In conclusion, baseline levels of the volume and the number of neurons and spine synapses in hippocampus were significantly smaller in the untreated FSL rats. Our findings indicate that chronic imipramine treatment reverses the suppression of neurogenesis and synaptogenesis in the hippocampus of the "depressed" FSL rats, and this occurs in correlation with behavioral effects. Our results support the neuronal plasticity hypothesis that depressive disorders may be related to impairments of structural plasticity and neuronal viability in hippocampus, furthermore, antidepressant treatment counteracts the structural impairments. (c) 2009 Wiley-Liss, Inc.

U2 - 10.1002/hipo.20718

DO - 10.1002/hipo.20718

M3 - Journal article

C2 - 19921703

VL - 20

SP - 1376

EP - 1384

JO - The Hippocampus

JF - The Hippocampus

SN - 1050-9631

IS - 12

ER -