Jens Randel Nyengaard

Chronic desipramine prevents acute stress-induced reorganization of medial prefrontal cortex architecture by blocking glutamate vesicle accumulation and excitatory synapse increase

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Chronic desipramine prevents acute stress-induced reorganization of medial prefrontal cortex architecture by blocking glutamate vesicle accumulation and excitatory synapse increase. / Nava, Nicoletta; Treccani, Giulia; Liebenberg, Nico; Chen, Fenghua; Popoli, Maurizio; Wegener, Gregers; Nyengaard, Jens Randel.

In: International Journal of Neuropsychopharmacology, 13.12.2014.

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

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@article{2c7945a1ee8b4a658cb15aa197f40fa9,
title = "Chronic desipramine prevents acute stress-induced reorganization of medial prefrontal cortex architecture by blocking glutamate vesicle accumulation and excitatory synapse increase",
abstract = "While a clear negative influence of chronic exposure to stressful experiences has been repeatedly demonstrated, the outcome of acute stress on key brain regions has only just started to be elucidated. Although it has been proposed that acute stress may produce enhancement of brain plasticity and that antidepressants may prevent such changes, we still lack ultrastructural evidence that acute stress-induced changes in neurotransmitter physiology are coupled with structural synaptic modifications. Rats were pretreated chronically (14 days) with desipramine (DMI; 10 mg/kg) and then subjected to acute foot-shock (FS)-stress. By means of serial section electron microscopy, the structural remodeling of medial prefrontal cortex (mPFC) glutamate synapses was assessed soon after acute stressor cessation and stress hormone levels were measured. FS-stress induced a remarkable increase in the number of docked vesicles and small excitatory synapses, partially and strongly prevented by DMI pretreatment, respectively. Acute stress-induced corticosterone elevation was not affected by drug treatment. Since DMI pretreatment prevented the stress-induced structural plasticity but not the hormone level increase, we hypothesize that the preventing action of DMI is located on pathways downstream of this process and/or other pathways. Moreover, because enhancement of glutamate system remodeling may contribute to overexcitation dysfunctions, this aspect could represent a crucial component in the pathophysiology of stress-related disorders.",
author = "Nicoletta Nava and Giulia Treccani and Nico Liebenberg and Fenghua Chen and Maurizio Popoli and Gregers Wegener and Nyengaard, {Jens Randel}",
note = "{\textcopyright} The Author 2014. Published by Oxford University Press on behalf of CINP.",
year = "2014",
month = dec,
day = "13",
doi = "10.1093/ijnp/pyu085",
language = "English",
journal = "International Journal of Neuropsychopharmacology",
issn = "1461-1457",
publisher = "Oxford University Press",

}

RIS

TY - JOUR

T1 - Chronic desipramine prevents acute stress-induced reorganization of medial prefrontal cortex architecture by blocking glutamate vesicle accumulation and excitatory synapse increase

AU - Nava, Nicoletta

AU - Treccani, Giulia

AU - Liebenberg, Nico

AU - Chen, Fenghua

AU - Popoli, Maurizio

AU - Wegener, Gregers

AU - Nyengaard, Jens Randel

N1 - © The Author 2014. Published by Oxford University Press on behalf of CINP.

PY - 2014/12/13

Y1 - 2014/12/13

N2 - While a clear negative influence of chronic exposure to stressful experiences has been repeatedly demonstrated, the outcome of acute stress on key brain regions has only just started to be elucidated. Although it has been proposed that acute stress may produce enhancement of brain plasticity and that antidepressants may prevent such changes, we still lack ultrastructural evidence that acute stress-induced changes in neurotransmitter physiology are coupled with structural synaptic modifications. Rats were pretreated chronically (14 days) with desipramine (DMI; 10 mg/kg) and then subjected to acute foot-shock (FS)-stress. By means of serial section electron microscopy, the structural remodeling of medial prefrontal cortex (mPFC) glutamate synapses was assessed soon after acute stressor cessation and stress hormone levels were measured. FS-stress induced a remarkable increase in the number of docked vesicles and small excitatory synapses, partially and strongly prevented by DMI pretreatment, respectively. Acute stress-induced corticosterone elevation was not affected by drug treatment. Since DMI pretreatment prevented the stress-induced structural plasticity but not the hormone level increase, we hypothesize that the preventing action of DMI is located on pathways downstream of this process and/or other pathways. Moreover, because enhancement of glutamate system remodeling may contribute to overexcitation dysfunctions, this aspect could represent a crucial component in the pathophysiology of stress-related disorders.

AB - While a clear negative influence of chronic exposure to stressful experiences has been repeatedly demonstrated, the outcome of acute stress on key brain regions has only just started to be elucidated. Although it has been proposed that acute stress may produce enhancement of brain plasticity and that antidepressants may prevent such changes, we still lack ultrastructural evidence that acute stress-induced changes in neurotransmitter physiology are coupled with structural synaptic modifications. Rats were pretreated chronically (14 days) with desipramine (DMI; 10 mg/kg) and then subjected to acute foot-shock (FS)-stress. By means of serial section electron microscopy, the structural remodeling of medial prefrontal cortex (mPFC) glutamate synapses was assessed soon after acute stressor cessation and stress hormone levels were measured. FS-stress induced a remarkable increase in the number of docked vesicles and small excitatory synapses, partially and strongly prevented by DMI pretreatment, respectively. Acute stress-induced corticosterone elevation was not affected by drug treatment. Since DMI pretreatment prevented the stress-induced structural plasticity but not the hormone level increase, we hypothesize that the preventing action of DMI is located on pathways downstream of this process and/or other pathways. Moreover, because enhancement of glutamate system remodeling may contribute to overexcitation dysfunctions, this aspect could represent a crucial component in the pathophysiology of stress-related disorders.

U2 - 10.1093/ijnp/pyu085

DO - 10.1093/ijnp/pyu085

M3 - Journal article

C2 - 25522419

JO - International Journal of Neuropsychopharmacology

JF - International Journal of Neuropsychopharmacology

SN - 1461-1457

ER -