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Mol Psychiatry. 2014 Apr;19(4):433-43. doi: 10.1038/mp.2014.5. Epub 2014 Feb 18.

Stress and corticosterone increase the readily releasable pool of glutamate vesicles in synaptic terminals of prefrontal and frontal cortex.

Author information

1
Laboratory of Neuropsychopharmacology and Functional Neurogenomics-Dipartimento di Scienze Farmacologiche e Biomolecolari and CEND, Università di Milano, Milano, Italy.
2
Laboratory of Cell Physiology-Dipartimento di Scienze Farmacologiche e Biomolecolari, Università di Milano, Milano, Italy.
3
Department of Pharmacy-Unit of Pharmacology and Toxicology, Center of Excellence for Biomedical Research, Università di Genova, Genova, Italy.
4
1] Stereology and Electron Microscopy Laboratory, Centre for Stochastic Geometry and Advanced Bioimaging, Aarhus University Hospital, Aarhus, Denmark [2] Translational Neuropsychiatry Unit, Department of Clinical Medicine, Aarhus University, Aarhus, Denmark.
5
Neurobiology of Learning Unit, Scientific Institute San Raffaele and Università Vita e Salute San Raffaele, Milano, Italy.
6
Department of Clinical and Molecular Biomedicine, Section of Pharmacology and Biochemistry, Università di Catania, Catania, Italy.
7
1] Laboratory of Neuropsychopharmacology and Functional Neurogenomics-Dipartimento di Scienze Farmacologiche e Biomolecolari and CEND, Università di Milano, Milano, Italy [2] IRCCS San Giovanni di Dio-Fatebenefratelli, Brescia, Italy.
8
Stereology and Electron Microscopy Laboratory, Centre for Stochastic Geometry and Advanced Bioimaging, Aarhus University Hospital, Aarhus, Denmark.
9
1] Translational Neuropsychiatry Unit, Department of Clinical Medicine, Aarhus University, Aarhus, Denmark [2] Centre of Excellence for Pharmaceutical Sciences, North West University, Potchefstroom, South Africa.

Abstract

Stress and glucocorticoids alter glutamatergic transmission, and the outcome of stress may range from plasticity enhancing effects to noxious, maladaptive changes. We have previously demonstrated that acute stress rapidly increases glutamate release in prefrontal and frontal cortex via glucocorticoid receptor and accumulation of presynaptic SNARE complex. Here we compared the ex vivo effects of acute stress on glutamate release with those of in vitro application of corticosterone, to analyze whether acute effect of stress on glutamatergic transmission is mediated by local synaptic action of corticosterone. We found that acute stress increases both the readily releasable pool (RRP) of vesicles and depolarization-evoked glutamate release, while application in vitro of corticosterone rapidly increases the RRP, an effect dependent on synaptic receptors for the hormone, but does not induce glutamate release for up to 20 min. These findings indicate that corticosterone mediates the enhancement of glutamate release induced by acute stress, and the rapid non-genomic action of the hormone is necessary but not sufficient for this effect.

PMID:
24535456
DOI:
10.1038/mp.2014.5
[Indexed for MEDLINE]

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