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.

Stress and corticosterone increase the readily releasable pool of glutamate vesicles in synaptic terminals of prefrontal and frontal cortex / G. Treccani, L. Musazzi, C. Perego, M. Milanese, N. Nava, T. Bonifacino, J. Lamanna, A. Malgaroli, F. Drago, G. Racagni, J.R. Nyengaard, G. Wegener, G. Bonanno, M. Popoli. - In: MOLECULAR PSYCHIATRY. - ISSN 1359-4184. - 19:4(2014 Apr), pp. 433-443. [10.1038/mp.2014.5]

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

G. Treccani
Primo
;
L. Musazzi
Secondo
;
C. Perego;G. Racagni;M. Popoli
Ultimo
2014-04

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.
Corticosterone; Glutamate release; Mood disorders; Presynaptic mechanisms; Stress
Settore BIO/14 - Farmacologia
Settore BIO/13 - Biologia Applicata
THE ACTION OF STRESS AND PSYCHIATRIC DRUGS ON GLUTAMATE RELEASE IN CORTICAL AREAS: RELEVANCE FOR STRESS-RELATED NEUROPSYCHIATRIC DISORDERS
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Utilizza questo identificativo per citare o creare un link a questo documento: http://hdl.handle.net/2434/235501
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