Acute stress rapidly increases the readily releasable pool of glutamate vesicles in prefrontal and frontal cortex through non-genomic action of corticosterone

• Published in: Molecular psychiatry Vol. 19; no. 4; p. 401
• Main Authors: Treccani, G, Musazzi, L, Perego, C, Milanese, M, Nava, N, Bonifacino, T, Lamanna, J, Malgaroli, A, Drago, F, Racagni, G, Nyengaard, J R, Wegener, G, Bonanno, G, Popoli, M
• Format: Journal Article
• Language: English
• Published: London Nature Publishing Group UK 01.04.2014; Nature Publishing Group
• Subjects: 631/378/1689/1831; 631/378/548/2590; 631/443/319/367; Animals; Behavioral Sciences; Biological Psychology; Cortex (frontal); Corticosterone; Corticosterone - metabolism; Corticosterone - pharmacology; Frontal Lobe - pathology; Frontal lobes; Glutamate; Glutamic Acid - metabolism; In Vitro Techniques; Medicine; Medicine & Public Health; Neurosciences; Pharmacotherapy; Physiological aspects; Prefrontal cortex; Presynaptic Terminals - drug effects; Presynaptic Terminals - metabolism; Properties; Psychiatry; Stress, Psychological - metabolism; Stress, Psychological - pathology; United Kingdom
• ISSN: 1359-4184; 1476-5578
• DOI: 10.1038/mp.2014.20

Stress and its mediators were shown to cause short- and long-lasting functional/structural changes in the brain, which may trigger neuropsychatric disorders. In this regard, changes in glutamate release/transmission were shown to play a primary role in the stress response (Popoli et al., 2012). We have previously found that Footshock (FS)-stress induces a marked increase of serum corticosterone (CORT) and of depolarization-dependent glutamate release from synaptosomes of prefrontal/frontal cortex (PC/FC), via activation of glucocorticoid receptor (GR) and SNARE complexes accumulation in synaptic membranes. The increase of glutamate release was prevented by chronic antidepressants (Musazzi et al., 2010). Main aim of the present work was to verify if the changes induced by stress on glutamate neurotransmission were mediated by a synaptic (non-genomic) effect of corticosterone (CORT), comparing the effects of acute stress in vivo with that of in vitro application of CORT on purified synaptosomes.