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Chronic treatment with agomelatine or venlafaxine reduces depolarization-evoked glutamate release from hippocampal synaptosomes

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Chronic treatment with agomelatine or venlafaxine reduces depolarization-evoked glutamate release from hippocampal synaptosomes. / Milanese, Marco; Tardito, Daniela; Musazzi, Laura; Treccani, Giulia; Mallei, Alessandra; Bonifacino, Tiziana; Gabriel, Cecilia; Mocaer, Elisabeth; Racagni, Giorgio; Popoli, Maurizio; Bonanno, Giambattista.

In: B M C Neuroscience, Vol. 14, 2013, p. 75.

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

Harvard

Milanese, M, Tardito, D, Musazzi, L, Treccani, G, Mallei, A, Bonifacino, T, Gabriel, C, Mocaer, E, Racagni, G, Popoli, M & Bonanno, G 2013, 'Chronic treatment with agomelatine or venlafaxine reduces depolarization-evoked glutamate release from hippocampal synaptosomes', B M C Neuroscience, vol. 14, pp. 75. https://doi.org/10.1186/1471-2202-14-75

APA

Milanese, M., Tardito, D., Musazzi, L., Treccani, G., Mallei, A., Bonifacino, T., ... Bonanno, G. (2013). Chronic treatment with agomelatine or venlafaxine reduces depolarization-evoked glutamate release from hippocampal synaptosomes. B M C Neuroscience, 14, 75. https://doi.org/10.1186/1471-2202-14-75

CBE

Milanese M, Tardito D, Musazzi L, Treccani G, Mallei A, Bonifacino T, Gabriel C, Mocaer E, Racagni G, Popoli M, Bonanno G. 2013. Chronic treatment with agomelatine or venlafaxine reduces depolarization-evoked glutamate release from hippocampal synaptosomes. B M C Neuroscience. 14:75. https://doi.org/10.1186/1471-2202-14-75

MLA

Vancouver

Author

Milanese, Marco ; Tardito, Daniela ; Musazzi, Laura ; Treccani, Giulia ; Mallei, Alessandra ; Bonifacino, Tiziana ; Gabriel, Cecilia ; Mocaer, Elisabeth ; Racagni, Giorgio ; Popoli, Maurizio ; Bonanno, Giambattista. / Chronic treatment with agomelatine or venlafaxine reduces depolarization-evoked glutamate release from hippocampal synaptosomes. In: B M C Neuroscience. 2013 ; Vol. 14. pp. 75.

Bibtex

@article{256b972c6eec406d8f95b1ce5f7aad8d,
title = "Chronic treatment with agomelatine or venlafaxine reduces depolarization-evoked glutamate release from hippocampal synaptosomes",
abstract = "BACKGROUND: Growing compelling evidence from clinical and preclinical studies has demonstrated the primary role of alterations of glutamatergic transmission in cortical and limbic areas in the pathophysiology of mood disorders. Chronic antidepressants have been shown to dampen endogenous glutamate release from rat hippocampal synaptic terminals and to prevent the marked increase of glutamate overflow induced by acute behavioral stress in frontal/prefrontal cortex. Agomelatine, a new antidepressant endowed with MT1/MT2 agonist and 5-HT2C serotonergic antagonist properties, has shown efficacy at both preclinical and clinical levels.RESULTS: Chronic treatment with agomelatine, or with the reference drug venlafaxine, induced a marked decrease of depolarization-evoked endogenous glutamate release from purified hippocampal synaptic terminals in superfusion. No changes were observed in GABA release. This effect was accompanied by reduced accumulation of SNARE protein complexes, the key molecular effector of vesicle docking, priming and fusion at presynaptic membranes.CONCLUSIONS: Our data suggest that the novel antidepressant agomelatine share with other classes of antidepressants the ability to modulate glutamatergic transmission in hippocampus. Its action seems to be mediated by molecular mechanisms located on the presynaptic membrane and related with the size of the vesicle pool ready for release.",
keywords = "Acetamides, Analysis of Variance, Animals, Antidepressive Agents, Calcium Ionophores, Cyclohexanols, Glutamic Acid, Hippocampus, Ionomycin, Male, Potassium Chloride, Rats, Rats, Sprague-Dawley, SNARE Proteins, Synaptosomes, Syntaxin 1, Venlafaxine Hydrochloride, gamma-Aminobutyric Acid, Journal Article, Research Support, Non-U.S. Gov't",
author = "Marco Milanese and Daniela Tardito and Laura Musazzi and Giulia Treccani and Alessandra Mallei and Tiziana Bonifacino and Cecilia Gabriel and Elisabeth Mocaer and Giorgio Racagni and Maurizio Popoli and Giambattista Bonanno",
year = "2013",
doi = "10.1186/1471-2202-14-75",
language = "English",
volume = "14",
pages = "75",
journal = "B M C Neuroscience",
issn = "1471-2202",
publisher = "BioMed Central Ltd.",

}

RIS

TY - JOUR

T1 - Chronic treatment with agomelatine or venlafaxine reduces depolarization-evoked glutamate release from hippocampal synaptosomes

AU - Milanese, Marco

AU - Tardito, Daniela

AU - Musazzi, Laura

AU - Treccani, Giulia

AU - Mallei, Alessandra

AU - Bonifacino, Tiziana

AU - Gabriel, Cecilia

AU - Mocaer, Elisabeth

AU - Racagni, Giorgio

AU - Popoli, Maurizio

AU - Bonanno, Giambattista

PY - 2013

Y1 - 2013

N2 - BACKGROUND: Growing compelling evidence from clinical and preclinical studies has demonstrated the primary role of alterations of glutamatergic transmission in cortical and limbic areas in the pathophysiology of mood disorders. Chronic antidepressants have been shown to dampen endogenous glutamate release from rat hippocampal synaptic terminals and to prevent the marked increase of glutamate overflow induced by acute behavioral stress in frontal/prefrontal cortex. Agomelatine, a new antidepressant endowed with MT1/MT2 agonist and 5-HT2C serotonergic antagonist properties, has shown efficacy at both preclinical and clinical levels.RESULTS: Chronic treatment with agomelatine, or with the reference drug venlafaxine, induced a marked decrease of depolarization-evoked endogenous glutamate release from purified hippocampal synaptic terminals in superfusion. No changes were observed in GABA release. This effect was accompanied by reduced accumulation of SNARE protein complexes, the key molecular effector of vesicle docking, priming and fusion at presynaptic membranes.CONCLUSIONS: Our data suggest that the novel antidepressant agomelatine share with other classes of antidepressants the ability to modulate glutamatergic transmission in hippocampus. Its action seems to be mediated by molecular mechanisms located on the presynaptic membrane and related with the size of the vesicle pool ready for release.

AB - BACKGROUND: Growing compelling evidence from clinical and preclinical studies has demonstrated the primary role of alterations of glutamatergic transmission in cortical and limbic areas in the pathophysiology of mood disorders. Chronic antidepressants have been shown to dampen endogenous glutamate release from rat hippocampal synaptic terminals and to prevent the marked increase of glutamate overflow induced by acute behavioral stress in frontal/prefrontal cortex. Agomelatine, a new antidepressant endowed with MT1/MT2 agonist and 5-HT2C serotonergic antagonist properties, has shown efficacy at both preclinical and clinical levels.RESULTS: Chronic treatment with agomelatine, or with the reference drug venlafaxine, induced a marked decrease of depolarization-evoked endogenous glutamate release from purified hippocampal synaptic terminals in superfusion. No changes were observed in GABA release. This effect was accompanied by reduced accumulation of SNARE protein complexes, the key molecular effector of vesicle docking, priming and fusion at presynaptic membranes.CONCLUSIONS: Our data suggest that the novel antidepressant agomelatine share with other classes of antidepressants the ability to modulate glutamatergic transmission in hippocampus. Its action seems to be mediated by molecular mechanisms located on the presynaptic membrane and related with the size of the vesicle pool ready for release.

KW - Acetamides

KW - Analysis of Variance

KW - Animals

KW - Antidepressive Agents

KW - Calcium Ionophores

KW - Cyclohexanols

KW - Glutamic Acid

KW - Hippocampus

KW - Ionomycin

KW - Male

KW - Potassium Chloride

KW - Rats

KW - Rats, Sprague-Dawley

KW - SNARE Proteins

KW - Synaptosomes

KW - Syntaxin 1

KW - Venlafaxine Hydrochloride

KW - gamma-Aminobutyric Acid

KW - Journal Article

KW - Research Support, Non-U.S. Gov't

U2 - 10.1186/1471-2202-14-75

DO - 10.1186/1471-2202-14-75

M3 - Journal article

C2 - 23895555

VL - 14

SP - 75

JO - B M C Neuroscience

JF - B M C Neuroscience

SN - 1471-2202

ER -