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Effect of triiodothyronine (T3) augmentation of acute milnacipran administration on monoamine levels: an in vivo microdialysis study in rats

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Title: Effect of triiodothyronine (T3) augmentation of acute milnacipran administration on monoamine levels: an in vivo microdialysis study in rats
Authors: Kitaichi, Yuji Browse this author
Inoue, Takeshi Browse this author →KAKEN DB
Nakagawa, Shin Browse this author →KAKEN DB
Boku, Shuken Browse this author →KAKEN DB
Kato, Akiko Browse this author
Kusumi, Ichiro Browse this author →KAKEN DB
Koyama, Tsukasa Browse this author →KAKEN DB
Keywords: depression
in vivo microdialysis
Issue Date: Oct-2012
Publisher: Dove Medical Press
Journal Title: Neuropsychiatric Disease and Treatment
Volume: 2012
Issue: 8
Start Page: 501
End Page: 507
Publisher DOI: 10.2147/NDT.S36906
Abstract: Background: Up to 30% of depressed patients are partially or totally resistant to antidepressant therapy. The administration of triiodothyronine (T3) to antidepressant nonresponders can be an effective augmentation strategy, although the mechanism is not fully understood. Methods: In vivo microdialysis was used to examine the effect of T3 augmentation of the antidepressant, milnacipran. Basal extracellular serotonin, norepinephrine, and dopamine levels were measured before and after acute milnacipran administration in the medial prefrontal cortex and amygdala of rats which had received subchronic (7 days) T3 treatment or control saline. Results: Subchronic administration of T3 at 0.1 mg/kg significantly increased basal extracellular levels of serotonin in the medial prefrontal cortex, but not in the amygdala. In contrast, subchronic administration of T3 at 0.2 mg/kg did not alter basal extracellular serotonin levels in the medial prefrontal cortex. Basal extracellular levels of norepinephrine and dopamine were not modified by either dose of T3 in either region. Acute administration of milnacipran, a serotonin-norepinephrine reuptake inhibitor, to control animals resulted in a significant increase of extracellular levels of serotonin, norepinephrine, and dopamine. When administered to animals treated subchronically with T3 at 0.1 mg/kg, milnacipran produced an additional increase in extracellular serotonin levels but not in levels of norepinephrine or dopamine in the medial prefrontal cortex of rats. Conclusion: These results suggest that the mechanism of the augmentation effect of milnacipran by T3 administration occurs via enhancement of serotonergic neurotransmission, but not through noradrenergic or dopaminergic neurotransmission.
Type: article
Appears in Collections:医学院・医学研究院 (Graduate School of Medicine / Faculty of Medicine) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

Submitter: 井上 猛

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