FC13-09 - Antidepressant tianeptine (TIA) action is based on the acceleration of serotonin turnover in the synapse: a hypothesis

Узбеков, М. Г.

doi:10.1016/s0924-9338(11)73594-5

Cited by 6 publications

(8 citation statements)

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“…Additionally, chronic tianeptine administration prolonged the climbing time in the modified Porsolt test in adult offspring. The effect of tianeptine may be due to its complex action including the unique properties on the serotoninergic system, by increasing reuptake and accelerate of serotonin turnover in the synapse (Uzbekov 2009 ). Moreover, tianeptine may modulate the glutamatergic and GABAergic systems (McEwen et al 2010 ), which as we previously demonstrated are impaired in prenatally stressed animals (Sowa et al 2015 ).…”

Section: Discussionmentioning

confidence: 99%

The Beneficial Impact of Antidepressant Drugs on Prenatal Stress-Evoked Malfunction of the Insulin-Like Growth Factor-1 (IGF-1) Protein Family in the Olfactory Bulbs of Adult Rats

et al. 2015

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Insulin-like growth factor-1 (IGF-1) promotes the growth, differentiation, and survival of both neurons and glial cells, and it is believed to exert antidepressant-like activity. Thus, disturbances in the IGF-1 system could be responsible for the course of depression. To date, there have been no papers showing the impact of chronic antidepressant treatment on the IGF-1 network in the olfactory bulb (OB) in an animal model of depression. Prenatal stress was used as model of depression. Twenty-four 3-month-old male offspring of control and stressed mothers were subjected to behavioral testing (forced swim test). The mRNA expression of IGF-1 and IGF-1 receptor (IGF-1R) and the protein level of IGF-1 and its phosphorylation, as well as the concentrations of IGF-binding proteins (IGFBP-2, -4, -3, and -6), were measured in OBs before and after chronic imipramine, fluoxetine, or tianeptine administration. Adult rats exposed prenatally to stressful stimuli displayed not only depression-like behavior but also decreased IGF-1 expression, dysregulation in the IGFBP network, and diminished mRNA expression, as well as IGF-1R phosphorylation, in the OB. The administration of antidepressants normalized most of the changes in the IGF-1 system of the OB evoked by prenatal stress. These results suggested a beneficial effect of chronic antidepressant drug treatment in the alleviation of IGF-1 family malfunction in OBs in an animal model of depression.

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Section: Discussionmentioning

confidence: 99%

The Beneficial Impact of Antidepressant Drugs on Prenatal Stress-Evoked Malfunction of the Insulin-Like Growth Factor-1 (IGF-1) Protein Family in the Olfactory Bulbs of Adult Rats

et al. 2015

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“…An unsettled question was whether tianeptine treatment caused hypersecretion of catecholamines in the adrenal medulla, resulting in lethal hypertensive crisis, because tianeptine facilitates fast turnover of serotonin at synaptic cleft (Uzbekov, 2009). However, the results of two previous studies are not in compliance with this presumption.…”

Section: Discussionmentioning

confidence: 99%

Tianeptine interferes with microtubule organization and hormone secretion of pheochromocytoma cells

Makani

Hall

Qamar

et al. 2013

Molecular and Cellular Endocrinology

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Pheochromocytoma originates from chromaffin cells in the adrenal medulla and sympathetic paraganglia. 36–53% of pheochromocytoma becomes malignant and, thereafter, resistant to conventional treatments. Pheochromocytoma also causes hyper-secretion of catecholamines that cause severe hypertension. We found that an antidepressant, tianeptine, interfered with normal life cycle of pheochromocytoma cells at its clinical doses. Treatment with tianeptine caused microtubule bundling and specific degradation of cytoplasmic dynein, a retrograde microtubule motor that mediates various microtubule-dependent processes during interphase and mitosis, in the rat pheochromocytoma PC12 cells. Tianeptine also increased the levels of pro-apoptotic proteins, slowed cell cycle progression, and increased apoptosis in PC12 cells. Importantly, tianeptine treatment decreased high K+-stimulated secretion of norepinephrine and chromogranin A in PC12 cells and of epinephrine in the mouse pheochromocytoma MPC cells. Our study demonstrates, for the first time, that tianeptine interferes with normal life cycle of pheochromocytoma cells.

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“…While venlafaxine is a member of SNRIs (serotonin-noradrenalin reuptake inhibitors), tianeptine is an atypical antidepressant drug. In contrast to tricycle antidepressants and selective serotonin reuptake inhibitors (SSRIs), it has been suggested that tianeptine decreases serotonin's bioactivity and its accumulation in serotonergic synapses of the central nervous system by promoting serotonin reuptake, and normalizing serotonergic neurotransmission [ 35 , 36 ]. Venlafaxine, which has a mechanism of action opposite to that of tianeptine (i.e.…”

Section: Discussionmentioning

confidence: 99%

Effect of venlafaxine on bone loss associated with ligature-induced periodontitis in Wistar rats

Carvalho

Souza

Neves

et al. 2010

J Negat Results BioMed

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BackgroundThe present study investigated the effects of venlafaxine, an antidepressant drug with immunoregulatory properties on the inflammatory response and bone loss associated with experimental periodontal disease (EPD).Materials and MethodsWistar rats were subjected to a ligature placement around the second upper left molar. The treated groups received orally venlafaxine (10 or 50 mg/kg) one hour before the experimental periodontal disease induction and daily for 10 days. Vehicle-treated experimental periodontal disease and a sham-operated (SO) controls were included. Bone loss was analyzed morphometrically and histopathological analysis was based on cell influx, alveolar bone, and cementum integrity. Lipid peroxidation quantification and immunohistochemistry to TNF-α and iNOS were performed.ResultsExperimental periodontal disease rats showed an intense bone loss compared to SO ones (SO = 1.61 ± 1.36; EPD = 4.47 ± 1.98 mm, p < 0.001) and evidenced increased cellular infiltration and immunoreactivity for TNF-α and iNOS. Venlafaxine treatment while at low dose (10 mg/kg) afforded no significant protection against bone loss (3.25 ± 1.26 mm), a high dose (50 mg/kg) caused significantly enhanced bone loss (6.81 ± 3.31 mm, p < 0.05). Venlafaxine effectively decreased the lipid peroxidation but showed no significant change in TNF-α or iNOS immunoreactivity.ConclusionThe increased bone loss associated with high dose venlafaxine may possibly be a result of synaptic inhibition of serotonin uptake.

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FC13-09 - Antidepressant tianeptine (TIA) action is based on the acceleration of serotonin turnover in the synapse: a hypothesis

Cited by 6 publications

References 0 publications

The Beneficial Impact of Antidepressant Drugs on Prenatal Stress-Evoked Malfunction of the Insulin-Like Growth Factor-1 (IGF-1) Protein Family in the Olfactory Bulbs of Adult Rats

The Beneficial Impact of Antidepressant Drugs on Prenatal Stress-Evoked Malfunction of the Insulin-Like Growth Factor-1 (IGF-1) Protein Family in the Olfactory Bulbs of Adult Rats

Tianeptine interferes with microtubule organization and hormone secretion of pheochromocytoma cells

Effect of venlafaxine on bone loss associated with ligature-induced periodontitis in Wistar rats

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