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Clues Revealed by Ketamine
Published in Scott Mendelson, Herbal Treatment of Major Depression, 2019
The active form of the thyroid hormone, triiodothyronine, is often successful as an augmentation when antidepressants are ineffective.30 Among its effects on neurons in the brain are decreases in GSK-3β, increases in BDNF,31 and activation of mTOR.32 Lamotrigine can also be effective when added to an antidepressant in patients with treatment-resistant MDD.33 Lamotrigine increases BDNF, decreases activity of GSK-3β,34 and increases activity of mTOR.35 Tianeptine, an antidepressant that enhances serotonin reuptake, also induces many of the same neuronal changes as the SSRIs. Both tianeptine and fluoxetine inhibit activation of GSK-3β in cortical neurons of prenatally stressed mice.36 Both fluoxetine37 and tianeptine38 increase the activity of mTOR. Finally, both fluoxetine and tianeptine reverse stress and inflammation-induced decreases in neuronal BDNF.39
Intracellular Signaling Transduction Dysregulation in Depression and Possible Future Targets for Antidepressant Therapy:Beyond the Serotonin Hypothesis
Published in Siegfried Kasper, Johan A. den Boer, J. M. Ad Sitsen, Handbook of Depression and Anxiety, 2003
Andrea Trentani, S. Kuipers, G.J. Ter Horst
Tianeptine is a novel antidepressant agent, both structurally (modified tricyclic) and in terms of its pharmacodynamic profile. Unlike other antidepressant agents, tianeptine stimulates the uptake of serotonin [132]. In patients with major depression without melancholia or psychotic features or with depressed bipolar disorder or dysthymic disorder, the antidepressant efficacy of short-term (4 weeks to 3 months) tianeptine therapy appears to be similar to that of amitriptyline, imipramine, and fluoxetine [28,133]. The hippocampus, most likely, is an important target for tianeptine’s therapeutic action. The human hippocampus undergoes atrophy in the aftermath of traumatic stress, recurrent depression, and Cushing’s syndrome [79,134–136]. Prolonged psychological stress in monkeys is associated with loss of hippocampal neurons [137], whereas repeated psychological stress in primitive primates and in rats causes hippocampal CA3 pyramidal neurons to undergo dendritic atrophy [138,139]. The atrophy is only seen in the apical dendritic tree and comprises a reduction in length and branching and must involve alterations in the apical dendritic cytoskeleton [140]. Three factors play a role in hippocampal damage. These include glucocorticoid hormones, which potentiate damage produced by other insults, endogenous excitatory amino acids, and serotonin [141,142]. Serotonin is released by stressors and plays a role in the actions of stress on nerve cells. It appears that stressors activate the release of excitatory amino acids from mossy fiber synapses and promote serotonin release and adrenal steroid secretion that concur to enhance the effect of stressful events in the hippocampus. Interestingly, tianeptine treatment prevents stress-induced atrophy of CA3 pyramidal neurons, whereas neither fluoxetine nor desipramine has such effects. Tianeptine treatment also prevents the stress-induced learning impairment. The molecular mechanisms by which tianeptine prevents stress-mediated dendritic atrophy is not yet fully understood, however [29].
When an obscurity becomes trend: social-media descriptions of tianeptine use and associated atypical drug use
Published in The American Journal of Drug and Alcohol Abuse, 2021
Kirsten E. Smith, Jeffery M. Rogers, Justin C. Strickland, David H. Epstein
Because tianeptine was so often co-used with kratom, phenibut, and racetams, we examined mentions of positive, adverse, and withdrawal effects in the context of co-use (Figure 3). People who used kratom were more likely to report positive effects from tianeptine, OR = 2.72[1.27,5.82], p = .01, but also more likely to report withdrawal symptoms, OR = 5.48[2.16,13.94], p < .001. Racetam use was also associated with a greater odds of positive effects from tianeptine, OR = 3.74[1.53,9.13], p = .004, but not with withdrawal symptoms, OR = 0.68[0.15,3.09], p = .62. Phenibut use was associated with neither. None of the three co-used drugs showed a statistically significant relationship with odds of non-withdrawal adverse effects of tianeptine.
Characteristics of tianeptine effects reported to a poison control center: a growing threat to public health
Published in Clinical Toxicology, 2021
William Rushton, Brian Whitworth, Julie Brown, Michael Kurz, Jessica Rivera
Tianeptine toxicity in the United States remains unfamiliar to most practitioners. A 2017 poison center review describes nine cases of tianeptine toxicity. Two of the nine cases exhibited symptoms of acute tianeptine toxicity and both required intensive care unit (ICU) admission following naloxone administration. Five cases were notable for withdrawal syndromes with agitation being the most common symptom; of these, four patients required the use of benzodiazepines for management [7]. Another scientific abstract identified 13 cases of tianeptine toxicity over a 10-year study period in North Carolina; almost all of the cases were chronic ingestions and presentation involved a combination of tachycardia, agitation, anxiety, and hypertension. In this report, lorazepam was the most commonly utilized agent for stabilization [8].
Poison control center experience with tianeptine: an unregulated pharmaceutical product with potential for abuse
Published in Clinical Toxicology, 2018
Jeanna M. Marraffa, Christine M. Stork, Robert S. Hoffman, Mark K. Su
There were nine reported cases of tianeptine exposure during the examined time period. No discrepancies in data extraction were noted. The first tianeptine exposure was reported in 2009, with the remainder of the cases occurring in 2015 or later (n = 8). Seven of the nine patients were male. Mean age was 27 years. There was one unintentional pediatric exposure. Three of the nine patients reported using tianeptine as a treatment for anxiety or depression. Five of the nine cases reported intentional abuse of tianeptine. Five of the nine cases complained of symptoms after discontinuing tianeptine. Three of the nine cases documented the dose of tianeptine: the unintentional pediatric exposure reported a dose of 12.5 mg; the other two cases reported abuse of 5 and 10 g daily. Discontinuation symptoms reported among the five withdrawal cases included anxiety, agitation, vomiting, diaphoresis, piloerection, lacrimation, and yawning. Two of the nine cases were originally believed to be opioid overdoses and were administered naloxone for central nervous system depression and/or respiratory depression. In one case, naloxone administration improved the mental status and respiratory drive. In the other case, no effect was observed after naloxone administration. None of the cases had seizures or electrocardiogram changes. Five of the nine cases were admitted to the hospital, and three of these cases were admitted to an intensive care unit. Outcomes reported in Toxicall® were minor in two cases, moderate in five cases, major in one case, and not reported in one case. Cases are summarized in Table 1.