Tianeptine: Challenging Antidepressant Model

 

L-tryptophan is an essential amino acid that is utilised in the brain to create serotonin. It has been stated that those who consume more L-tryptophan in their diet are less likely to commit suicide than those who do not consume much of the amino acid. SSRIs, which are the most common treatment for depression, work by binding to the serotonin transporter, thus preventing the reuptake of serotonin into the presynaptic nerve cells. This process results in more serotonin being available for use in the nerve synapse. Popular examples of SSRIs include fluoxetine (Prozac) and sertraline (Zoloft).

 

Working as a selective serotonin reuptake enhancer (SSRE), Tianeptine acts in the opposite fashion. Rather than preventing the reuptake of serotonin, Tianeptine actually aids this process in the hippocampus and the cortex. Since this process also appears to help to treat depression, Tianeptine has further complicated the understanding that having a deficit of serotonin is the cause of depression.

 

Precisely how Tianeptine works to increase the speed of serotonin reuptake remains unclear, particularly as the drug does not appear to act noticeably at the sites of neurotransmitter receptors or monoamine transporters. It has been presumed that the effect of Tianeptine is dependent upon the changes in neurons and the relationships between them that take place in the longer term – over the period of a few weeks. This theory does however remain conjecture.

 

Tianeptine’s not like other antidepressants: Truly Unique Properties

 

In the summer of 2014, a study revealed that tianeptine operates as a complete agonist at the delta and mu opioid receptors, whilst having no significant impact at the kappa receptors. It is understood that selective kappa agonists usually cause dysphoria and conversely, selective mu agonists in certain parts of the brain (known as hedonic hotspots) usually cause euphoria. The effect of delta opioid receptors however, is not yet known. Opioids that have been widely used for the treatment of psychiatric conditions in the past are known for their addictive properties as well as their effects as mood-improvers. The action of Tianeptine on mu, and to a lesser extent delta opioid, receptors may however offer the key to a drug that brightens the mood without the side effect of dependence.

 

Tianeptine’s action – Challenging the classic Antidepressant model


L-tryptophan
 is an essential amino acid that is utilised in the brain to create serotonin. It has been stated that those who consume more L-tryptophan in their diet are less likely to commit suicide than those who do not consume much of the amino acid. SSRIs, which are the most common treatment for depression, work by binding to the serotonin transporter, thus preventing the reuptake of serotonin into the presynaptic nerve cells. This process results in more serotonin being available for use in the nerve synapse. Popular examples of SSRIs include fluoxetine (Prozac) and sertraline (Zoloft).

 

Working as a selective serotonin reuptake enhancer (SSRE), Tianeptine acts in the opposite fashion. Rather than preventing the reuptake of serotonin, Tianeptine actually aids this process in the hippocampus and the cortex. Since this process also appears to help to treat depression, Tianeptine has further complicated the understanding that having a deficit of serotonin is the cause of depression.

 

Precisely how Tianeptine works to increase the speed of serotonin reuptake remains unclear, particularly as the drug does not appear to act noticeably at the sites of neurotransmitter receptors or monoamine transporters. It has been presumed that the effect of Tianeptine is dependent upon the changes in neurons and the relationships between them that take place in the longer term – over the period of a few weeks. This theory does however remain conjecture.

 

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