The principle of drug treatment for depression is based on the assumption that this disease is caused by a lack of serotonin. In addition, norepinephrine should at least be responsible for the (motor) lack of drive.
Antidepressants make use of this knowledge by increasing the concentration of both messenger substances in the synaptic gap.
For very interested laypeople:
This is the space between two synapses that must be overcome by these messenger substances in order to be able to transmit a signal. If the so-called presynapse is excited by a signal, it releases neurotransmitters into the synaptic gap. These then overcome the route by diffusion to the next synapse, the so-called postsynapse. The transmitters bind to the receptors on the surface. As a result, the postsynapse is now also excited and can then pass the signal on.
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A Increased concentration can on three ways respectively:
1. Inhibition of the neuronal monoamine transporter:
These transporters normally ensure that noradrenaline / serotonin is taken back up from the synaptic gap into the presynapse, so that the transmitted signal ends.
The following antidepressants inhibit this process: tricyclic antidepressants, selective serotonin reuptake inhibitors, norepinephrine and serotonin reuptake inhibitors.
2. Increase in release from the presynapse:
The release of the specific transmitter is usually limited by the activation of so-called autoreceptors on your neurons. Antidepressants that inhibit these receptors thus achieve an increased release and consequently also an increased concentration in the synaptic gap:? 2-adrenoceptor antagonists
3. Inhibition of monoamine oxidase A:
The enzyme monoamine oxidase A normally builds "our" Neurotransmitters after transmission in the synaptic gap again. By inhibiting it, less serotonin and noradrenaline are broken down and more are absorbed into the presynaptic stores. The now “overfilled” memories release a larger number of transmitters as a result.
The following antidepressants have this effect: MAOIs
However, it is important for therapy to know that the concentrations of neurotransmitters change immediately after the start of therapy and so too possible adverse effects almost immediately deploy.
The desired antidepressant effect sets against it only after 1-3 weeks a.
The drug inhibition of the transporter is responsible for this. Because of the permanently increased concentration of neurotransmitters in the synaptic gap, the synapse reacts with a reduced release of these.
An antidepressant effect can therefore not occur at this point in time. At a long-standing inhibition then it comes to one Down-regulation (desensitization) of the autoreceptorswho are responsible for limiting the release from the presynapse. This gradually leads to a slow increase in the release.
As a result, the patient must be aware of this or the attending physician must point out that this "Adaptive changes" a certain time need.
Because often it comes to premature discontinuation of therapy, as the patient complains about side effects early on and the desired effect is supposed to be absent. It is also worth knowing that antidepressants are not addictive and that the side effects caused by the development of tolerance are often only temporary.
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In the course of therapy With Antidepressants many patients report one continuously decreasing effect of the respective preparation.
This is often due to the fact that, in addition to having a direct, rapid effect (e.g. increasing the concentration of the transmitters in the synaptic gap), many active ingredients also lead to various adaptation processes in the brain in the long term.
Patients usually report a waning antidepressant effect after several weeks or a few months, as the direct and rapid effect is increasingly waning. There are various options how this development can be counteracted. However, these should be discussed and discussed with the treating doctor in any case. A premature and abrupt discontinuation of a drug can to significant side effects to lead.
Read more about the topic here: Side effects of antidepressants
In principle, there are three options available if the effect declines: For many drugs (including SSRIs), the therapy begins in low doses and can be increased continuously over time. In addition, there are many different antidepressant drug groups that also have different approaches to action. Depending on the patient, a preparation can work differently. For this reason, a change of antidepressant may be indicated. Finally, in certain forms of depression, accompanying psychotherapy can lead to a significantly improved therapeutic success.
To transmit signals, a nerve cell releases various neurotransmitters into the synaptic gap, which bind to receptors in another nerve cell and transmit the signal. The remaining neurotransmitters are then broken down and taken back into the nerve cells via transporters. A deficiency of the transmitters serotonin and norepinephrine is suspected for the development of depression. By increasing these transmitter concentrations in the central nervous system, antidepressants increase drive and reduce anxiety.
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Read more on this topic: The role of serotonin / neurotransmitters in depression
The various antidepressants use different approaches and can be classified accordingly. In principle, a distinction is made between three different approaches: inhibiting the resumption of transmitters, inhibiting the degradation of a transmitter and influencing the release of transmitters by inhibiting receptors on nerve cells.
Find out more about the topic here: Antidepressant medication
The exact mechanism of action of lithium salts is not yet known. But should they be in important transport systems intervene, which should ultimately lead to a weakened signal transmission in certain receptors. This is also the case with the autoreceptors at the synapse, which regulate the release of serotonin into the synaptic gap. If these are inhibited, more is released. The production of serotonin should also be increased.
In the treatment of depression, lithium can be given in addition to an antidepressant if this alone has no effect (so-called. Lithium augmentation).
Find out more about the topic here: lithium
When combining different antidepressants with the Pill there may be some interactions. One of the reasons for this is that both the pill and numerous antidepressants are metabolized by the liver. Due to the heavy load on the liver from the antidepressants, the effective levels of the pill can be influenced in rare cases and the hormone levels deviate significantly. Conversely, an already existing depression can also be aggravated by the changed hormone levels.$config[ads_text1] not found
Often it happens to Interactions with an antidepressant use of Johannis herbs and taking the pill at the same time. A strong weakening of the effect up to a loss of effectiveness is possible. For this reason, during a Therapy with St. John's wort refrains from taking the pill or another preparation may be used.
The other antidepressants used (tricyclic antidepressants, SSRIs, MAO inhibitors, etc.) show, according to study results, no relevant effects on the effectiveness of the pill. Still it should Combination always agreed with the attending physician become.
As studies have shown, treating healthy people with antidepressants has increased too no effect on the mood of those affected. Very few patients have reported a slight euphoria and drive feeling within the first few days. However, the mechanism of action has not been clarified. It is therefore not possible to use it to permanently lighten the mood.
At the same time, however, it can be to some extent significant side effects come during treatment with common antidepressants. This is because the preparations not only work in the central nervous system but also in many other organs of the human body. Depending on the drug, the typical side effects were like sleep disorders, one restricted libido (sexual desire) as well Nausea, diarrhea and a headache reported.
Read more about the topic here: Side effects of antidepressants