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Depression and How Antidepressants Work in Your Brain

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Depression – a pathological sadness – affects a large proportion of people. It has many forms:

  • Endogenous depression without any obvious reason
  • Reactive depression as a reaction to unfavourable events
  • Symptomatic depression, which looks like a depression but in fact it is a consequence of e.g. some poisoning, dementia or a tumor
  • Masked or blurred depression, which manifests itself with physical symptoms only – e.g. indigestion, backache, giddiness etc.
  • According to its intensity we distinguish small and major depression; then there is psychotic depression and depression without psychotic symptoms, then dysthymia as a chronic small depression and many other types

Depression can be cured by drugs - antidepressants, psychotherapy and ECT - electroconvulsive therapy which is used very rarely when other deep depression treatment fails. The f irst antidepressant was imipramine and was synthesized in 1956 by Roland Kuhn, a Swiss. Since that time antidepressants have changed a lot. There are more and more preparations available, belonging to one of the antidepressant groups – tricyclic (TCA), bicyclic and tetracyclic (TeCA) antidepressants, selective serotonin reuptake inhibitors SSRI, serotonin-norepinephrine reuptake inhibitors SRNI, monoamine oxidase inhibitors MAOI, Reversible Monoamine Oxidase Inhibitor RIMA and others. Their producers' aim is to eliminate or reduce their side effects. Most antidepressants work upon the neurotransmitters serotonin and/or noradrenalin.

And how, actually, do antidepressants function in your brain?

We must take a  large view but don't worry, it will be as simple as possible.
In our brain there are cells called neurons. The e ntire brain activity works that one neuron gets a signal and passes it to another, that one to another and so on and so forth. That is how our hands move , blinking, digestion, mood and all such things are controlled.

So a nervous signal goes through a neuron and passes on at the end of the neuron's projection – but there is a gap! Neurons are not connected to each other (don't ask me why). So this neuron releases a signal transmitter (neurotransmitter) into the gap. The transmitter's molecules penetrate the other neuron and by this the signal is passed further. The molecules that do not reach the other neuron are either eliminated or recycled. The gap (or precisely "synaptic gap" as all that loose connection of neurons is called "synapse") must be kept in good order.

There are many types of neurotransmitters and their imbalance causes various problems including depression. With depression, there are two most important transmitters: serotonin and noradrenalin.

If there is a lack of serotonin, depression is caused , so drugs are supposed to increase the quantity of serotonin at synapses. Let's take some of the SSRI antidepressants as an example. These drugs increase the quantity of serotonin so, that they block or slow down the process of cleaning the unexpended serotonin out of the synaptic gaps. This function is in these drugs' name, too – Selective Serotonin Reuptake Inhibitors.

If there is a lack of serotonin molecules, not enough of them reach the other neuron (and accordingly this neuron is not activated) and the rest of the molecules are removed too quickly. Thanks to SSRI, serotonin molecules have more time to join to the other neuron.

So, as you can see, no mystery. And so there is no reason to be afraid of antidepressants, because they just boost desirable and natural processes.

And how, actually, do antidepressants function in your brain?

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

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