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Blocked up passageways

Antidepressant drugs work as roadblocks for brain chemicals.

The way in which antidepressants exert their effects on brain cells has been revealed by two separate teams of researchers working independently of each other.

Read more here.

Posted by Oliver Morton on August 9, 2007 07:00 PM |

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To know how antidepressants are blocking the reuptake proteins could help to develop more potent agents for to do just that: the re-uptake, which does not mean exactly to have a more effective antidepressants. Escitalopram or its precursor citalopram, which are among the most potent and selective agents that block SERT (serotonin reuptake protein), but that doesn’t mean that they are above the rest of antidepressants. In fact as Danish University Antidepressant Group, have shown that there is no antidepressant, until now more efficient than clomipramine (Side effects are different issue).
Beside that, there are some antidepressants that do not work though a re-uptake inhibition as mono amino oxidize inhibitors (MAOIs), and mirtazapine that work though blocking presinaptic receptors (alpha-2 and 5-HT1a, mainly).
As Dr. Artigas et al., in Barcelona had shown ,once antidepressant start working at re-uptake proteins, auto receptors (i.e., somato-dendritic 5-HT1a or alpha-2), then poduce an "antagonic reaction" and there are reduction of both synthesis and release of neurotransmitters (Autoreceptors had a hyper reaction because the low levels of NTs pre-tratmment). That is one explanation of the delay of clinical noticeable effect of antidepressants. The overall problem is inside the neuron, because regulatory mechanism that keep receptors and neurotransmitters in fine homeostatic tune are not doing their work, and in fact those cells, probably mono aminergics have been working more in alostasis for long time. More clear targets could be BDNF.

Posted by: Rafael J. Salin-Pascual MD, PhD | August 10, 2007 09:56 PM

It is scary to see that they give drug and they do not even know how they work in the brain

Posted by: natacha | August 10, 2007 10:39 PM

The commentary stated that the human mutations resulted in anti-depressant loss of function. On the contrary these mutations that Zhou et. al created were gain of function, increasing desipramine's ability to block transport in SERT and DAT.

Quite right: the story has been corrected on this matter. Thanks very much for pointing it out. Ed

Posted by: Bryan | August 13, 2007 07:16 PM

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