Selective serotonin reuptake inhibitors (SSRIs) achieve their therapeutic effect by modifying synaptic availability of the neurotransmitter serotinin. This is accomplished, first of all, by blocking the proteins that normally transport serotonin back into the cells that release them (presynaptic cell). In doing so, synaptic levels of serotonin are temporarily boosted. This phase is normally associated with an acute increase in anxiety. However, this subsides over several days as subtypes of postsynaptic5-HT receptors down-regulate in response to the excess serotonin. During this time another kind of protein called an autoreceptor (in this case 5-HT1 autoreceptors) located on the presynaptic cell begins to desensitize. Normally these types of receptor proteins provide a kind of feedback mechanism that limits the production of neurotransmitters.With these desensitized, the cell receives less feedback and the rate of serotonin synthesis and release increases. Since not all postsynaptic 5-HT receptors down-regulate in response to increased synaptic levels of serotonin - the ones that don't are able to bind more serotonin and this is thought to account for the longer term effects of SSRIs. Similar processes occur as 'secondary effects' on cells that release noradrenaline - as these express 5-HT2a heteroceptors - and this also is thought to contribute to their therapeutic efficacy. The reason serotonin is targeted by SSRIs in the first place is that the same regions of the brain that contain a high density of serotinin-releasing neurons (Raphe nuclei) are known to regulate mood directly as well as indirectly via interactions with other brain areas and neurotransmitter systems (like noradrenaline and dopamine in other parts of the limbic system as well as frontal cortex). However, because it's so complex, and no two brains are the same, responses to SSRIs can vary. In most cases of mild to moderate depression they offer a benefit .
It is observed in post-mortem examinations of depressed people that committed suicide that serotonin levels were low at some parts of the brain. SSRI's reduce the rate of destruction of serotonin therefore increasing it's concentration.
SSRIs definitely increase serotonin levels in all patients immediately, but anti-depressant action is NOT guaranteed and when it is achieved, it is after 20 days or more. So other factors may be contributing as well, but they are yet to be discovered.
No. They are SSRIs and work on the nervous systems where statins work in the liver and metabolism of lipids.
Mental depression is believed to be related to the low activity of one or more neurotransmitters in the brain.Although it is not understood exactly how most SSRIs work, they are designed to increase the level of serotonin in the brain.
There is no definitive answer, but if two months have passed, consider changing meds.
the long-term effects of SSRIs are unknown
As far as I know, food has minimal impact on SSRIs, if at all. If you are not satisfied with the results of your SSRIs, ask your doctor to either increase dosage or try other agent.
I think it is believed to act faster than SSRIs, within two weeks. But give it a month or two before changing it.
Selective serotonin reuptake inhibitors are medicines that relieve symptoms of depression. Selective serotonin reuptake inhibitors, also known as SSRIs or serotonin boosters
The most common side effects of SSRIs include: dry mouth.dizziness.sour or acid stomach or gas.heartburn.decreased appetite.stomach upset.diarrhea.sweating.headache.fatigue.drowsiness.insomnia.nervousness.tremors.sexual problems
Antidepressants: SSRIs, MAOIs, and tricyclics are three major categories of antidepressants. SSRIs are the most common and include Celexa, Zoloft, and Lexapro among others.
fluoxentine (an example of SSRIs).
If you are depressed, it makes you feel normal again, but it takes 3-5 weeks to kick in.
SSRIs or any drug that increases serotonin