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Misc How does an SSRI work?

bronson

Bluelighter
Joined
Jan 14, 2010
Messages
5,141
Location
NE USA
First off, if this isn't the right place for this sort of question, please move it to somewhere that you feel it would get more appropriate responses.

I've been trying to figure out how selective serotonin reuptake inhibitor work for a long time now, and have done a good deal of reading on the subject.

I understand, that they stop the reuptake of serotonin which helps fix a chemical imbalance an individual may have. Yet there are still a few points of confusion.

-->Does a depressed individual start out with excess serotonin and the reuptake inhibition brings serotonin levels down to a reasonable level?

-->Or is the depressed person deficient in serotonin and reuptake inhibition keeps a larger more constant amount of serotonin moving through the central nervous system?

The biggest point of confusion is what reuptake inhibition is exactly, and how it happens.

If someone knowledgeable in this area could better explain these things to me I would be most appreciative. :\
 
dam just went of neurons in psychology. I believe reuptake is where left over neurotransmitters in the synapse are taken back into the neuron from which they were fired.
So in this case left over serotonin in the synapse is taken back into the neuron. So inhibition of this action would mean that serotonin is left within the synapse and not taken back into the neuron, what this accomplishes im not sure perhaps it mimics a firing of the original neuron for the receiving neuron without the actual firing of the original neuron... lol im confusing myself

http://upload.wikimedia.org/wikipedia/commons/8/8e/Reuptake_both.png
 
Re-uptake inhibition means that the neurotransmitter (serotonin) is kept in the synapse for a longer period of time, by inhibiting its re-absorption into the pre-synaptic neuron. The more serotonin that is in the synapse, the greater chance of communication between the pre-synaptic and post-synaptic neurons. This is because it binds to receptor sites on the post-synaptic neuron and at sufficient concentrations causes an action potential (basically when a neuron fires.)

PSolz.jpg


This image illustrates some of what I've said here (5HT is the chemical name abbreviation for serotonin.)

In a nutshell, SSRIs increase serotonin between neurons. The more serotonin between neurons, the more likely the secondary neuron is to fire. This treatment is based on the idea that depression and other symptoms are caused by a deficiency of serotonin in the synapse.
 
dokomo: Wonderful response. I now feel like I actually fully understand it. Thanks! :)

And, so then with SSRI, they are 'selective'. Does that mean that they leave most types of serotonin alone. But cause just the target types to stay in the synaptic gap longer?
 
^ good explanation .

I guess it's the same for DRI's and NDRI's?

Exactly. In each case the medication targets the re-uptake pumps for that particular neurotransmitter.

dokomo: Wonderful response. I now feel like I actually fully understand it. Thanks! :)

And, so then with SSRI, they are 'selective'. Does that mean that they leave most types of serotonin alone. But cause just the target types to stay in the synaptic gap longer?

The term "selective" simply means that the medication will only (primarily) affect reuptake pumps for serotonin. This is an advance over the previous generation of medications (MAOIs) that increased all monoamine neurotransmitters (dopamine, norepinephrine, etc.) Because they had such a broad effect, the side effect profile was much worse, so the selectivity of an SSRI makes it a much more attractive treatment option.
 
while we're on the (general) subject of serotonin, can anybody explain to me why serotonin agonists like triptans - sumatriptan, FI - do not cause psychedelic effects?

they're not 5-HT2A subset receptor agonists like the psychedelic drugs ?

Exactly right, triptan medications do not act on 5-HT2A receptors (involved in intense, visual hallucinations from psychedelics.)
 
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