can anyone please break down how SSRIs work for me? please? i really do not understand…despite what i have read…
thank you.
what part do you want to be explained? how serotonin is supposed to improve mood or how serotonin reuptake is inhibited to produce more serotonin effects?
The whole thing about synapse is a theory, because we can’t see down that far as of yet. However, there are two theories of how the brain works. One theory is called the strand theory (if I remember correctly) and that states that the brain is one continuous nerve strand. The idea is that the nerve impulses, or information, travels around in your brain non-stop. This has been put to the side because it does not provide a neat explanation.
So, the synaptic theory was developed. That is based on electrical circuit theory. A circuit is like a light switch in the when you flip the switch the circuit (connection) is completed and electricity flows freely through the wires and to the light bulb. The theory is that your brain has tiny “circuits†in it called synapse. However, instead of electricity flowing, there are chemicals (some do create a type of electricity) that complete the circuit.
Supposedly, there are two bits of nerve tissue that are extremely close but not touching that act as the circuit. There are many different types of these and each type handles different sensations or functions. Serotonin is just one chemical that leaks out of these nerve bits and the completes the circuit by filling the gap in-between.
Theoretically, serotonin has been seen to be low in depressed people. So, the theory goes that their serotonin must not be leaking out to complete the circuit that may cause increased good spirits. The drug is supposed to inhibit the nerve from sucking the serotonin back up and breaking the circuit.
All of this is a theory and facts about the medication will state that they really have no idea about how or why it works if it works at all.
Trust me when I say that if you get work putting your mind in order that you will feel much better.
Enough of that though, how did you like the explanation? Did it make sense?
So then you believe that “uppers” are merely placebo effects???
And then how exactly does one pu their mind “in order”?
BTW, embracetrees,
To add to the notion of “we have no idea how these meds REALLY work,” a few years back it was argued that SSRIs do NOT exert their effect as their name implies, given the time it takes for them to work (4-6 weeks). The newer theory I found (no, I didn’t come up with it–I just found out about it…but it doesn’t seem to get any play in any of the many texts I teach from) argues that SSRIs make the brain (or the post-synaptic neruons in it) MORE SENSITIVE to the serotonin that is released into the synaptic gap.
I remember seeing some pretty compelling arguments for this theory, and my first impression was “there’s no way they’re going to promote this newer theory b/c it would require them to come up with a new acronym; but the drug companies have done such a great job of making ‘SSRI’ a houshold name.” Just a few thoughts…
PhilosophyGirl,
Uppers may stimulate the brain and then the body, but they can’t make you happy that your mom just died. There’s a difference between opinions held and how you body feels.
I seem to remember from my biology days that antidepressants in general work by altering the dynamic equilibrium between receptor count and neurotransmitter (seratonin/dopamine for example) concentration back to within normal mean levels - hence the delay in therapuetic effect whilst the brain’s neurophysiology adapts.
I’d be very surprised if a drug was released for public consumption without a fairly definite idea of its biochemistry, and acute/chronological toxicity/terratogenicity.
Purely personal note - don’t take em unless you’re seriously thinking of applying razor to wrist - your brain chemistry is too delicate a balance to go chucking bricks at. The side-effects are seriously wonky too.
Go to pub, talk to friends. Go to Gym - exhaust the body.
no tab, SSRIs work on only one part of the brain, making the serotonin receptors more sensitive, because in depression, sometimes the receiving neurons arent stimulated by serotonin. what i was asking was how this worked…
S.elective S.erotonin R.euptake I.nhibitors…?
Sorry if I was unspecific… Here’s how I remember the model:
Picture a synapse: Make two fists, move your arms in front of your body till your knuckles almost touch. This resembles a synapse.
Serotonin is secreted by your left fist, after recieving nervous stimulation. It jumps the gap, and binds to receptors on your right fist. Your right fist triggers and sends an impulse along it’s neuron to the next outbranchings of synapses. But only if enough serotonin finds receptors to bind to.
Now, usually that Serotonin is reabsorbed by the neurons, to clear the synapse for re-firing (this happens very quickly) but under the influence of SSRI’s this happens less quickly, and the concentration of serotonin within the synapse is increased. ie: There’s more serotonin floating in the gap. This means the synapse is now always ‘half’ on (imagine a light switch with the switch moved and held at the mid position, it takes now only a very little effort to switch it fully on.)
Equating in the body to a lowered threshold of stimulation, required to fire the neuron/synapse. As only a little hike in the concentration of serotonin is enough to fill the receptors and fire the recipient neuron. This state is acute, and persists only as long as the medicine is taken.
Now the brain and the body in general exists in a state of dynamic equilibrium. Imagine a see-saw. Taking SSRIs pushes the see-saw down on the serotonin side, the body doesn’t like this imbalance, so begins to make more Serotonin receptors on the other side of the synapse, to deal with the increased concentrations. Pushing the see-saw back to the neutral postition. This takes a little time.
Now, with all these extra receptors, the chemical chances of a binding event occuring for any given molecule of serotonin secreted is raised, and the overall sensitivity of the synapse increased, allowing quicker passage of even a lowered threshold of stimulation to pass along the neurons of the effected area. This state is relatively chronologicaly stable, and persists even after medication is discontinued. As long as the pyschological state of depression has lessened/stopped, and the trigggering event causing said depression come to terms with. Psyque/Adler will know more on that front.
SSRI’s flood the circulation of the general brain, but only effect the area sensitive to their effects: ie: the serotonin-policed synaptic ganglia.
The Good Drug Guide;
Selective serotonin re-uptake inhibitors increase the amount of serotonin in the synapse by blocking the re-uptake of serotonin by the serotonin re-uptake transporter.
Over time (>2 weeks) re-regulation occurs in the brain which lessens the activity of the HPA (hypothalamus-pituitary-adrenal) axis - lowering stress response.
It is postulated that overactivity of the HPA axis (chronicly high glucocorticoid levels) leads to depression;
biopsychiatry.com/hpa.htm
biopsychiatry.com/lhpa.htm
It is also postulated that new neuronal cell growth in the hippocampal region is at least partly responsible for the clinical efficacy of SSRIs;
biopsychiatry.com/antidepressants/index.htm
Towards the Abolition of Suffering through Science
abolitionist-society.com