Posted by SLS on February 25, 2014, at 12:21:33
In reply to Re: Returned to Abilify. Adding Saphris. » SLS, posted by johnLA on February 25, 2014, at 10:57:13
Hi John.
> i am curious as to your response to remeron.
>
> could you put it in 'laymen's' termsDon't I always?
;-)
> it's mode of action and your specific response?
Gosh. It is so hard to describe depression. With Remeron and idazoxan, I felt an anxious depression. I wanted it to end. I was, for the most part, motionless. I was too vegetative to think. Suicide was out of the question, as I didn't have the energy or wits to do it. It was actually painful. I just wanted to be left alone, yet, I was dependent on others to survive. The depression was hideous. It had no beginning and had no end.
5-HT = serotoin
NE = norepinephrine (noradrenalin)
H = histamineRemeron binds to and acts as an antagonist at receptors of several different neurotransmitters. These are a few of them.
1. 5-HT2a
2. 5-HT2b
3. 5-HT3
4. NE alpha-2a
5. H1A neurotransmitter is like a key that fits into a lock; the lock being the receptor. Generally speaking, a receptor is specific for one neurotransmitter.
* Agonist = a substance that binds to a receptor and stimulates it to perform its duties.
* Antagonist = a substance that binds to a receptor and blocks it from being stimulated.
* Inverse agonist = a substance that binds to a receptor and fools the receptor complex into acting in a manner opposite to that produced by an agonist.
Remeron is an antagonist at the five receptors listed above.
1. When stimulated, 5-HT2a and 5-HT2c receptors antagonize (inhibit) the release of excitatory neurotransmitters like dopamine in several brain structures. Remeron is very "sticky" and will bind to these same receptors tighter than serotonin does, thus inhibiting the action of serotonin. So, Remeron is inhibiting the inhibiting function of serotonin receptors on dopamine release. This is what is known as disinhibition. Confusing, I know. The bottom line is that to block 5-HT2a/c receptors releases more dopamine.
2. When stimulated, NE alpha-2a receptors increase the synthesis and release of NE. They are located on the terminal presynaptic membrane, and act as autoreceptors. (self-recognition). When NE levels decrease, the number of autoreceptors being stimulated by NE also decreases. This is a signal to the presynaptic neuron terminal to make more and release more NE. This is what it is known as a negative-feedback loop. So, when Remeron blocks the NE alpha-2a receptors, it is as if a blindfold was placed over them. They don't "see" the NE floating around in the synapse. The presynaptic neuron is therefore fooled into thinking it is time to make more and release more NE. The bottom line is that Remeron increases NE activity.
3. H1 receptors are one type of histamine receptor. They are involved in wakefulness, perceived energy, immune system activation, and appetite. H1 antagonist antihistamines like Remeron reduce wakefulness, cause fatigue, inhibit metabolism, inhibit immune activity, and increase appetite.
So, where does this leave you?
I don't know. Remeron can poop out just like SSRIs do, although I doubt it occurs as often. You could try adding a SRI drug (SSRI or SNRI) first, and then attempt to discontinue the Remeron if you feel better. You might need both drugs. You might not do well with them at all.
What are your main symptoms?
If you have to ask whether or not you are feeling well, then you probably aren't.
Sorry for any mistakes. I don't have the energy to proofread this. :-(
- ScottSome see things as they are and ask why.
I dream of things that never were and ask why not.- George Bernard Shaw
poster:SLS
thread:1059698
URL: http://www.dr-bob.org/babble/20140214/msgs/1061299.html