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Dr. Bob is Robert Hsiung, MD,
bob@dr-bob.orgShown: posts 1 to 3 of 3. This is the beginning of the thread.
Posted by Janelle on March 15, 2002, at 2:40:30
The same med (say Serzone) can both block certain receptors from getting Norepinephrine and also do the reuptake inhibiting thing to other receptors? This seems weird, like the med is defeating its own purpose!
I ask this because you said "there is something sitting on the alpha-1 receptor blocking some norepinephrine, but at the same time the reuptake inhibitor is causing more norepinephrine to "hang around" at the receiving neuron."
WHAT is that something sitting on the alpha-1 receptor (which I gather is a receiving neuron) blocking some NE?
Thanks
-Janelle
Posted by JohnX2 on March 15, 2002, at 4:54:15
In reply to JohnX2 are you saying that ..., posted by Janelle on March 15, 2002, at 2:40:30
> The same med (say Serzone) can both block certain receptors from getting Norepinephrine and also do the reuptake inhibiting thing to other receptors? This seems weird, like the med is defeating its own purpose!
maybe, it depends if the alpha-1 receptor is important for what we are treating?......
>
> I ask this because you said "there is something sitting on the alpha-1 receptor blocking some norepinephrine, but at the same time the reuptake inhibitor is causing more norepinephrine to "hang around" at the receiving neuron."
>
> WHAT is that something sitting on the alpha-1 receptor (which I gather is a receiving neuron) blocking some NE?The medicine is sitting on the alpha-1 receptor.
The people who designed the chemical try to build it to do something very specific. They call this "selective". But this is very difficult. Many times the chemical may inadvertantly bind to some other receptor/whatever that is not important.The older antidepressants were very "non-selective". These were the tricyclic antidepressants. They would mess with all sorts of chemicals/receptors that had nothing to do with depression, but still treat the depression. So they would have lots of side effects.
When Eli Lilly came out with Prozac, the first "SSRI", it was somewhat of a stepping stone. It was the first commercially available medicine that selectively targeted a chemical that was thought to be important for depression. It did not goof with a lot of other less important receptors/chemicals. So people found the medicine more tolerable.
Obviously the scientists can still do better.
John
> Thanks
> -Janelle
Posted by Janelle on March 15, 2002, at 15:32:49
In reply to Re: JohnX2 are you saying that ... » Janelle, posted by JohnX2 on March 15, 2002, at 4:54:15
John,
Believe it or not, I understand as completely as possible the difference between the *older generation* of tricyclic a-d's (I even know why they are called trycyclics!) and the *newer generation* of SSRI's.
The first a-d I took was Elavil/Amitryptline, which is a tricyclic! Luckily, the side effects I had were minor and wore off, which I was told they often do. I did miss the nice calming, sedative effect it had for me which got me to sleep like a baby (I took it at night for awhile).
Have you ever taken a tricyclic, and if so which one(s)?
Also, I have a question from a thread further above that you apparently didn't see my note to go back up there - what are GENOMIC changes? I couldn't find the word genomic in the dictionary.
Thanks!
-Janelle
This is the end of the thread.
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