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Dr. Bob is Robert Hsiung, MD,
bob@dr-bob.orgShown: posts 1 to 9 of 9. This is the beginning of the thread.
Posted by chess on February 11, 2004, at 10:58:13
I've read all the posts on Buspar, but I'm still a little confused.
Is it correct to say that Buspar decreases anxiety because it decreases the amount of serotonin being released into the synapse?
If that is correct, and that anxiety is caused by too much serotonin in the synapse, then why does an SSRI like Lexapro also decrease anxiety if it increases the amount of serotonin in the synapse?
Posted by linkadge on February 12, 2004, at 10:20:29
In reply to Buspar mechanism of action, posted by chess on February 11, 2004, at 10:58:13
Serotonin at the 5ht1a receptor decreases anxiety while serotonin at the 5ht2a receptor can cause anxiety.
Buspar tries to acitvate the 5ht1a receptor and decrease serotonin, thereby reducing the serotonin at the 2a receptor.
SSRI's activate all receptors. They activate the 1a receptor which can decrease anxiety but they also activate the 2a receptor which can cause initial anxiety till the system adjusts.
As you can see it is not an exact science.
But those are the basics of it.
Linkadge
Posted by chess on February 12, 2004, at 22:43:24
In reply to Re: Buspar mechanism of action, posted by linkadge on February 12, 2004, at 10:20:29
I've read that Buspar actually reduces anxiety because it eventually desensitizes the 5ht1a receptor over a period of time of activating it, and this desensitization ends up promoting serotonin release which then over time down-regulates the 5ht2a receptor and thus reduces anxiety.
Does that sound correct?
Or is Linkadge correct that Buspar basically reduces anxiety because it activates the 5ht1a receptor which decreaes serotonin release which thus reduces serotonin available at the 2a receptor?
Posted by scott-d-o on February 12, 2004, at 23:25:44
In reply to Re: Buspar mechanism of action, posted by chess on February 12, 2004, at 22:43:24
> I've read that Buspar actually reduces anxiety because it eventually desensitizes the 5ht1a receptor over a period of time of activating it, and this desensitization ends up promoting serotonin release which then over time down-regulates the 5ht2a receptor and thus reduces anxiety.
>
> Does that sound correct?
>
> Or is Linkadge correct that Buspar basically reduces anxiety because it activates the 5ht1a receptor which decreaes serotonin release which thus reduces serotonin available at the 2a receptor?my advice is just to take the med and see if it works for you instead of trying to figure all of this out. really there is even more to it than you are considering.
However, i will attempt to explain the best I can. it's a full agonist at 5-HT1a autoreceptors and a partial agonist at postsynaptic 5-HT1a receptors. Meaning it can attenuate or potentiate serotonin transmission dependant mostly on extracellular serotonin levels.
buspirone most closely resembles atypical antipsychotics, which can also be anxiolytic at low doses. i think it's anti-anxiety affect is primarily due to dopamine release caused indirectly by 5-HT1a agonism, and antagonism of D2 autoreceptors, also causing dopamine release. this is only my theory however and I don't think anyone could tell you the true answer with any great deal of certainty.
scott
Posted by jonh kimble on February 13, 2004, at 0:24:00
In reply to Re: Buspar mechanism of action, posted by scott-d-o on February 12, 2004, at 23:25:44
i think your right that endless speculation does little, but it does some. take this. seroquel made me more anxious. buspar makes me more anxious. if they are related in effect that points to something, does it not?
Posted by scott-d-o on February 13, 2004, at 1:35:18
In reply to Re: Buspar compared to seroquel crazy!!, posted by jonh kimble on February 13, 2004, at 0:24:00
> i think your right that endless speculation does little, but it does some. take this. seroquel made me more anxious. buspar makes me more anxious. if they are related in effect that points to something, does it not?
well, that is what the psychiatrist is there for.. anyhow, you are speaking from personal experience with particular medications and I would agree that making comparisons with a similar med or class of meds is viable.
however, going on theory alone, even after doing a sh*t load of research, it is extremely unlikely you will be able to plug your symptoms into a theoretical formula and get your miracle drug as a solution. every action in the brain is going to have several reactions, i.e. my example of having to consider indirect dopamine release resulting from 5-HT1a agonism in the case of buspar.
scott
Posted by chess on February 13, 2004, at 10:10:17
In reply to Re: Buspar mechanism of action, posted by scott-d-o on February 12, 2004, at 23:25:44
The interesting point is that it takes Buspar around 4 weeks for its therapeutic action to take effect.
So what it initially does (full agonist at 5-HT1a autoreceptors and a partial agonist at postsynaptic 5-HT1a receptors) is not what I'm asking about specifically, but rather what effect it has caused after 4 weeks is the question, which is why I remarked and asked for confirmation about Buspar reducing anxiety because over time (around 4 weeks) it eventually desensitizes the 5ht1a autoreceptor which then causes more serotonin to be released which then over time down-regulates the postsynaptic 5ht2a receptor and thus reduces anxiety.
I understand why some people say "just take it", but if buspar's effect is due primarily to it's enhancement of serotonin release after 4 weeks then it seems to me that the SSRIs are doing the same thing, so why not just take an SSRI?
Posted by scott-d-o on February 14, 2004, at 22:30:30
In reply to Re: Buspar mechanism of action, posted by chess on February 13, 2004, at 10:10:17
> The interesting point is that it takes Buspar around 4 weeks for its therapeutic action to take effect.
> So what it initially does (full agonist at 5-HT1a autoreceptors and a partial agonist at postsynaptic 5-HT1a receptors) is not what I'm asking about specifically, but rather what effect it has caused after 4 weeks is the question, which is why I remarked and asked for confirmation about Buspar reducing anxiety because over time (around 4 weeks) it eventually desensitizes the 5ht1a autoreceptor which then causes more serotonin to be released which then over time down-regulates the postsynaptic 5ht2a receptor and thus reduces anxiety.
> I understand why some people say "just take it", but if buspar's effect is due primarily to it's enhancement of serotonin release after 4 weeks then it seems to me that the SSRIs are doing the same thing, so why not just take an SSRI?Why not just take a SSRI? Good question... First of all, buspirone was invented way before SSRI's existed, so there wasn't always that option. Buspirone, like SSRI's, is useless for anxiety in my opinion, unless the anxiety is being caused by a depressive disorder, thus I think it should have been marketed as an antidepressant. I guess perhaps they thought that they might be able to steal some market share from the benzodiazepine class of meds by marketing it as a "non-addictive anti-anxiety med."
Nowadays, buspirone is most commonly used in conjunction with a SSRI. It increases dopamine and norepinephrine thru DA2 antagonism and alpha-2 adrenergic antagonism and thus reduces common SSRI-induced side effects such as bruxism, and sexual dysfunction. Most find a SSRI and buspirone to be a good combination. Personally, I could not even tolerate a SSRI without buspirone or another dopaminergic medication.
If you do not want to take multiple medications and just want an pure anti-anxiety effect, look at the benzodiazepines such as clonazepam. They are non-addictive but can cause dependency like the SSRI's. Hope this helps.
scott
Posted by csc on December 16, 2004, at 1:55:52
In reply to Re: Buspar mechanism of action, posted by scott-d-o on February 12, 2004, at 23:25:44
Buspiron is a 5HT1A agonist and DA partial agonist. It has been used to treat patient in confusional or delirium state also, as trazodone does.
I have the experience to give buspirone in patient with frontal lobe syndrome with response.
It's believed that 5HT1A makes its action to enhance mesocortical but not mesolimbic dopaminergic transmission, but I do not know whthere its action sites are mesencephalum or prefrontal corteces.
I think that 5HT1A can up-regulate post-synaptic dopmine receptors in prefrontal cortex, and the receptor number correlates to the frontal lobe function. Diinhibition, impulsivity, delusion, and even anxiety may represent the dysfunction of prefrontal cortex. A good example is diffuse lewy body dementia (DLBD), in which hallucination is one cardinal symptom. Sometimes I see a hallucination as a "negative" symptom, and its because the hypofunction of frefrontal region. Therefore I would give DA agonist in combination with buspirone in treating a case of DLBD.
This is the end of the thread.
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