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Im quoting this from another persons perspective from another forum…… its quite convincing…..
Basically, why should we mess with serotonin as a whole when the benefits are from 5-ht1 receptor stimulation? Or is this a vast over simplification of things?
“paradoxically, activation of the entire serotonin system as a whole is actually quite dysphoric and self-defeating in many ways. In fact, the only part of the entire system that produces relief from anxiety and depression upon activation is the 5-HT1 receptor complex. The other receptors, including the 5-HT2, 5-HT3, 5-HT6, and 5-HT7 receptors, are all anxiogenic and pro-depressive in nature. In addition, along with the 5-HT4 and 5-HT5 receptors, activation of these receptors is also largely responsible for the bulk of negative side effects attributed to all drugs that increase extracellular serotonin concentrations across the entire 5-HT system.
Unlike the other receptor complexes, the 5-HT1 complex has complicated pre-synaptic autoreceptor functions that limit and modulate 5-HT1-specific neurotransmission. Upon agonization of these autoreceptors, serotonin release is inhibited, therefore agonization causes a paradoxical release-limiting effect. So, for example, upon first starting a SSRI such as escitalopram (lexapro), the activity of the 5-HT1 complex is actually lowered, while the rest of the 5-HT receptors are stimulated, producing nothing but negative, depressive, and dysphoric effects. This is marked by temporary side effects such as increased anxiety, depression, and suicidal thoughts and idealizations, which are observed in many patients first commencing SSRI therapy.
After several weeks, the 5-HT1 autoreceptors manage to downregulate and become desensitized, which results in a mild but nonetheless beneficial increase in serotonin neurotransmission in the 5-HT1 complex, though nowhere near as strong an increase as observed in the other 5-HT complexes. This light increase in the activity of the 5-HT1 complex is fully responsible for the therapeutic benefits of the SSRIs, while the increased activity of the other 5-HT complexes is responsible for the vast majority of the side effects.”
(ps. i gota start cutting back on the topics i make, seems like im flooding the place, LOL)
@The450Man 1132 wrote:
Im quoting this from another persons perspective from another forum…… its quite convincing…..
Basically, why should we mess with serotonin as a whole when the benefits are from 5-ht1 receptor stimulation? Or is this a vast over simplification of things?
“paradoxically, activation of the entire serotonin system as a whole is actually quite dysphoric and self-defeating in many ways. In fact, the only part of the entire system that produces relief from anxiety and depression upon activation is the 5-HT1 receptor complex. The other receptors, including the 5-HT2, 5-HT3, 5-HT6, and 5-HT7 receptors, are all anxiogenic and pro-depressive in nature. In addition, along with the 5-HT4 and 5-HT5 receptors, activation of these receptors is also largely responsible for the bulk of negative side effects attributed to all drugs that increase extracellular serotonin concentrations across the entire 5-HT system.
Unlike the other receptor complexes, the 5-HT1 complex has complicated pre-synaptic autoreceptor functions that limit and modulate 5-HT1-specific neurotransmission. Upon agonization of these autoreceptors, serotonin release is inhibited, therefore agonization causes a paradoxical release-limiting effect. So, for example, upon first starting a SSRI such as escitalopram (lexapro), the activity of the 5-HT1 complex is actually lowered, while the rest of the 5-HT receptors are stimulated, producing nothing but negative, depressive, and dysphoric effects. This is marked by temporary side effects such as increased anxiety, depression, and suicidal thoughts and idealizations, which are observed in many patients first commencing SSRI therapy.
After several weeks, the 5-HT1 autoreceptors manage to downregulate and become desensitized, which results in a mild but nonetheless beneficial increase in serotonin neurotransmission in the 5-HT1 complex, though nowhere near as strong an increase as observed in the other 5-HT complexes. This light increase in the activity of the 5-HT1 complex is fully responsible for the therapeutic benefits of the SSRIs, while the increased activity of the other 5-HT complexes is responsible for the vast majority of the side effects.”
(ps. i gota start cutting back on the topics i make, seems like im flooding the place, LOL)
There are about 15 different serotonin receptors. Each one of them is stimulated by serotonin.
It is extremely difficult to stimulate only one of type of serotonin receptor.
When one substance stimulates one type of serotonin receptor, it is bound to stimulate most, if not all of them, and other receptors as well. Since serotonin is also similar to melatonin, it may also stimulate melatonin receptors also. With foreign substances, this is bound to happen.
The serotonin 2A receptors are pretty nice to block. This results in an increase in dopamine signaling. It is fairly specific for the frontal cortex. I wouldn’t mind finding something that can do this while minimally affecting the other systems. Unfortunately, the current medications (the atypical antipsychotics like Zyprexa) that affect serotonin 2A receptors also affect multiple other systems also.
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Cellular signaling systems work by a summation of all of the signals. A group of signals have to work together in order to go in any one particular direction. This is what makes things difficult to isolate the function of a single signal, and makes it even more difficult to isolate the functions of a single receptor subtype.
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You only have 24 posts. What are you talking about? You are more like a trickle than a flood. 😉
Keep the questions coming. I love it. The more questions we have, the more we learn. So keep stimulating our minds.
One of these days, we’ll catch up to the larger forums. 🙂
Known serotonin subtypes/functions
@The450Man 1193 wrote:
Known serotonin subtypes/functions
That is a good textbook. I have it in my book collection. It was a good read few years back one summer.
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