Time&energy
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- Joined
- Aug 21, 2018
- Messages
- 28
Serotonergic agents that activate 5HT2A receptors prevent NMDA antagonist neurotoxicity. - PubMed - NCBI
Are all serotonin receptors equally as bad as one another?
In my opinion serotonin has multiple opposing outcomes on various different receptor sites, making it more of a neuromodulator than a neurotransmitter.
I have speculated in the past that serotonin could be classified as a harm avoidance chemical, due to the studies pointing to high serotonin levels being negatively associated with novelty.
With this in light I could see how an extreme manifestation from novel sensation could provoke an extreme reaction, IE an autistic person exposed to loud noise or large crowds.
I have experienced these sensations myself from taking stupendously large doses of 5HTP, before I knew of the detrimental effects of serotonin.
In regards to substances that classify as agonists to the 5HT1 receptors, like Creatine, ALCAR or Fluoxetine, it seems like they amplify anxiety, movement problems and produce hypersensitive reactions to stimulus.
I can't help wondering however, why it is the opposite reaction is imparted through 5HT2A agonists on me.
It seems that this receptor type can have positive effects on cognition. As I understand it the 5HT2A receptor is bound to glutamate receptors and is pivotal for the functioning of dopamine receptors. It seems that agonists such as Inositol hexonoate and Ashwanghanda have beneficial effects in terms of social mediation, anxiety and cognition.
Why therefore would this serotonin receptor be as bad as the others?
Are all serotonin receptors equally as bad as one another?
In my opinion serotonin has multiple opposing outcomes on various different receptor sites, making it more of a neuromodulator than a neurotransmitter.
I have speculated in the past that serotonin could be classified as a harm avoidance chemical, due to the studies pointing to high serotonin levels being negatively associated with novelty.
With this in light I could see how an extreme manifestation from novel sensation could provoke an extreme reaction, IE an autistic person exposed to loud noise or large crowds.
I have experienced these sensations myself from taking stupendously large doses of 5HTP, before I knew of the detrimental effects of serotonin.
In regards to substances that classify as agonists to the 5HT1 receptors, like Creatine, ALCAR or Fluoxetine, it seems like they amplify anxiety, movement problems and produce hypersensitive reactions to stimulus.
I can't help wondering however, why it is the opposite reaction is imparted through 5HT2A agonists on me.
It seems that this receptor type can have positive effects on cognition. As I understand it the 5HT2A receptor is bound to glutamate receptors and is pivotal for the functioning of dopamine receptors. It seems that agonists such as Inositol hexonoate and Ashwanghanda have beneficial effects in terms of social mediation, anxiety and cognition.
Why therefore would this serotonin receptor be as bad as the others?