Weltmeister
Bluelighter
- Joined
- Oct 23, 2015
- Messages
- 231
Love that theyre advertising it as a potent antagonist of 5-ht3 receptors yet according to the sources they cite it doesnt even bind to the receptor.
N&PD Moderators: Skorpio | someguyontheinternet
would the dizzy stuff have gone away had I taken it for longer ? took it maybe 1 week. And wouldnt 5ht1a activation decrease serotonin?Those side effects are 5-HT1A activation related, and are apparently the reason why 5-HT1A full agonists haven't made it to market even though they may otherwise be helpful for some conditions.
With regards to Zyprexa's efficacy for your anxiety, this could be due to any number of reasons. Have you tried other antipsychotics that achieve appreciable dopamine receptor blockade, e.g. Risperidone? I wouldn't count Seroquel/quetiapine unless you've been up to very high doses, and even then its still different from other antipsychotics. The anti-dopamine properties can occasionally be helpful for some issues in particular people, such as intrusive thoughts/OCD/anxiety.
It says buspar is an agonist on presynaptic 5ht1 receptors... so not the synapse 5ht1a receptor which if there is a lot serotonin matter since thats were serotonin receptors get activated? and it says on wiki its an agonist on postsynaptic 5-HT1A receptors.. so both pre and post synaptic activation but not in the synapse? When I say in the synapse I mean like the middel dont know whats it called I think its synapse? or synaptic cleft or somth.,
Does anyone know if Vortioxetine or viibryd increases 5ht1a activation in the SYNAPSE so it decreases serotonin receptors activation.
Agonism at 5-HT1A and antagonism at 5-HT2 (notably 2A) receptors induces anxiolysis. I don't know much about 5-HT6 but I would assume antagonism would tend towards promoting anxiolysis more so than agonism would at this receptor. 5-HT3 agonists are anxiogenic, and with a lot of antidepressants and antipsychotics acting as antagonists this receptor it would seem that it indeed plays a part in their anxiolytic effects.
Edit: Quick look around determined that it is actually agonism, not antagonism, that may induce anxiolytic effects when it comes to the 5-HT6 receptor.
IIRC the predominant expression of 5-HT3 in hippocampus is on interneurons (no expression on principal cells I believe), and more active hippocampi may help combat some mental illnesses better. So in that sense, decreased 5-HT3/decreased GABA may actually be helpful to some, with regards to the hippocampi.Question though on this. 5HT3 receptors are located on GABA interneurons. Antagonism of the 5HT3 receptors in PET scans of vortioxetine-treated patients showed that even at 5mg were it is only a 5HT3 antagonist + SRI this reduced GABA firing and increased the release of glutamate (as well as virtually all of the other neurotransmitters including acetylcholine and histamine). I would theorize that for some people this could make anxiety worse and would explain why a lot of people with anxious depression don't do well on vortioxetine
IIRC the predominant expression of 5-HT3 in hippocampus is on interneurons (no expression on principal cells I believe), and more active hippocampi may help combat some mental illnesses better. So in that sense, decreased 5-HT3/decreased GABA may actually be helpful to some, with regards to the hippocampi.
Serotonin can inhibit GABA interneurons via effects on 5-HT2 receptors as well.
This reminds me that there are actually some electrical synapse autoreceptors, named autapses (some are also regular chemical synapses as well), whereby a neuron's axon projects back onto its own dendrites https://www.nature.com/articles/srep30914Well there is also fast transmission via connexon and pannexin gap-junction channels. And possibly some contribution via ephaptic coupling effects between nearby neurons is there not? although the ephaptic coupling effect isn't strong, it wouldn't surprise me if such an emergent phenomenon is not being wasted, since the body, and particularly the nervous system does seem to be such a complex, subtle and quite astonishing organ, in its efficiency.
Since you were off on an "increasing NMDA receptor activation tangent", I'll throw out there that blocking NMDA receptors increases dopamine/norepinephrine.I have a question about receptors. Blocking 5ht2c increases dopamine / norepherpine in one part of the brain. Are there any other receptors in which when you block or agonize which increases those two neurontransmitters?
Since you were off on an "increasing NMDA receptor activation tangent", I'll throw out there that blocking NMDA receptors increases dopamine/norepinephrine.
hmm sounds like ur lying to stop me from trying NMDA. too bad im not smart enough to understand .Since you were off on an "increasing NMDA receptor activation tangent", I'll throw out there that blocking NMDA receptors increases dopamine/norepinephrine.