The functional relevance of serotonin 5-HT1A receptors in many mental health disorders should be revealed here, these receptors not only act on many peripheral, central, neuroendocrine levels - but have direct actions on stress responses - the agonism (stimulation) of which tends to have both pro-cortisol and pro-stress effects through the inhibition of serotonin release in other areas/receptors.
It also is a receptor directly acting on both pre-synaptic and post-synaptic nerve terminals to inhibit dopaminergic firing, and to inhibit glutamate and acetylcholine activity - by doing this it causes the depression of the central nervous system, but the activation can ironically, also cause anxiety because of the net reduction in serotonin tone and also of the inhibition of GABA in both the PVN (ParaVentrical Nucleus) and the hippocampus.
Based on my research, this receptor can alter neuro-endocrine parameter's by the above effects, and directly - mainly increasing cortisol, prolactin and beta-endorphin, and while it does increase oxytocin - it does not do so enough to cause any measurable or noticeable good effects if in theory, the reduction of serotonin or eventual enhancement of serotonin by de-sensitization of these receptors will overpower that oxytocin increase - making it irrelevant.
In addition, this receptor seems to be doing more harm than good, not only because of it's negative endocrine effects and dopamine antagonistic properties, but it has direct histamine inhibiting and NMDA inhibiting properties, thus , this likely proves why the overactivation of this receptor can cause psychosis , co-occurring with anxiety and other disorders , especially apathy/emotional blunting. Also explains why many antipsychotic drugs block this receptor, by antagonizing 5-ht1A; we are disinhibiting NMDA and histamine - effectively modulating the net increase in dopaminergic tone also increased by the blockade of this receptor.
As one would see by research, NMDA receptors, glutamate and / or Histamine is generally lower in schizophrenics, and while glutamate is heightened in obsessive-compulsive-subjects, it is only certain glutamate receptors that tend to by hyper active while others are HYPO ACTIVE. Interestingly, the one receptor found hypoactive in schizophrenia is also hypoactive in OCD subjects; NMDA-glutamate receptors, which are primarily inhibited by histamine H3, serotonin 5-HT1A receptors and by an overmethylated state in the body/liver.
http://www.acnp.org/g4/GN401000117/CH115.html
http://www.ncbi.nlm.nih.gov/pubmed/23757185
It also is a receptor directly acting on both pre-synaptic and post-synaptic nerve terminals to inhibit dopaminergic firing, and to inhibit glutamate and acetylcholine activity - by doing this it causes the depression of the central nervous system, but the activation can ironically, also cause anxiety because of the net reduction in serotonin tone and also of the inhibition of GABA in both the PVN (ParaVentrical Nucleus) and the hippocampus.
Based on my research, this receptor can alter neuro-endocrine parameter's by the above effects, and directly - mainly increasing cortisol, prolactin and beta-endorphin, and while it does increase oxytocin - it does not do so enough to cause any measurable or noticeable good effects if in theory, the reduction of serotonin or eventual enhancement of serotonin by de-sensitization of these receptors will overpower that oxytocin increase - making it irrelevant.
In addition, this receptor seems to be doing more harm than good, not only because of it's negative endocrine effects and dopamine antagonistic properties, but it has direct histamine inhibiting and NMDA inhibiting properties, thus , this likely proves why the overactivation of this receptor can cause psychosis , co-occurring with anxiety and other disorders , especially apathy/emotional blunting. Also explains why many antipsychotic drugs block this receptor, by antagonizing 5-ht1A; we are disinhibiting NMDA and histamine - effectively modulating the net increase in dopaminergic tone also increased by the blockade of this receptor.
As one would see by research, NMDA receptors, glutamate and / or Histamine is generally lower in schizophrenics, and while glutamate is heightened in obsessive-compulsive-subjects, it is only certain glutamate receptors that tend to by hyper active while others are HYPO ACTIVE. Interestingly, the one receptor found hypoactive in schizophrenia is also hypoactive in OCD subjects; NMDA-glutamate receptors, which are primarily inhibited by histamine H3, serotonin 5-HT1A receptors and by an overmethylated state in the body/liver.
http://www.acnp.org/g4/GN401000117/CH115.html
http://www.ncbi.nlm.nih.gov/pubmed/23757185
