https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6724987/
Here we show that serotonin, by activating 5-HT1A receptors, inhibited NMDA receptor-mediated ionic and synaptic currents in PFC pyramidal neurons, and the NR2B subunit-containing NMDA receptor is the primary target of 5-HT1A receptors. This effect of 5-HT1A receptors was blocked by agents that interfere with microtubule assembly, as well as by cellular knock-down of the kinesin motor protein KIF17 (kinesin superfamily member 17), which transports NR2B-containing vesicles along microtubule in neuronal dendrites. Inhibition of either CaMKII (calcium/calmodulin-dependent kinase II) or MEK/ERK (mitogen-activated protein kinase kinase/extracellular signal-regulated kinase) abolished the 5-HT1A modulation of NMDAR currents. Biochemical evidence also indicates that 5-HT1A activation reduced microtubule stability, which was abolished by CaMKII or MEK inhibitors. Moreover, immunocytochemical studies show that 5-HT1A activation decreased the number of surface NR2B subunits on dendrites, which was prevented by the microtubule stabilizer. Together, these results suggest that serotonin suppresses NMDAR function through a mechanism dependent on microtubule/kinesin-based dendritic transport of NMDA receptors that is regulated by CaMKII and ERK signaling pathways.
Apparently these are postsynaptic receptors (once mentioned at another point). My theory is that presynpatic 5HT1a or autoreceptors - which are independent units with different location by my understanding - do almost nothing, except inhibit serotonin when upregulated, which improves my motivation and emotional anhedonia (terrible motivation and emotional anhedonia when downregulated with Ashwagandha).
In any case, the important thing is that NNMDAR-inhibition. And this could explain why - sometimes - St. John's Wort, which is a postsynaptic 5HT1a antagonist, temporarily inceases genital sensitivity for me (again, sometimes). Or maybe this has nothing to do with it, it is just a sidenote.