https://www.eurekaselect.com/55536/article
Knockout mice lacking the 5-HT1B gene have shown an increase in aggression and a higher preference for alcohol.[14] Under basal conditions, knockout mice present with a "normal" phenotype and exhibit a sucrose preference (lack of sucrose preference is considered a measure of anhedonia). However, after undergoing chronic unpredictable stress treatment to induce a "depression-like" phenotype these animals do not benefit from administration of selective serotonin reuptake inhibitor (SSRIs).[11]
Psychoneuroendocrinology. 2002 Jul;27(5):609-18.
Involvement of the 5-HT(1A) and 5-HT(1B) serotonergic receptor subtypes in sexual arousal in male mice.
Popova NK1, Amstislavskaya TG.
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Abstract
The presence of a sexually receptive female behind a partition that prevents physical contact, but not seeing or smelling, increases blood testosterone level and induces the specific behavior in CBA male mice so that they more frequently approach the partition and spend more time near it in an attempt to make their way to the female. Treatment with the selective 5-HT(1A) serotonin receptor agonist 8-OH-DPAT (0.1, 0.25, 0.5 and 2.0 mg/kg) induced a dose-dependent decreasein the amount of time spent by the males near the partition, or "partition time", which is considered the main pattern of sexual motivation. The activating effect of female exposure on the male's pituitary-testicular system was totally blocked, as no increase in plasma testosterone level was observed. The 5-HT(1A) antagonist p-MPPI (0.1, 0.2 and 0.4 mg/kg) itself did not affect behavior or alter plasma testosterone, but attenuated the inhibiting effect of 8-OH-DPAT on behavior and totally antagonised the effect of the 5-HT(1A) agonist on testosterone response. The 5-HT(1B) agonist CGS-12066A (1.0 and 2.0 mg/kg) has no influence on the plasma testosterone increase exhibited by the male in response to female exposure. At the same time, either dose of CGS-12066A significantly reduced the partition time. The conclusion was made that the 5-HT(1A) subtype is involved in controlling both behavioral and hormonal indices of sexual arousal in male mice, while the 5-HT(1B) receptors antagonise sexual motivation, but do not modify the hypothalamic-pituitary-testicular response.
PMID: 11965359 [PubMed - indexed for MEDLINE]
My theory is that by inhibiting SERT, 5-HT1B and 5-HT1A autoreceptors downregulate, thus stop inhibiting serotonin flow to postsynaptic receptors, which ends up killing libido and also producing anhedonia
Basically 5-HT1B and 5-HT1A antagonist should in theory raise libido, while agonists should kill it.
Buspirone 5HT1A agonist downregulates autoreceptors, effect similar to SERT inhibitors. Using deductive reasoning 5-HT1A and 5-HT1B antagonists should in theory after few weeks (depending on affinity) upregulate autoreceptors, thus bringing back more normal flow of serotonin to the synapse.