Compound 5-HT1A 5-HT2A 5-HT2B 5-HT3
4-HO-TMT 4,400 670.0 120.0 >10,000
4-AcO-TMT >10,000 >10,000 >10,000 >10,000
Psilocin 567.4 107.2 4.6 >10,000
Psilocybin >10,000 >10,000 98.7 >10,000

4-AcO-TMT showed no binding activity at any of the receptors tested. However, 4-HO-TMT had activity at 5-HT1A, 5-HT2A, and 5-HT2B. Agonist activity at 5-HT2A is regarded by experts as the hallmark of psychedelic activity.16

Although 4-HO-TMT showed less binding affinity at 5-HT2A than psilocin, the authors concluded that the Ki values were comparable (670.0 nM and 107.2 nM, respectively). Also, the data showed that 4-HO-TMT has a similar affinity for 5-HT2B compared to psilocybin.

Recall that one of the hypotheses Chadeayne et al. was testing was that aeruginascin’s active metabolite 4-HO-TMT would have an affinity for 5-HT3 like bufotenine. The data showed this was not the case. The Ki for 4-HO-TMT at 5-HT3 was >10,000 nM.
[...]
Despite the value gained from these tests, it is unclear why Chadeayne et al. did not test the two compounds at nicotinic acetylcholine receptors. The results may have shed some light on the possible role of aeruginascin (or its metabolite) in the phenomenon known as wood lover paralysis.

Of the 7 known serotonin receptor families, 5-HT3 is unique in that it works via a different mechanism than the others. Serotonin receptor families 1, 2, and 4-7 are G-protein coupled receptors that have a distinct structure of 7 coils that traverse the cell membrane.7 When these receptors bind serotonin and other compounds, they activate signaling pathways in the cell that use phosphatidylinositol and cyclic AMP (cAMP). The 5-HT3 receptor, however, works via a ligand-gated sodium and potassium channel. For these receptors, the binding of serotonin opens ion channels, allowing sodium and potassium to enter the cell, leading to an excitatory response. The ion-gated mechanism by which 5-HT3 receptors work is more like the way acetylcholine binds to neurons at neural-muscle junctions in the body, creating signaling for muscles to contract.

Studies have found that the frog venom bufotenidine (the one that causes paralysis) binds to the 5-HT3 receptor with ten times the affinity of serotonin.8 Recall the structural similarities between bufotenidine and aeruginascin (Figure 5). If aeruginascin is dephosphorylated in the body and carbon 4 receives a hydroxyl group as a result, then the only difference between the paralysis-causing bufotenidine and the Wood Lover Paralysis-causing candidate aeruginascin is whether carbon 4 or 5 has the hydroxyl group. Both molecules have the charged and reactive trimethylammonium group, so it is feasible they may affect the same receptor and cause the same effect. Also, based on its chemical structure, bufotenidine may be confined to the PNS and not be able to cross the blood-brain barrier, just like aeruginascin.

So my question is now, what is causing this effect in species not found to contain aeruginascin?

I have a fair ammount of experience picking and eating especially psilocybe cyanescens, and while the paralysis is usually absent, there are some specimens that will cause it - and it's pretty damn powerful.