Abstract/Summary

The venoms of some spider species are medically relevant, causing skeletal muscle damage and pain, while others are being bioprospected for potentially useful components. These factors justify the examination of their biochemical activity and their effects in vitro and in vivo. Two tarantula spider venoms were studied in this work, the Poecilotheria regalis and the Thrixopelma pruriens. The P. regalis venom has limited content characterisation and reportedly causes muscle damage symptoms and severe pain, while some T. pruriens venom toxins are instead being developed as analgesics, despite one having an affinity for a sodium ion channel related to muscle excitability. Muscle’s innate regenerative capacity for repair requires stem cells called satellite cells which become myoblasts. Their survival, migration, and fusion into myotubes can be impacted by venoms, which can also induce atrophy. Undifferentiated myoblasts in vitro were unaffected by either venom. However, both inhibited fusion and induced atrophy in the C2C12 mouse muscle cell line, in contrast to the AB1190 cell line from human paravertebral muscle. Treatment of atrophy from P. regalis venom by soluble activin receptor type IIB was investigated, however, improvement was not found. The in vivo study found that P. regalis caused muscle damage and delayed regeneration including some aspects unresolved by day 20. Nociception related to pain from P. regalis venom was also studied in vivo. Neuronal activity was quantified in mouse spinal cords, with a trend of increased reactive oxygen species, which supports published observations of hyperalgesia or pain sensitivity. In a preliminary in vivo study T. pruriens venom appeared to cause only localised minor skeletal muscle damage, even at a higher concentration than P. regalis venom. Overall, this study gives novel insight into the two venom’s activities in skeletal muscle and quantifiable nociception-related measures caused by a tarantula venom, as well as suggesting mechanisms.