text: Yo, check it out, let me break it down for you
  Populations of nociceptors, muscle pain syndromes, what they do?
  We tryna understand the function, but it's still unclear
  Comparing two classes, let me make it crystal clear
  
  IB4-positive, IB4-negative, nociceptors in the mix
  Inflammatory pain, chronic or acute, which one sticks?
  Gastrocnemius muscle in rats, that's where we test
  IB4-saporin treatment, destroyin' the best
  
  Baseline mechanical nociceptive threshold, we observe
  In rats treated with IB4-saporin, what's the word?
  Models of inflammation, carrageenan we inject
  Or ergonomic intervention, exercise or vibrate, you bet
  
  Hyperalgesia induced, acute pain transitionin'
  From acute to chronic, that's the mission we been given
  PGE(2)-induced hyperalgesia, we check the prolongation
  After recovery from acute pain, what's the situation?
  
  Baseline threshold ain't affected by the treatment
  But IB4-saporin rats, they got an improvement
  Shorter duration hyperalgesia, that's the deal
  In all three models, it's the real deal, for real
  
  Peak hyperalgesia, it be attenuated too
  In the ergonomic pain models, that's what it do
  IB4-saporin treatment, it be on point
  Preventin' prolongation of PGE(2)-induced joint
  
  So listen up, IB4(+) and IB4(-) neurons play a role
  In acute muscle hyperalgesia, they take control
  But when it comes to the long term, only IB4+ they choose
  That's the consequence of acute hyperalgesia, no excuse