Neuromuscular nicotinic receptors mediate bladder contractions following bladder reinnervation with somatic to autonomic nerve transfer after decentralization by spinal root transection

This study investigates whether the reinnervated neuronal pathway mediates contraction via the same neurotransmitter and receptor mechanisms as the original pathway. Following bladder decentralization by transection of sacral roots, peripheral nerve transfer was performed with bilateral genitofemoral to pelvic nerve transfer (GFNT) and unilateral (left) femoral nerve to bilateral pelvic nerve transfer (FNT). The present study details a SCh-sensitive component of bladder contraction and α1 nicotinic receptor subunit immunostaining that appears following nerve transfer and bladder reinnervation, which is not present in control dogs.

• 1
  Succinylcholine (SCh) virtually eliminated bladder pressure increases induced by electrical stimulation of the transferred somatic nerves or the lumbar spinal segments that contribute axons to these donor nerves.
• 2
  The reinnervated detrusor muscles of GFNT and FNT animals also contained increased alpha1 nicotinic receptor subunit immunoreactivity in punctate dots on detrusor muscle fascicles and in neuronal cell bodies, staining not observed in control animals.
• 3
  In control animals (either un-operated or sham-operated) SCh had no effect on nerve evoked bladder pressure increases