SPINAL cord injury disrupts micturition reflexes, which produces morbi
dity. The contribution of endogenous opioid systems to urinary retenti
on were assessed in chronic spinal cats by administering the opioid re
ceptor antagonist, naloxone (5-500 mu g kg(-1), i.p.), to unanesthetiz
ed paraplegic cats while monitoring lower urinary tract function and o
bserving hind limb reflexes. While naloxone had no overt effect in acu
te spinal cats, in chronic spinal cats naloxone induced the release of
large volumes of urine and produced marked hind limb hyper-reflexia.
Prominent tachyphylaxis and tolerance to the effects of naloxone were
evident. Immunohistochemical studies indicated a marked increase in le
ucine enkephalin and dynorphin in sacral spinal neurons. Together, the
se data indicate hyperactivity of the endogenous spinal opioid system
following recovery from spinal cord injury and, furthermore, suggest t
hat the spinal neural circuitry may become 'dependent' upon elevated l
evels of endogenous opioid peptides.