Abstract
We have investigated whether bladder afferent neurons are likely to be targets for
circulating estrogens by mapping estrogen receptor (ER) distribution in lumbosacral
dorsal root ganglia (DRG) of adult female rats. Sensory neurons innervating either
the detrusor or trigone regions were identified by application of fluorescent retrograde
tracer dyes to the bladder wall. Labelled neurons were classified by their immunoreactivity
for either type of ER (ERα or ERβ) and further compared with subpopulations of neurons
containing substance P, calcitonin gene-related peptide and vanilloid receptor (a
marker of polymodal nociceptors). Both ER types were expressed in numerous sensory
neurons of either upper lumbar (L1/L2) or lower lumbar/sacral (L6/S1) ganglia and
there was almost complete coexpression of ERα and ERβ. ER-positive neurons were mainly
small–medium size (18–25-μm diameter), indicating that they may be nociceptors and/or
supply visceral targets. Most bladder-projecting neurons expressed ERs and the majority
of these also expressed neuropeptides or vanilloid receptor. Afferent neurons supplying
detrusor and trigone regions had similar immunohistochemical features. About a third
of the bladder-projecting neurons expressed both ER and vanilloid receptor, suggesting
a mechanism by which estrogens could influence bladder pain. The prevalence of different
chemical classes of ER-positive bladder-projecting neurons was reflected throughout
the entire population of neurons in dorsal root ganglia of these spinal levels, suggesting
that neurons supplying other pelvic visceral targets may have similar chemical profiles.
These results suggest that many functional classes of sensory neurons innervating
the lower urinary tract are likely to be targets for circulating estrogens, including
many nociceptor neurons. The coexistence of ERα and ERβ suggests a broad range of
potential mechanisms by which estrogens may exert their genomic effects in this system.
Keywords
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Article info
Publication history
Accepted:
February 20,
2003
Received in revised form:
February 11,
2003
Received:
December 9,
2002
Identification
Copyright
© 2003 Elsevier Science B.V. Published by Elsevier Inc. All rights reserved.