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University of Vermont College of Medicine, Departments of Neurology and Anatomy and Neurobiology, Burlington, Vermont 05405
These studies examined
Fos protein expression in spinal cord neurons synaptically activated by
stimulation of bladder afferent pathways after spinal cord injury
(SCI). In urethan-anesthetized Wistar rats after SCI for 6 wk,
intravesical saline distension significantly (P 
0.005)
increased the number of Fos-immunoreactive (IR) cells in the
rostrolumbar (L1, 38 cells/section; L2, 29 cells/section) and caudal
lumbosacral (L6, 140 cells/section; S1, 110 cells/section) spinal cord
compared with control animals, but Fos expression in the L5 segment was
not altered. The distribution of Fos-IR cells was also altered in the
lumbosacral spinal cord. Significantly greater numbers of Fos-IR cells
were distributed in the dorsal commissure and medial and lateral dorsal
horn after intravesical distension in SCI animals. Large percentages of
parasympathetic (75%) and sympathetic (85%) preganglionic neurons
also expressed Fos-IR after intravesical distension in SCI animals.
These results demonstrate that bladder distension produces increased
numbers and an altered distribution pattern of Fos-IR cells after SCI. This pattern resembles that after noxious irritation of the bladder in
control animals. Pretreatment with capsaicin significantly reduced the
number of Fos-IR cells induced by bladder distension after SCI. These
data suggest that SCI can reveal an altered Fos expression pattern in
response to a nonnoxious bladder stimulus that is partially mediated by
capsaicin-sensitive bladder afferents.
lumbosacral spinal cord; neurotrophic factors; choline acetyltransferase; preganglionic neurons; urinary bladder dysfunction; capsaicin
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