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  • Title: Alterations in afferent pathways from the urinary bladder of the rat in response to partial urethral obstruction.
    Author: Steers WD, Ciambotti J, Etzel B, Erdman S, de Groat WC.
    Journal: J Comp Neurol; 1991 Aug 15; 310(3):401-10. PubMed ID: 1723990.
    Abstract:
    Afferent pathways from the urinary bladder were examined with axonal tracing techniques in normal female Wistar rats and in those with partial urethral ligation. Following injection of wheat germ agglutinin-horseradish peroxidase (HRP) into the bladder wall, HRP was detected in lumbosacral dorsal root ganglion cells and in afferent projections to the L6-S1 spinal cord at sites in laminae I, II, V-VII, and X known to receive visceral afferent input. Partial urethral ligation (6 weeks) produced a sixfold increase in bladder weight and altered the morphology of bladder afferent pathways. Changes included an increase in the average cross-sectional area of labelled neuronal profiles in L6 and S1 dorsal root ganglia in obstructed (766 +/- 378 microns 2, P less than 0.001) compared to control rats (528 +/- 189 mu 2). The cross-sectional area of the largest profiles also increased by approximately 40%. The mean number of labelled dorsal root ganglion cell profiles was similar in ligated (837 +/- 198) and control (883 +/- 352) groups. When compared to control animals the obstructed animals exhibited a 60% increase in the area of the labelled afferent terminal field in the intermediolateral region of the L6-S1 spinal cord. This increased labelling was even more remarkable given that the volume of tracer per bladder weight injected into the hypertrophied bladder was 87% less than controls. These results provide evidence that bladder afferents project to regions of the spinal cord known to regulate micturition and that these afferents can undergo morphological alterations and/or changes in axoplasmic transport in response to urethral ligation. Changes may occur in response to increased target organ mass, increased neural activity, or alterations in the levels or activity of neurotrophic factors.
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