Morphological plasticity in efferent pathways to the urinary bladder of the rat following urethral obstruction

Steers, WD; Ciambotti, Jonathan; Erdman, S; Groat, WC de

doi:10.1523/jneurosci.10-06-01943.1990

Cited by 129 publications

(58 citation statements)

References 34 publications

(38 reference statements)

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“…Dilution of the sympathetic myometrial nerve fibers that fail to keep pace with the size of the uterus was also seen in the rat during puberty (Brauer et al 1992) and after acute (Brauer et al 1995) and chronic exposure to estrogen of young adult rats (Chávez-Genaro et al, In press). This unusual behavior of uterine sympathetic nerves clearly contrasts with the responses of similar nerves in other hypertrophic target tissues, including muscular visceral organs, in which changes in target size induce coordinated changes in their innervating neurons (Gabella 1984;Steers et al 1990). …”

Section: Discussionmentioning

confidence: 85%

Effects of Infantile/Prepubertal Chronic Estrogen Treatment and Chemical Sympathectomy with Guanethidine on Developing Cholinergic Nerves of the Rat Uterus

Richeri

Viettro

Chávez-Genaro

et al. 2002

J Histochem Cytochem.

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(TC) S U M M A R Y The innervation of the uterus is remarkable in that it exhibits physiological changes in response to altered levels in the circulating levels of sex hormones. Previous studies by our group showed that chronic administration of estrogen to rats during the infantile/prepubertal period provoked, at 28 days of age, an almost complete loss of norepinephrine-labeled sympathetic nerves, similar to that observed in late pregnancy. It is not known, however, whether early exposure to estrogen affects uterine cholinergic nerves. Similarly, it is not known to what extent development and estrogen-induced responses in the uterine cholinergic innervation are affected by the absence of sympathetic nerves. To address this question, in this study we analyzed the effects of infantile/prepubertal chronic estrogen treatment, chronic chemical sympathectomy with guanethidine, and combined sympathectomy and chronic estrogen treatment on developing cholinergic nerves of the rat uterus. Cholinergic nerves were visualized using a combination of acetylcholinesterase histochemistry and the immunohistochemical demonstration of the vesicular acetylcholine transporter (VAChT). After chronic estrogen treatment, a well-developed plexus of cholinergic nerves was observed in the uterus. Quantitative studies showed that chronic exposure to estrogen induced contrasting responses in uterine cholinergic nerves, increasing the density of large and medium-sized nerve bundles and reducing the intercept density of fine fibers providing myometrial and perivascular innervation. Estrogen-induced changes in the uterine cholinergic innervation did not appear to result from the absence/impairment of sympathetic nerves, because sympathectomy did not mimic the effects produced by estrogen. Estrogen-induced responses in parasympathetic nerves are discussed, considering the direct effects of estrogen on neurons and on changes in neuron-target interactions.

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Section: Discussionmentioning

confidence: 85%

Effects of Infantile/Prepubertal Chronic Estrogen Treatment and Chemical Sympathectomy with Guanethidine on Developing Cholinergic Nerves of the Rat Uterus

Richeri

Viettro

Chávez-Genaro

et al. 2002

J Histochem Cytochem.

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“…Analogous to spinal cord injury, which disrupts supraspinal regulation of micturition, this could contribute to the development of local spinal regulation of the micturition reflex, which is thought to underlie the hyperreflexia that characterizes overactive bladder (20). Thus, consequences of bladder obstruction on Barrington's nucleus neuronal activity may feed-forward to further contribute to the bladder dysfunction.…”

Section: Discussionmentioning

confidence: 99%

Impact of overactive bladder on the brain: Central sequelae of a visceral pathology

Rickenbacher¹,

Baez²,

Hale³

et al. 2008

Proc. Natl. Acad. Sci. U.S.A.

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Neural circuits that allow for reciprocal communication between the brain and viscera are critical for coordinating behavior with visceral activity. At the same time, these circuits are positioned to convey signals from pathologic events occurring in viscera to the brain, thereby providing a structural basis for comorbid central and peripheral symptoms. In the pons, Barrington's nucleus and the norepinephrine (NE) nucleus, locus coeruleus (LC), are integral to a circuit that links the pelvic viscera with the forebrain and coordinates pelvic visceral activity with arousal and behavior. Here, we demonstrate that a prevalent bladder dysfunction, produced by partial obstruction in rat, has an enduring disruptive impact on cortical activity through this circuit. Within 2 weeks of partial bladder obstruction, the activity of LC neurons was tonically elevated. LC hyperactivity was associated with cortical electroencephalographic activation that was characterized by decreased low-frequency (1-3 Hz) activity and prominent theta oscillations (6 -8 Hz) that persisted for 4 weeks. Selective lesion of the LC-NE system significantly attenuated the cortical effects. The findings underscore the potential for significant neurobehavioral consequences of bladder disorders, including hyperarousal, sleep disturbances, and disruption of sensorimotor integration, as a result of central noradrenergic hyperactivity. The results further imply that pharmacological manipulation of central NE function may alleviate central sequelae of these visceral disorders.Barrington's nucleus ͉ bladder obstruction ͉ electroencephalographic activity ͉ locus coeruleus O veractive bladder is a prevalent disorder, affecting 17% of the population and negatively impacting quality of life (1). Partial bladder obstruction is a common cause of overactive bladder in males and is used to model overactive bladder in laboratory animals (2). Whereas the structural and functional changes induced in bladder by partial obstruction are well studied (3, 4), the impact on brain function has been neglected. The potential for central consequences of bladder dysfunctions exists because neural circuits are present that communicate pelvic visceral status to the brain so that behavior can be coordinated with visceral functions. Barrington's nucleus (the pontine micturition center) and the locus coeruleus (LC) are integral components of a circuit that performs this task (5). Barrington's nucleus neurons project to spinal preganglionic parasympathetic neurons, where they regulate activity of the bladder and other pelvic viscera (6). These projections form the efferent limb of the micturition reflex, in which Barrington's nucleus neurons are activated by bladder distention and in response, initiate bladder contraction (7). The same Barrington's nucleus neurons project to the LC, a major norepinephrine (NE)-containing nucleus with divergent efferent projections that densely innervate the forebrain (8, 9). Among its functions, the LC regulates arousal, shifts in attention, and involv...

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“…A manifestation of bladder dysfunction seen in 60-75% of patients with BPH is bladder hyperactivity (2). Because obstruction ofthe bladder leads to changes in neuronal morphology and function, these alterations in neural pathways could contribute to bladder dysfunction and alter treatment outcome (3)(4)(5)(6)(7).…”

mentioning

confidence: 99%

Nerve growth factor in the urinary bladder of the adult regulates neuronal form and function.

Steers¹,

Kolbeck²,

Creedon³

et al. 1991

J. Clin. Invest.

352

229

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Urethral obstruction produces increased voiding frequency (0.7±0.06 to 1.1±0.08 h-') and hypertrophy of the urinary bladder (89±1.7 to 708±40 mg) with profound increments in the dimensions of afferent (4, 6) and efferent neurons (299±4.7 to 573±8.6 gm2) supplying this organ in the rat. We discovered that hypertrophied bladders of rat and human contain significantly more nerve growth factor (NGF) per milligram wet weight, protein, and DNA than normal bladders. The temporal correlation between NGF content, neuronal hypertrophy, and bladder weight was consistent with a role for this growth factor in the neurotrophic effects associated with obstruction. Autoimmunity to NGF abolished the hypertrophy of NGF-sensitive bladder neurons in the pelvic ganglion after obstruction. Relief of urethral obstruction reduced bladder size (349±78 mg), but neuronal hypertrophy (460.2±10.2 Mm2) and elevated NGF levels were only partially reversed. Bladder hypertrophy (133±43 mg) induced by osmotic diuresis slightly increased ganglion cell area (365.2±6.1 gm2) and only doubled NGF content of the bladder. These findings provide important new evidence that parenchymal cells in the hypertrophied bladder can synthesize NGF and possibly other molecular messengers that act to alter the size and function of neurons in adult animals and man. (J.

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Morphological plasticity in efferent pathways to the urinary bladder of the rat following urethral obstruction

Cited by 129 publications

References 34 publications

Effects of Infantile/Prepubertal Chronic Estrogen Treatment and Chemical Sympathectomy with Guanethidine on Developing Cholinergic Nerves of the Rat Uterus

Effects of Infantile/Prepubertal Chronic Estrogen Treatment and Chemical Sympathectomy with Guanethidine on Developing Cholinergic Nerves of the Rat Uterus

Impact of overactive bladder on the brain: Central sequelae of a visceral pathology

Nerve growth factor in the urinary bladder of the adult regulates neuronal form and function.

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