Intrinsic Innervation of the Uterus in Guinea Pig and Rat

Mustafa, Fatima; Fatani, J A; El-Eishi, Hamdi; el-Badawi, M G

doi:10.1159/000146377

Cited by 10 publications

(7 citation statements)

References 7 publications

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“…In agreement with previous studies (Adham and Schenk 1969; Moscarini et al 1982;Papka et al 1985;Garfield 1986;Mustafa et al 1987;Prud'homme et al 2000), we observed that cholinergic nerves were extremely sparse in the cephalic portion of the uterine horn but were concentrated in the caudal region, where they formed a well-developed plexus in association with blood vessels and myometrial smooth muscle. This regional pattern of distribution clearly contrasts with that shown by sympathetic (Adham and Schenk 1969;Houdeau et al 1998;Zoubina et al 1998) and sensory nerve fibers (Zoubina et al 1998), which appear more concentrated in the cephalic portion of the uterine horn.…”

Section: Discussionsupporting

confidence: 93%

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: Discussionsupporting

confidence: 93%

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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“…Unlike reports for the PG, descriptions of the cholinergic innervation of the uterine cervix and horns are more consistent; some report a dense nerve supply to the myometrium, basal epithelium and glands (Mustafa et al 1987), dense supply to vasculature and myometrium (Kanerva et al 1972b;Garfield 1986) and especially the cervix (Mäkelä and Grönroos 1959;Papka et al 1985;Melo and Machado 1993;Sullivan et al 1994). In addition, bilateral destruction of the PG causes loss of AChE-positive fibers from the rat uterine myometrium and perivascular space, indicating that the PG is a major source of such fibers (Kanerva et al 1972b).…”

Section: Cholinergic Elements In the Uterusmentioning

confidence: 90%

“…For example, Kanerva (1971) reported intense AChE activity in one-fifth to one-third of the PG neurons, but Papka et al (1987) and Sullivan et al (1994) reported that the majority of PG neurons were AChEpositive and "cholinergic." "Cholinergic" innnervation of the rat uterine cervix and horns is described as moderate to dense in the myometrium and vasculature, moderate to weak in the endometrium, and with thick branching nerve trunks (Kanerva et al 1972b;Papka et al 1985;Garfield 1986;Mustafa et al 1987;Melo and Machado 1993). Consequently, the cholinergic innervation of the uterus has not been precisely elucidated because of variable results of nonspecific histochemical methods.…”

Section: Introductionmentioning

confidence: 99%

Cholinergic neurons of the pelvic autonomic ganglia and uterus of the female rat: distribution of axons and presence of muscarinic receptors

et al. 1999

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Acetylcholine (ACh) stimulates contraction of the uterus and dilates the uterine arterial supply. Uterine cholinergic nerves arise from the paracervical ganglia and were, in the past, characterized based on acetylcholinesterase (AChE) histochemistry. However, the histochemical reaction for acetylcholinesterase provides only indirect evidence of acetylcholine location and is a nonspecific marker for cholinergic nerves. The present study: (1) reevaluated cholinergic neurons of the paracervical ganglia, (2) examined the cholinergic innervation of the uterus by using retrograde axonal tracing and antibodies against molecules specific to cholinergic neurons, choline acetyltransferase and the vesicular acetylcholine transporter, and (3) examined muscarinic receptors in the paracervical ganglia using autoradiography and a radiolabeled agonist. Most ganglionic neurons were choline acetyltransferase-and vesicular acetylcholine transporter-immunoreactive and were apposed by choline acetyltransferase/vesicular acetylcholine transporter-immunoreactive terminals. Retrograde tracing showed that some cholinergic neurons projected axons to the uterus. These nerves formed moderately dense plexuses in the myometrium, cervical smooth muscle and microarterial system of the uterine horns and cervix. Finally, the paracervical ganglia contain muscarinic receptors. These results clearly reveal the cholinergic innervation of the uterus and cervix, a source of these nerves, and demonstrate the muscarinic receptor content of the paracervical ganglia. Cholinergic nerves could play significant roles in the control of uterine myometrium and vasculature.

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“…These nerves are particularly well developed in the tubo-uterine junction, suggesting a role in sphincter control (Moustafa et al, 1987). Oviductal efferent nerves express a range of neuropeptides including neuropeptide Y (NPY) and vasoactive intestinal polypeptide (VIP) and peptide histidine isoleucine (PHI), (Helm et al, 1982; Papka et al, 1985; Kannisto et al, 1986; Owman et al, 1986b; Czaja et al, 1996).…”

Section: Innervation Of the Female Reproductive Tract: An Overviewmentioning

confidence: 99%

“…There is considerable interspecies variation in the density of uterine cholinergic nerves, being well-develop in mice and humans but almost absent in the guinea pig (Moustafa et al, 1987). NPY co-localizes with acetylcholine (Ach) in neurons of the paracervical ganglia innervating the cervix (Traurig and Papka, 1993).…”

Section: Innervation Of the Female Reproductive Tract: An Overviewmentioning

confidence: 99%

Estrogen and female reproductive tract innervation: Cellular and molecular mechanisms of autonomic neuroplasticity

Brauer

Smith

2015

Autonomic Neuroscience

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The female reproductive tract undergoes remarkable functional and structural changes associated with cycling, conception and pregnancy, and it is likely advantageous to both individual and species to alter relationships between reproductive tissues and innervation. For several decades, it has been appreciated that the mammalian uterus undergoes massive sympathetic axon depletion in late pregnancy, possibly representing an adaptation to promote smooth muscle quiescence and sustained blood flow. Innervation to other structures such as cervix and vagina also undergo pregnancy-related changes in innervation that may facilitate parturition. These tissues provide highly tractable models for examining cellular and molecular mechanisms underlying peripheral nervous system plasticity. Studies show that estrogen elicits rapid degeneration of sympathetic terminal axons in myometrium, which regenerate under low-estrogen conditions. Degeneration is mediated by the target tissue: under estrogen's influence, the myometrium produces proteins repulsive to sympathetic axons including BDNF, neurotrimin, semaphorins, and pro-NGF, and extracellular matrix components are remodeled. Interestingly, nerve depletion does not involve diminished levels of classical sympathetic neurotrophins that promote axon growth. Estrogen also affects sympathetic neuron neurotrophin receptor expression in ways that appear to favor pro-degenerative effects of the target tissue. In contrast to the uterus, estrogen depletes vaginal autonomic and nociceptive axons, with the latter driven in part by estrogen-induced suppression BMP4 synthesis. These findings illustrate that hormonally mediated physiological plasticity is a highly complex phenomenon involving multiple, predominantly repulsive target-derived factors acting in concert to achieve rapid and selective reductions in innervation.

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Intrinsic Innervation of the Uterus in Guinea Pig and Rat

Cited by 10 publications

References 7 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

Cholinergic neurons of the pelvic autonomic ganglia and uterus of the female rat: distribution of axons and presence of muscarinic receptors

Estrogen and female reproductive tract innervation: Cellular and molecular mechanisms of autonomic neuroplasticity

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