Cholinergic neuronal differentiation factors: evidence for the presence of both CNTF-like and non-CNTF-like factors in developing rat footpad

Development ◽  
1992 ◽  
Vol 114 (3) ◽  
pp. 689-698 ◽  
Author(s):  
H. Rohrer

Catecholaminergic sympathetic neurons are able to change their transmitter phenotype during development and to acquire cholinergic properties. Cholinergic sympathetic differentiation is only observed in fibers innervating specific targets like the sweat glands in the rat footpad. A function for ciliary neurotrophic factor (CNTF) in this process has been implied as it is able to induce cholinergic properties (ChAT, VIP) in cultured chick and rat neurons. We show here that a CNTF-like, VIP-inducing activity is present in rat footpads and that its increases 6-fold during the period of cholinergic sympathetic differentiation. Immunohistochemical analysis of P21 rat footpads demonstrated CNTF-like immunoreactivity in Schwann cells but not in sweat glands, the target tissue of cholinergic sympathetic neurons. The expression of this factor in footpads seems to be dependent on the presence of intact nerve axons, as nerve transection results in a loss of CNTF-like cholinergic activity and immunoreactivity. Immunoprecipitation experiments with rat footpad extracts provided evidence for the presence of ChAT-inducing factors other than CNTF, which may independently or together with CNTF be involved in the determination of sympathetic neuron phenotype.

1996 ◽  
Vol 134 (2) ◽  
pp. 487-497 ◽  
Author(s):  
K M Albers ◽  
T N Perrone ◽  
T P Goodness ◽  
M E Jones ◽  
M A Green ◽  
...  

Target-derived influences of nerve growth factor on neuronal survival and differentiation are well documented, though effects of other neurotrophins are less clear. To examine the influence of NT-3 neurotrophin overexpression in a target tissue of sensory and sympathetic neurons, transgenic mice were isolated that overexpress NT-3 in the epidermis. Overexpression of NT-3 led to a 42% increase in the number of dorsal root ganglia sensory neurons, a 70% increase in the number of trigeminal sensory neurons, and a 32% increase in sympathetic neurons. Elevated NT-3 also caused enlargement of touch dome mechanoreceptor units, sensory end organs innervated by slowly adapting type 1 (SA1) neurons. The enlarged touch dome units of the transgenics had an increased number of associated Merkel cells, cells at which SA1s terminate. An additional alteration of skin innervation in NT-3 transgenics was an increased density of myelinated circular endings associated with the piloneural complex. The enhancement of innervation to the skin was accompanied by a doubling in the number of sensory neurons expressing trkC. In addition, measures of nerve fibers in cross-sectional profiles of cutaneous saphenous nerves of transgenics showed a 60% increase in myelinated fibers. These results indicate that in vivo overexpression of NT-3 by the epidermis enhances the number of sensory and sympathetic neurons and the development of selected sensory endings of the skin.


2021 ◽  
Vol 14 (1) ◽  
pp. 24-28
Author(s):  
Tainá Zuchi ◽  
◽  
Claudia Lopatini ◽  
Joice Faria

Mammary gland tumors are one of the most commonly diagnosed tumors in female dogs, with a reported prevalence ranging from 26 to 73% in Brazil. In recognition of the importance of these tumors veterinary researchers and clinicians in Brazil produced the first consensus statement regarding canine mammary tumors in 2010. The intention was to establish criteria for diagnosis, prognosis, and treatment. This study evaluated the methods of prevention, diagnosis, treatment, and determination of prognosis used by veterinarians in Brazil, and sought to quantify the number of veterinarians who were aware of the consensus statement. One hundred and three veterinary clinics participated in the study, 87.37% of which recommend early neutering as a preventative treatment for mammary tumors. For diagnosis, 100% of these use laboratory testing, 94.17% perform chest radiography, 78.64% incisional biopsies, 44.66% cytological analysis, and 13.59% immunohistochemical analysis. The most common surgical procedure is unilateral mastectomy (72.81%), and chemotherapy is performed in 49.51% of the clinics. Of the 103 clinics, 66.01% were aware of the consensus. Although knowledge of the consensus statement is widespread among veterinarians in Brazil, not all its recommendations are being followed. Preventive actions for canine mammary tumors are well established in most parts of the country. However, the consensus statement has had little influence on informing prognostic and therapeutic approaches, with a poor uptake of surgical removal of lymph nodes and immunohistochemical examination.


1996 ◽  
Vol 271 (3) ◽  
pp. L392-L399 ◽  
Author(s):  
T. M. Nguyen ◽  
H. Guillozo ◽  
L. Marin ◽  
C. Tordet ◽  
S. Koite ◽  
...  

Rat fetal lung is a target tissue for 1 alpha,25-dihydroxyvitamin D3 [1 alpha,25 (OH)2 D3]. We have identified the cells that respond to the hormone and tested the hypothesis that the lung is also a source of 1 alpha,25(OH)2D3. We found that 1) at the end of pregnancy (days 20-21) alveolar type II cells (ATII) bore 1 alpha,25(OH)2D3 receptors and responded to the hormone. Incubating these cells with 10(-9) M 1 alpha,25(OH)2D3 for 48 h stimulated the synthesis (87.3 +/- 9.1%) and release (61.7 +/- 6.1%) of disaturated phosphatidylcholine; 2) EB-1213, a 1 alpha,25(OH)2D3 analogue with low calcemic activity, had similar effects on ATII; 3) neither fetal lung fibroblasts nor neonatal ATII (day 2 postpartum) expressed 1 alpha,25(OH)2D3 receptors; and 4) in contrast, fetal lung fibroblasts taken on days 19-22 of gestation converted [3H]25(OH)D3 to [3H]1 alpha,25(OH)2D3, whereas ATII and skin fibroblasts did not. These findings suggest that 1 alpha,25(OH)2D3 is a local mediator of epithelial-mesenchymal cell interactions in the developing rat lung and that 1 alpha,25(OH)2D3 or EB-1213 might be therapeutically useful in treating the respiratory distress syndrome of premature neonates.


2016 ◽  
Vol 48 (1) ◽  
pp. 1-7 ◽  
Author(s):  
Haihong Li ◽  
Liyun Chen ◽  
Mingjun Zhang ◽  
Bingna Zhang

2000 ◽  
Vol 278 (2) ◽  
pp. H404-H411 ◽  
Author(s):  
Deborah H. Damon

Sympathetic nerves are purported to stimulate blood vessel growth. The mechanism(s) underlying this stimulation has not been determined. With use of an in vitro coculture model, the present study tests the hypothesis that sympathetic neurons stimulate the growth of vascular smooth muscle (VSM) and evaluates potential mechanisms mediating this stimulation. Sympathetic neurons isolated from superior cervical ganglia (SCG) stimulated the growth of VSM. Growth of VSM in the presence of SCG (856 ± 81%) was significantly greater than that in the absence of SCG (626 ± 66%, P < 0.05). SCG did not stimulate VSM growth in transwell cocultures. An antibody that neutralized the activity of transforming growth factor-β2 (TGF-β2) inhibited SCG stimulation of VSM growth in coculture. SCG stimulation of VSM growth was also inhibited by an endothelin A receptor antagonist. These data suggest novel mechanisms for sympathetic modulation of vascular growth that may play a role in the physiological and/or pathological growth of the vasculature.


2007 ◽  
Vol 67 (16) ◽  
pp. 7825-7832 ◽  
Author(s):  
Yan Weng ◽  
Cheng Fang ◽  
Robert J. Turesky ◽  
Melissa Behr ◽  
Laurence S. Kaminsky ◽  
...  

1998 ◽  
Vol 140 (4) ◽  
pp. 911-923 ◽  
Author(s):  
Shernaz X. Bamji ◽  
Marta Majdan ◽  
Christine D. Pozniak ◽  
Daniel J. Belliveau ◽  
Raquel Aloyz ◽  
...  

Abstract. To determine whether the p75 neurotrophin receptor (p75NTR) plays a role in naturally occurring neuronal death, we examined neonatal sympathetic neurons that express both the TrkA tyrosine kinase receptor and p75NTR. When sympathetic neuron survival is maintained with low quantities of NGF or KCl, the neurotrophin brain-derived neurotrophic factor (BDNF), which does not activate Trk receptors on sympathetic neurons, causes neuronal apoptosis and increased phosphorylation of c-jun. Function-blocking antibody studies indicate that this apoptosis is due to BDNF-mediated activation of p75NTR. To determine the physiological relevance of these culture findings, we examined sympathetic neurons in BDNF−/− and p75NTR−/− mice. In BDNF−/− mice, sympathetic neuron number is increased relative to BDNF+/+ littermates, and in p75NTR−/− mice, the normal period of sympathetic neuron death does not occur, with neuronal attrition occurring later in life. This deficit in apoptosis is intrinsic to sympathetic neurons, since cultured p75NTR−/− neurons die more slowly than do their wild-type counterparts. Together, these data indicate that p75NTR can signal to mediate apoptosis, and that this mechanism is essential for naturally occurring sympathetic neuron death.


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