Prenatal and postnatal requirements of NT-3 for sympathetic neuroblast survival and innervation of specific targets

Development ◽  
1996 ◽  
Vol 122 (2) ◽  
pp. 491-500 ◽  
Author(s):  
W.M. ElShamy ◽  
S. Linnarsson ◽  
K.F. Lee ◽  
R. Jaenisch ◽  
P. Ernfors
Keyword(s):  
Pineal Gland ◽  
Internal Carotid ◽  
Sympathetic Neurons ◽  
Sympathetic Innervation ◽  
Mutant Mice ◽  
Normal Complement ◽  
Normal Number ◽  
Neurotrophin 3 ◽  
Cervical Ganglion ◽  
Functional Copy

Postnatal homozygous neurotrophin-3 mutant mice display a loss of about half the sympathetic superior cervical ganglion (SCG) neurons (Ernfors, P., Lee, K.-F., Kucera, J. and Jaenisch, R. (1994a) Cell 77, 503–512; Farinas, I., Jones, K. R., Backus, C., Wang, X. Y. and Reichardt, L. F. (1994) Nature 369, 658–661). We found that this loss is caused by excessive apoptosis of sympathetic neuroblasts leading to a failure to generate a normal number of neurons during neurogenesis. NT-3 was also found to be required postnatally. In Nt-3−/− mice, sympathetic fibers failed to invade pineal gland and external ear postnatally; whereas other targets of the external and internal carotid nerves, including the submandibular gland and the iris, displayed a normal complement of sympathetic innervation. Sympathetic fibers of mice carrying one functional copy of the Nt-3 gene (Nt-3+/− mice) invaded the pineal gland, but failed to branch and form a ground plexus. Cultured neonatal sympathetic neurons responded to NT-3 by neurite outgrowth and mRNA upregulation of the NT-3 receptor, trkC. Exogenously administered NT-3 promoted sympathetic growth and rescued the sympathetic target deficit of the mutant mice. We conclude that NT-3 is required for the survival of sympathetic neuroblasts during neurogenesis and for sympathetic innervation and branching in specific targets after birth.

scholarly journals p75-deficient embryonic dorsal root sensory and neonatal sympathetic neurons display a decreased sensitivity to NGF

Development ◽  
1994 ◽  
Vol 120 (4) ◽  
pp. 1027-1033 ◽  
Author(s):  
K.F. Lee ◽  
A.M. Davies ◽  
R. Jaenisch
Keyword(s):  
Nervous System ◽  
Peripheral Nervous System ◽  
Neural Development ◽  
Dorsal Root ◽  
Sympathetic Neurons ◽  
Mutant Mice ◽  
Neurotrophin Receptor ◽  
Cervical Ganglion ◽  
Response Specificity

To understand the role of low-affinity neurotrophin receptor p75 in neural development, we previously generated mice carrying a null mutation in the p75 locus (Lee, K. F., Li, E., Huber, L. J., Landis, S. C., Sharpe, A. H., Chao, M. V. and Jaenisch, R. (1992) Cell 69, 737–749). To elucidate the mechanisms leading to deficits in the peripheral nervous system in p75 mutant mice, we have employed dissociated cultures to examine the responses of p75-deficient dorsal root ganglion (DRG) and superior cervical ganglion (SCG) neurons to different neurotrophins. We found that p75-deficient DRG and SCG neurons displayed a 2- to 3-fold decreased sensitivity to NGF at embryonic day 15 (E15) and postnatal day 3 (P3), respectively, ages that coincide with the peak of naturally occurring cell death. Furthermore, while p75-deficient E15 DRG neurons did not change their response specificity to BDNF, NT-3, and NT-4/5, P3 SCG neurons became more responsive to NT-3 at higher concentrations (nanomolar ranges). These results may help explain the deficits in the peripheral nervous system in p75 mutant mice and provide evidence that p75 can modulate neurotrophin sensitivity in some neurons.

scholarly journals Structural changes of the human superior cervical ganglion following ischemic stroke

Medicina ◽  
2007 ◽  
Vol 43 (5) ◽  
pp. 390 ◽  
Author(s):  
Gineta Liutkienė ◽  
Rimvydas Stropus ◽  
Anita Dabužinskienė ◽  
Mara Pilmane
Keyword(s):  
Ischemic Stroke ◽  
Superior Cervical Ganglion ◽  
Sympathetic Neurons ◽  
Sympathetic Innervation ◽  
Sympathetic Ganglia ◽  
Neuronal Cell Body ◽  
Control Group ◽  
Superior Cervical Ganglia ◽  
Cervical Ganglion ◽  
Cervical Ganglia

Objective. The sympathetic nervous system participates in the modulation of cerebrovascular autoregulation. The most important source of sympathetic innervation of the cerebral arteries is the superior cervical ganglion. The aim of this study was to investigate signs of the neurodegenerative alteration in the sympathetic ganglia including the evaluation of apoptosis of neuronal and satellite cells in the human superior cervical ganglion after ischemic stroke, because so far alterations in human sympathetic ganglia related to the injury to peripheral tissue have not been enough analyzed. Materials and methods. We investigated human superior cervical ganglia from eight patients who died of ischemic stroke and from seven control subjects. Neurohistological examination of sympathetic ganglia was performed on 5 μm paraffin sections stained with cresyl violet. TUNEL method was applied to assess apoptotic cells of sympathetic ganglia. Results. The present investigation showed that: (1) signs of neurodegenerative alteration (darkly stained and deformed neurons with vacuoles, lymphocytic infiltrates, gliocyte proliferation) were markedly expressed in the ganglia of stroke patients; (2) apoptotic neuronal and glial cell death was observed in the human superior cervical ganglia of the control and stroke groups; (3) heterogenic distribution of apoptotic neurons and glial cells as well as individual variations in both groups were identified; (4) higher apoptotic index of sympathetic neurons (89%) in the stroke group than in the control group was found. Conclusions. We associated these findings with retrograde reaction of the neuronal cell body to axonal damage, which occurs in the ischemic focus of blood vessels innervated by superior cervical ganglion.

Timing of sympathetic innervation affects growth of myocardium in oculo

1995 ◽  
Vol 269 (1) ◽  
pp. H140-H148
Author(s):  
T. C. Love ◽  
D. C. Tucker
Keyword(s):  
Superior Cervical Ganglion ◽  
Cellular Proliferation ◽  
Internal Carotid ◽  
Sympathetic Innervation ◽  
Adult Rats ◽  
Cardiac Growth ◽  
Superior Cervical Ganglionectomy ◽  
Cervical Ganglion ◽  
Whole Heart

The effects of sympathetic innervation on myocardial growth during the proliferative and hypertrophic phases of cardiac growth were examined with the use of embryonic day 12 whole hearts or ventricles cultured in the anterior eye chamber of adult rats for 8 wk. Sympathetic innervation of whole heart and ventricular grafts was prevented by removing the superior cervical ganglion 1 wk before grafting or was limited to the cellular proliferation phase of growth by superior cervical ganglionectomy after grafts had been in oculo for 4 wk. Grafts in sympathetically innervated eye chambers were significantly larger than grafts in eye chambers denervated at 4 wk and grafts in eye chambers sympathectomized 1 wk before grafting. Innervation of grafts was delayed until 5-6 wk in oculo by crushing the internal carotid nerve. Delayed innervation produced grafts that were as large as those in innervated eye chambers. Together, these experiments suggest that the effects of sympathetic innervation on myocardial growth in oculo are most apparent during the second 4 wk in oculo (i.e., during the cellular enlargement phase of growth.

TRPC1, TRPC3, and TRPC4 in Rat Orofacial Structures

2017 ◽  
Vol 204 (5-6) ◽  
pp. 293-303 ◽  
Author(s):  
Masatoshi Fujita ◽  
Tadasu Sato ◽  
Takehiro Yajima ◽  
Eiji Masaki ◽  
Hiroyuki Ichikawa
Keyword(s):  
Transient Receptor Potential ◽  
Sympathetic Neurons ◽  
Receptor Potential ◽  
Monovalent Cation ◽  
Calcitonin Gene ◽  
Cervical Ganglion ◽  
Parasympathetic Neurons ◽  
Transient Receptor ◽  
And Function ◽  
And Control

TRPC (transient receptor potential cation channel subfamily C) members are nonselective monovalent cation channels and control Ca2+ inflow. In this study, immunohistochemistry for TRPC1, TRPC3, and TRPC4 was performed on rat oral and craniofacial structures to elucidate their distribution and function in the peripheries. In the trigeminal ganglion (TG), 56.1, 84.1, and 68.3% of sensory neurons were immunoreactive (IR) for TRPC1, TRPC3, and TRPC4, respectively. A double immunofluorescence method revealed that small to medium-sized TG neurons co-expressed TRPCs and calcitonin gene-related peptide. In the superior cervical ganglion, all sympathetic neurons showed TRPC1 and TRPC3 immunoreactivity. Parasympathetic neurons in the submandibular ganglion, tongue, and parotid gland were TRPC1, TRPC3, and TRPC4 IR. Gustatory and olfactory cells were also IR for TRPC1, TRPC3, and/or TRPC4. In the musculature, motor endplates expressed TRPC1 and TRPC4 immunoreactivity. It is likely that TRPCs are associated with sensory, autonomic, and motor functions in oral and craniofacial structures.

Plasticity of postganglionic sympathetic neurons in the rat superior cervical ganglion after axotomy

1994 ◽  
Vol 29 (2) ◽  
pp. 120-130 ◽  
Author(s):  
Lars Klimaschewski ◽  
Thang D. Tran ◽  
Rainer Nobiling ◽  
Christine Heym
Keyword(s):  
Superior Cervical Ganglion ◽  
Sympathetic Neurons ◽  
Cervical Ganglion

Postganglionic sympathetic neurons express endothelin

1998 ◽  
Vol 274 (3) ◽  
pp. R873-R878 ◽  
Author(s):  
Deborah H. Damon
Keyword(s):  
Spinal Cord ◽  
Superior Cervical Ganglion ◽  
Sympathetic Neurons ◽  
Northern Analysis ◽  
Rat Pups ◽  
Cervical Ganglion ◽  
Brain And Spinal Cord ◽  
The Brain

Endothelin (ET) is a peptide originally identified as an endothelial-derived vasoconstrictor. It is now recognized that ET is produced by and acts on many other tissues including the brain and spinal cord, where it is believed to modulate neurotransmission. The present studies demonstrate that ET is synthesized by and secreted from postganglionic sympathetic neurons. With the use of Northern analysis, ET-1 mRNA was detected in cultures of sympathetic superior cervical ganglion (SCG) neurons isolated from 3- to 5-day old rat pups. ET-1 and ET-3 peptides were also detected in cultured SCG neurons using immunohistochemistry. ET-1 (50 pg/106 cells) and ET-3 (173 pg/106 cells) were detected by radioimmunoassay of media conditioned by cultured SCG. ET-1 (77 pg/mg protein) and ET-3 (30 pg/mg protein) were also detected by radioimmunoassay of extracts of adult SCG.

scholarly journals Regulatory Function of Sympathetic Innervation on the Endo/Lysosomal Trafficking of Acetylcholine Receptor

2021 ◽  
Vol 12 ◽  
Author(s):  
Tatjana Straka ◽  
Charlotte Schröder ◽  
Andreas Roos ◽  
Laxmikanth Kollipara ◽  
Albert Sickmann ◽  
...  
Keyword(s):  
Neuromuscular Junction ◽  
Acetylcholine Receptor ◽  
Ribosomal Proteins ◽  
Neuromuscular Junctions ◽  
Sympathetic Neurons ◽  
Sympathetic Innervation ◽  
Regulatory Function ◽  
Hindlimb Muscles ◽  
Nerve Muscle

Recent studies have demonstrated that neuromuscular junctions are co-innervated by sympathetic neurons. This co-innervation has been shown to be crucial for neuromuscular junction morphology and functional maintenance. To improve our understanding of how sympathetic innervation affects nerve–muscle synapse homeostasis, we here used in vivo imaging, proteomic, biochemical, and microscopic approaches to compare normal and sympathectomized mouse hindlimb muscles. Live confocal microscopy revealed reduced fiber diameters, enhanced acetylcholine receptor turnover, and increased amounts of endo/lysosomal acetylcholine-receptor-bearing vesicles. Proteomics analysis of sympathectomized skeletal muscles showed that besides massive changes in mitochondrial, sarcomeric, and ribosomal proteins, the relative abundance of vesicular trafficking markers was affected by sympathectomy. Immunofluorescence and Western blot approaches corroborated these findings and, in addition, suggested local upregulation and enrichment of endo/lysosomal progression and autophagy markers, Rab 7 and p62, at the sarcomeric regions of muscle fibers and neuromuscular junctions. In summary, these data give novel insights into the relevance of sympathetic innervation for the homeostasis of muscle and neuromuscular junctions. They are consistent with an upregulation of endocytic and autophagic trafficking at the whole muscle level and at the neuromuscular junction.

scholarly journals Adipose tissue-derived neurotrophic factor 3 regulates sympathetic innervation and thermogenesis in adipose tissue

2020 ◽  
Author(s):  
Xin Cui ◽  
Jia Jing ◽  
Rui Wu ◽  
Qiang Cao ◽  
Fenfen Li ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Neurotrophic Factor ◽  
Sympathetic Innervation ◽  
Neurite Growth ◽  
Sympathetic Neuron ◽  
Beige Adipocyte ◽  
Diet Induced Obesity ◽  
Neurotrophin 3 ◽  
Beige Adipocytes ◽  
Adipocyte Development

AbstractActivation of brown fat thermogenesis increases energy expenditure and alleviates obesity. Sympathetic nervous system (SNS) is important in brown/beige adipocyte thermogenesis. Here we discover a novel fat-derived “adipokine” neurotrophic factor neurotrophin 3 (NTF3) and its receptor Tropomyosin receptor kinase C (TRKC) as key regulators of SNS growth and innervation in adipose tissue. NTF3 is highly expressed in brown/beige adipocytes, and potently stimulates sympathetic neuron neurite growth. NTF3/TRKC regulates a plethora of pathways in neuronal axonal growth and elongation. Adipose tissue sympathetic innervation is significantly increased in mice with adipocyte-specific NTF3 overexpression, but profoundly reduced in mice with TRKC haploinsufficiency (TRKC+/-). Increasing NTF3 via pharmacological or genetic approach promotes beige adipocyte development, enhances cold-induced thermogenesis and protects against diet-induced obesity (DIO); whereas TRKC+/- mice or SNS TRKC deficient mice are cold intolerant and prone to DIO. Thus, NTF3 is an important fat-derived neurotrophic factor regulating SNS innervation, energy metabolism and obesity.

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