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.

scholarly journals The effect of preganglionic stimulation on the incorporation of l-[U-14C]valine into the protein of the superior cervical ganglion of the guinea pig

1970 ◽  
Vol 118 (5) ◽  
pp. 813-818 ◽  
Author(s):  
P. Banks
Keyword(s):  
Guinea Pig ◽  
Superior Cervical Ganglion ◽  
Superior Cervical Ganglia ◽  
Cervical Ganglion ◽  
Cervical Ganglia ◽  
Preganglionic Stimulation ◽  
Energy Dependent ◽  
Stimulation Of

1. Superior cervical ganglia from the guinea pig carry out an energy-dependent incorporation of l-[14C]valine into protein in vitro. 2. Stimulation of the preganglionic nerve at a physiological frequency for more than a few minutes decreases the ability of the ganglia to incorporate labelled valine into protein.

Evidence for a Blood Ganglion Barrier in the Superior Cervical Ganglion of the Rat

1982 ◽  
Vol 40 ◽  
pp. 204-204
Author(s):  
D. M. DePace
Keyword(s):  
Blood Vessels ◽  
Superior Cervical Ganglion ◽  
Peripheral Nerves ◽  
Time Schedule ◽  
Transmission Electron ◽  
Cervical Ganglion ◽  
The Central Nervous System ◽  
Cervical Ganglia ◽  
Capillary Circulation ◽  
And Control

The majority of blood vessels in the superior cervical ganglion possess a continuous endothelium with tight junctions. These same features have been associated with the blood brain barrier of the central nervous system and peripheral nerves. These vessels may perform a barrier function between the capillary circulation and the superior cervical ganglion. The permeability of the blood vessels in the superior cervical ganglion of the rat was tested by intravenous injection of horseradish peroxidase (HRP). Three experimental groups of four animals each were given intravenous HRP (Sigma Type II) in a dosage of.08 to.15 mg/gm body weight in.5 ml of.85% saline. The animals were sacrificed at five, ten or 15 minutes following administration of the tracer. Superior cervical ganglia were quickly removed and fixed by immersion in 2.5% glutaraldehyde in Sorenson's.1M phosphate buffer, pH 7.4. Three control animals received,5ml of saline without HRP. These were sacrificed on the same time schedule. Tissues from experimental and control animals were reacted for peroxidase activity and then processed for routine transmission electron microscopy.

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.

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.

Late Discharges in Dog's Sympathetic Ganglia

1972 ◽  
Vol 50 (3) ◽  
pp. 263-269 ◽  
Author(s):  
S. S. Chen
Keyword(s):  
Superior Cervical Ganglion ◽  
Stimulus Frequency ◽  
Sympathetic Ganglia ◽  
Late Response ◽  
Before And After ◽  
Cervical Ganglion ◽  
High Stimulus ◽  
Time Courses ◽  
Preganglionic Stimulation ◽  
Muscarinic And Nicotinic Receptors

In the dog a preganglionic stimulation at a high stimulus frequency for 10–15 s elicited a two-wave response, early and late responses in the perfused ear (vasoconstriction), as well as early and late contractions in the nictitating membrane. Both the late contraction and the late response could be aborted by cooling the superior cervical ganglion, and restored by rewarming the ganglion. Both were resistant to atropine and hexamethonium combined. Their magnitude depended upon the duration of stimulation and upon the stimulus frequency used. Their time courses were similar both before and after hexamethonium or chilling. Therefore, it is concluded that they are manifestations of late discharges in the superior cervical ganglion, which are independent of both muscarinic and nicotinic receptors in the ganglion. A similar but less prominent phenomenon was demonstrated in the lumbosacral sympathetic ganglion of the dog by studying the responses of the retractor penis muscle and the perfused hind limb to preganglionic stimulation.

Vascular-derived artemin: a determinant of vascular sympathetic innervation?

2007 ◽  
Vol 293 (1) ◽  
pp. H266-H273 ◽  
Author(s):  
Deborah H. Damon ◽  
Jaclyn A. teRiele ◽  
Stephen B. Marko
Keyword(s):  
Important Determinant ◽  
Sympathetic Neurons ◽  
Sympathetic Innervation ◽  
Axon Growth ◽  
Neurite Growth ◽  
Sympathetic Ganglia ◽  
Neonatal Rat ◽  
Rt Pcr ◽  
Adult Rats ◽  
Sympathetic Axon

Vascular sympathetic innervation is an important determinant of blood pressure and blood flow. The mechanisms that determine vascular sympathetic innervation are not well understood. The present study tests the hypothesis that vascular-derived artemin promotes the development of sympathetic innervation to blood vessels by promoting sympathetic axon growth. RT-PCR and Western analyses indicate that artemin is expressed by cultured vascular smooth muscle and arteries, and artemin coreceptors, glial cell-derived neurotrophic factor family receptor α3 and ret, are expressed by postganglionic sympathetic neurons. The effects of artemin on axon growth were assessed on explants of neonatal rat sympathetic ganglia. In the presence, but not in the absence, of nerve growth factor, exogenous artemin stimulated neurite growth. Femoral arteries (FA) from adult rats contain artemin, and these arteries stimulated sympathetic neurite growth. Growth in the presence of FA was 92.2 ± 11.9 mm, and that in the absence of FA was 26.3 ± 5.4 mm ( P < 0.05). FA stimulation of axon growth was reduced by an antibody that neutralized the activity of artemin ( P < 0.05). These data indicate that artemin is expressed in arteries, and its receptors are expressed and functional in the postganglionic sympathetic neurons that innervate them. This suggests that artemin may be a determinant of vascular sympathetic innervation.

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