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.

The Effect of Hemicholinium-3 on Choline and Acetylcholine Levels in a Sympathetic Ganglion

1975 ◽  
Vol 53 (3) ◽  
pp. 451-457 ◽  
Author(s):  
J. C. Khatter ◽  
A. J. D. Friesen
Keyword(s):  
Superior Cervical Ganglion ◽  
Sympathetic Ganglion ◽  
Transport Systems ◽  
Cholinergic Nerves ◽  
Choline Transport ◽  
Site Of Action ◽  
Cervical Ganglion ◽  
Preganglionic Stimulation ◽  
Rate Of Decline ◽  
Stimulation Of

Preganglionic stimulation of the cat's superior cervical ganglion in the presence of hemicholinium-3 (HC-3) produced the expected depletion of acetylcholine (ACh) stores, but failed to cause a corresponding reduction in the choline content. These results suggest that either HC-3 possesses an intracellular site of action or that in lower doses it selectively inhibits a specialized choline transport system in cholinergic nerves. At a dose of 2 mg/kg, HC-3 probably blocked ACh synthesis completely in ganglia stimulated at 20 Hz. Under these conditions, there was a rapid depletion of ACh to about 50% of control levels during the first 5 min of stimulation and thereafter the rate of decline in ACh levels proceeded at a much slower pace. Since the 2 mg/kg dose of HC-3 did not raise plasma choline concentrations, it may be assumed that non-specialized choline transport systems in other tissues were not significantly inhibited by this dose of HC-3. However, when the dose of HC-3 was increased to 4 mg/kg, plasma choline levels increased by 58%.

A comparative study of the acute effects of cetamolol (AI-27,303), atenolol, propranolol, and dexpropranolol on blood pressure, sympathetic nerve and ganglion activity of cats

1983 ◽  
Vol 61 (7) ◽  
pp. 693-698 ◽  
Author(s):  
J. Jaramillo
Keyword(s):  
Blood Pressure ◽  
Comparative Study ◽  
Intravenous Administration ◽  
Superior Cervical Ganglion ◽  
Sympathetic Nerve ◽  
Sympathetic Ganglia ◽  
Acute Effects ◽  
Cervical Ganglion ◽  
Sympathetic Discharge ◽  
Nerve Discharge

The effects of cetamolol (AI-27,303, Betacor®), atenolol, propranolol, and dexpropranolol were evaluated in 36 chloralose–urethane anesthetized cats. Blood pressure, sympathetic nerve discharge, and ganglionic activity (from the superior cervical ganglion) were recorded after the intravenous administration of 2.5, 5.0, and 10 mg/kg doses of the compounds. The results indicate that cetamolol and atenolol decreased blood pressure and discharge in the postganglionic sympathetic nerve and impaired transmission at the level of sympathetic ganglia. Propranolol and dexpropranolol given at the same doses produced a larger decrease in blood pressure, but increased the sympathetic discharge and had no effect on ganglionic spike amplitude.

Common origin and developmental dependence on c-ret of subsets of enteric and sympathetic neuroblasts

Development ◽  
1996 ◽  
Vol 122 (1) ◽  
pp. 349-358 ◽  
Author(s):  
P.L. Durbec ◽  
L.B. Larsson-Blomberg ◽  
A. Schuchardt ◽  
F. Costantini ◽  
V. Pachnis
Keyword(s):  
Nervous System ◽  
Neural Crest ◽  
Enteric Nervous System ◽  
Superior Cervical Ganglion ◽  
Normal Development ◽  
Sympathetic Ganglia ◽  
Tyrosine Kinase Receptor ◽  
Control Mechanisms ◽  
Enteric Ganglia ◽  
Cervical Ganglion

c-ret encodes a tyrosine kinase receptor that is necessary for normal development of the mammalian enteric nervous system. Germline mutations in c-ret lead to congenital megacolon in humans, while a loss-of-function allele (ret.k-) causes intestinal aganglionosis in mice. Here we examine in detail the function of c-ret during neurogenesis, as well as the lineage relationships among cell populations in the enteric nervous system and the sympathetic nervous system that are dependent on c-ret function. We report that, while the intestine of newborn ret.k- mice is devoid of enteric ganglia, the esophagus and stomach are only partially affected; furthermore, the superior cervical ganglion is absent, while more posterior sympathetic ganglia and the adrenal medulla are unaffected. Analysis of mutant embryos shows that the superior cervical ganglion anlage is present at E10.5, but absent by E12.5, suggesting that c-ret is required for the survival or proliferation of sympathetic neuroblasts. In situ hybridization studies, as well as direct labelling of cells with DiI, indicate that a common pool of neural crest cells derived from the postotic hindbrain normally gives rise to most of the enteric nervous system and the superior cervical ganglion, and is uniquely dependent on c-ret function for normal development. We term this the sympathoenteric lineage. In contrast, a distinct sympathoadrenal lineage derived from trunk neural crest forms the more posterior sympathetic ganglia, and also contributes to the foregut enteric nervous system. Overall, our studies reveal previously unknown complexities of cell lineage and genetic control mechanisms in the developing mammalian peripheral nervous system.

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.

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