The effects of sympathetic nerve damage on satellite glial cells in the mouse superior cervical ganglion

2019 ◽  
Vol 221 ◽  
pp. 102584 ◽  
Author(s):  
Rachel Feldman-Goriachnik ◽  
Menachem Hanani
1904 ◽  
Vol 73 (488-496) ◽  
pp. 99-99
Author(s):  
John Newport Langley ◽  
Hugh Kerr Anderson

It is well known that the cervical sympathetic nerve and the chorda tympani have opposite actions upon the blood-vessels of the sub-maxillary gland, the former causing contraction of the vessels, and the latter, dilatation. Evidence has been given by one of us that the chorda tympani if united with the cervical sympathetic, can in time make connection with the nerve cells of the superior cervical ganglion and become in part vaso-constrictor fibres. Our experiments have been directed to determine whether the cervical sympathetic if allowed an opportunity of becoming connected with the peripheral nerve cells in the course of the chorda tympani will in part change their function from vaso-constrictor to vaso-dilator. Two experiments were made on anæsthetised cats, both give similar results, but one was much more conclusive on the point at issue than the other, and here we shall speak of that only. The superior cervical ganglion was excised and the central end of the cervical sympathetic nerve was joined to the peripheral end of the lingual, which contains the chorda tympani fibres. After allowing time for union and regeneration of the nerves, the cervical sympathetic was stimulated; it caused prompt flushing of the sub-maxillary glands, and the effect was repeatedly obtained.


1983 ◽  
Vol 61 (7) ◽  
pp. 693-698 ◽  
Author(s):  
J. Jaramillo

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.


1890 ◽  
Vol 47 (286-291) ◽  
pp. 379-390 ◽  

It is well known that by stimulating the sympathetic nerve in the neck the following effects can be produced :—(1) Retraction of the nictitating membrane; (2) protrusion of the eyeball and opening of the eye; (3) turning the eye, if previous to stimulation the optic axis is directed nasally, so that the optic axis is directed straight forwards, or it may be forwards and a little outwards


1996 ◽  
Vol 75 (1) ◽  
pp. 514-517 ◽  
Author(s):  
D. F. Bossut ◽  
V. K. Shea ◽  
E. R. Perl

1. The effects of ipsilateral removal of the superior cervical ganglion on the subsequent responsiveness of C-fiber polymodal nociceptors (CPMs) of the ear to close-arterial injections of norepinephrine (NE) were evaluated in adult, anesthetized rabbits. 2. In normal unanesthetized rabbits, the two ears were usually at the same temperature. Immediately after the ganglionectomy, the ipsilateral ear was warmer; however, at the time of electrophysiological recordings (4-23 days) the majority of animals had the ipsilateral ear cooler by > or = 1 degree C, suggestive of denervation supersensitivity. 3. NE (50 ng) did not activate any CPMs (n = 28) from intact animals. 4. Seven of 22 CPMs recorded from sympathectomized ears were activated by NE (50 ng). The responses varied considerably but typically consisted of 2-4 impulses in the 60 s after the NE injection. In some instances, repetitive activity continued for many minutes. Such prolonged discharge differs from the adrenergic responses seen after partial nerve damage. 5. The induction of adrenergic excitability in CPMs by sympathectomy is suggested to be a counterpart to postsympathectomy neuralgia in human beings and a possible part of the mechanism leading to sympathetically related pain states.


Sign in / Sign up

Export Citation Format

Share Document