scholarly journals VII. On the progressive paralysis of the different classes of nerve cells in the superior cervical ganglion

1890 ◽  
Vol 47 (286-291) ◽  
pp. 379-390 ◽  
Keyword(s):  
Superior Cervical Ganglion ◽  
Sympathetic Nerve ◽  
Nerve Cells ◽  
Optic Axis ◽  
Nictitating Membrane ◽  
Cervical Ganglion

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

scholarly journals On the effects of joining the cervical sympathetic nerve with the chorda tympani.

1904 ◽  
Vol 73 (488-496) ◽  
pp. 99-99
Author(s):  
John Newport Langley ◽  
Hugh Kerr Anderson
Keyword(s):  
Peripheral Nerve ◽  
Blood Vessels ◽  
Superior Cervical Ganglion ◽  
Sympathetic Nerve ◽  
Nerve Cells ◽  
The Other ◽  
Chorda Tympani ◽  
Cervical Ganglion ◽  
Cervical Sympathetic ◽  
Cervical Sympathetic Nerve

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.

The Actions of Polymyxin B and Histamine on Ganglionic Transmission

1972 ◽  
Vol 50 (8) ◽  
pp. 824-831 ◽  
Author(s):  
H. E. Brezenoff ◽  
S. B. Gertner
Keyword(s):  
Superior Cervical Ganglion ◽  
Action Potentials ◽  
Polymyxin B ◽  
Low Doses ◽  
Nictitating Membrane ◽  
Contrast Administration ◽  
Blocking Effects ◽  
Cervical Ganglion ◽  
Ganglionic Transmission ◽  
Higher Doses

The ganglionic effects of histamine and the histamine-liberating agent polymyxin B were studied in the cat. Nictitating membrane contractions and postganglionic action potentials were used to monitor the actions of these drugs on the superior cervical ganglion. Close arterial injections of low doses of histamine (1 μg) directly stimulated the ganglion while considerably higher doses (above 300 μg) caused a block of transmission. The two effects were due to separate and independent mechanisms. In contrast, administration of polymyxin B (100–500 μg) only caused ganglion block.The effects of histamine on the ganglion were prevented by chlorpheniramine while those of polymyxin B were potentiated by this antihistamine. The results of this study indicate that the ganglion blocking effects of polymyxin B are not mediated by released ganglionic histamine.

Supersensitivity of denervated superior cervical ganglion to acetylcholine

1960 ◽  
Vol 198 (5) ◽  
pp. 949-954 ◽  
Author(s):  
Shu Chien
Keyword(s):  
Superior Cervical Ganglion ◽  
The Other ◽  
Nictitating Membrane ◽  
Indirect Determination ◽  
Cervical Sympathetic Trunk ◽  
Cervical Ganglion ◽  
Cervical Sympathetic ◽  
Two Sides

The supersensitivity of denervated superior cervical ganglion to acetylcholine was studied in cats at 2 weeks after the section of cervical sympathetic trunk on one side, with the other side as a control. The control ganglion required about four times as much of acetylcholine as the denervated side, in order to release the same amount of norepinephrine at the postganglionic endings. The relative quantity of norepinephrine released on acetylcholine administration to ganglia was determined indirectly by using the in vivo nictitating membrane as an indicator, whose responses to various doses of norepinephrine had been calibrated. The validity of such indirect determination of norepinephrine was shown by experiments in which the eyeballs were removed or the lever magnifications were made unequal. With control cats in which both cervical sympathetic trunks were cut acutely, the sensitivity of the ganglia on two sides to acetylcholine was almost equal.

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.

An AF-DX 116 sensitive inhibitory mechanism modulates nicotinic and muscarinic transmission in cat superior cervical ganglion in the presence of anticholinesterase

1992 ◽  
Vol 70 (12) ◽  
pp. 1535-1541 ◽  
Author(s):  
M. Bachoo ◽  
C. Polosa
Keyword(s):  
Action Potential ◽  
Receptor Antagonist ◽  
Muscarinic Receptor ◽  
Superior Cervical Ganglion ◽  
Cholinesterase Activity ◽  
Compound Action Potential ◽  
Arterial Supply ◽  
Nictitating Membrane ◽  
Cervical Ganglion ◽  
Compound Action

The effect of the muscarinic receptor antagonist AF-DX 116 on the inhibitory action of muscarinic agonists and on responses mediated by nicotinic or muscarinic ganglionic transmission was studied in the superior cervical ganglion of the anesthetized cat. The postganglionic compound action potential evoked by cervical sympathetic trunk stimulation was depressed by methacholine or acetylcholine (ACh) injected into the ganglionic arterial supply. The depression was blocked by AF-DX 116. The compound action potentials evoked by preganglionic stimulus trains were also depressed when the intratrain frequency was 2 Hz or greater. This intratrain depression was, however, insensitive to AF-DX 116. The anticholinesterase drug physostigmine markedly enhanced the intratrain depression of the compound action potential. This effect was reversed by AF-DX 116. During nicotinic receptor block with hexamethonium, preganglionic stimulus trains with intratrain frequencies of 5 Hz or greater produced nictitating membrane contractions that could be blocked by the M1 muscarinic receptor antagonist pirenzepine. The amplitude of the contractions increased with frequency and reached a maximum at 20–40 Hz. AF-DX 116 had no effect on these responses. After administration of physostigmine, the amplitude of the nictitating membrane responses decreased with increasing intratrain frequency. AF-DX 116 reversed this effect. The data suggest that, in the superior cervical ganglion, AF-DX 116 sensitive muscarinic receptors which depress synaptic transmission are activated by exogenous agonists but not by the ACh released by the preganglionic axon terminals unless cholinesterase activity is inhibited. This may result from the fact that these receptors, although accessible to agonists injected into the ganglionic arterial supply, are remote from synaptic release sites and that, under normal conditions, cholinesterase activity prevents sufficient activation of these receptors by the nerve-released ACh to result in modulation of synaptic transmission.Key words: muscarinic inhibition, M2 receptors, sympathetic ganglion modulation.

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