Synaptic transmission in the chronically decentralized middle cervical and stellate ganglia of the dog

1983 ◽  
Vol 61 (10) ◽  
pp. 1149-1155 ◽  
Author(s):  
J. A. Armour
Keyword(s):  
Central Nervous System ◽  
Action Potentials ◽  
Autonomic Nerves ◽  
Autonomic Ganglia ◽  
Afferent Nerves ◽  
Stellate Ganglia ◽  
Compound Action Potentials ◽  
The Central Nervous System ◽  
Compound Action ◽  
Stimulation Of

Afferent stimulation of one thoracic cardiopulmonary nerve generated compound action potentials in the efferent axons of other ipsilateral cardiopulmonary nerves in dogs, 14 days after their thoracic autonomic ganglia had been decentralized. The compound action potentials were influenced by the frequency of activation and (in 5 of 12 dogs) by pharmacological autonomic blocking agents (hexamethonium, atropine, phentolamine, and propranolol). Moreover, they were abolished transiently when chymotrypsin was injected locally into the ganglia, and extendedly when manganese was injected. Thus, synapses that can be activated by stimulation of afferent nerves exist in chronically decentralized thoracic autonomic nerves and ganglia. It is proposed that regulation of the heart and lungs occurs in part via thoracic autonomic neural elements independent of the central nervous system.

Synaptic transmission in thoracic autonomic ganglia of the dog

1983 ◽  
Vol 61 (8) ◽  
pp. 793-801 ◽  
Author(s):  
J. A. Armour
Keyword(s):  
Neural Activity ◽  
Action Potentials ◽  
Compound Action Potentials ◽  
Cervical Ganglion ◽  
Cervical Ganglia ◽  
Frequency Of Stimulation ◽  
Synaptic Mechanisms ◽  
Adrenergic And Cholinergic Receptors ◽  
Compound Action ◽  
Stimulation Of

Afferent stimulation of one canine thoracic cardiopulmonary nerve can generate compound action potentials in another ipsilateral cardiopulmonary nerve. These compound action potentials persist after acute decentralization of the middle cervical ganglion, indicating that they result from neural activity in the middle cervical ganglion and thoracic nerves. Changing the frequency of stimulation can alter the compound action potentials, suggesting that temporal facilitation or inhibition occurs in this middle cervical ganglion preparation. The compound action potentials can be modified by stimulation of sympathetic preganglionic fibers and by hexamethonium, atropine, phentolamine, propranolol, and (or) manganese. It thus appears that afferent cardiopulmonary nerves can activate efferent cardiopulmonary nerves via synaptic mechanisms in the stellate and middle cervical ganglia. It also appears that these mechanisms involve adrenergic and cholinergic receptors and are influenced by preganglionic sympathetic fibers arising from the cord.

Stretch of mammalian nerve in vitro: Effect on compound action potentials

2000 ◽  
Vol 5 (4) ◽  
pp. 227-235 ◽  
Author(s):  
Sidney Ochs ◽  
Rahman Pourmand ◽  
Kenan Si ◽  
Richard N. Friedman
Keyword(s):  
Action Potentials ◽  
Compound Action Potentials ◽  
Vitro Effect ◽  
Mammalian Nerve ◽  
Compound Action

scholarly journals Site of cochlear stimulation and its effect on electrically evoked compound action potentials using the MED-EL standard electrode array

2009 ◽  
Vol 8 (1) ◽  
pp. 40 ◽  
Author(s):  
Stefan Brill ◽  
Joachim Müller ◽  
Rudolf Hagen ◽  
Alexander Möltner ◽  
Steffi-Johanna Brockmeier ◽  
...  
Keyword(s):  
Action Potentials ◽  
Electrode Array ◽  
Compound Action Potentials ◽  
Compound Action

Using Evoked Compound Action Potentials to Assess Activation of Electrodes and Predict C-Levels in the Tempo+ Cochlear Implant Speech Processor

2010 ◽  
Vol 31 (1) ◽  
pp. 134-145 ◽  
Author(s):  
Isaac Alvarez ◽  
Angel de la Torre ◽  
Manuel Sainz ◽  
Cristina Roldán ◽  
Hansjoerg Schoesser ◽  
...  
Keyword(s):  
Cochlear Implant ◽  
Action Potentials ◽  
Speech Processor ◽  
Compound Action Potentials ◽  
Compound Action

scholarly journals VI. —Anaphylaxis and anaphylatoxins

1923 ◽  
Vol 211 (382-390) ◽  
pp. 273-315 ◽  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Guinea Pig ◽  
Anaphylactic Shock ◽  
The Body ◽  
Muscle Fibres ◽  
Direct Stimulation ◽  
Fundamental Conception ◽  
The Central Nervous System ◽  
Stimulation Of

In the study of the phenomena of anaphylaxis there are certain points on which some measure of agreement seems to have been attained. In the case of anaphylaxis to soluble proteins, with which alone we are directly concerned in this paper, the majority of investigators probably accept the view that the condition is due to the formation of an antibody of the precipitin type. Concerning the method, however, by which the presence of this antibody causes the specific sensitiveness, the means by which its interaction with the antibody produces the anaphylactic shock, there is a wide divergence of conception. Two main currents of speculation can be discerned. One view, historically rather the earlier, and first put forward by Besredka (1) attributes the anaphylactic condition to the location of the antibody in the body cells. There is not complete unanimity among adherents of this view as to the nature of the antibody concerned, or as to the class of cells containing it which are primarily affected in the anaphylactic shock. Besredka (2) himself has apparently not accepted the identification of the anaphylactic antibody with a precipitin, but regards it as belonging to a special class (sensibilisine). He also regards the cells of the central nervous system as those primarily involved in the anaphylactic shock in the guinea-pig. Others, including one of us (3), have found no adequate reason for rejecting the strong evidence in favour of the precipitin nature of the anaphylactic antibody, produced by Doerr and Russ (4), Weil (5), and others, and have accepted and confirmed the description of the rapid anaphylactic death in the guinea-pig as due to a direct stimulation of the plain-muscle fibres surrounding the bronchioles, causing valve-like obstruction of the lumen, and leading to asphyxia, with the characteristic fixed distension of the lungs, as first described by Auer and Lewis (6), and almost simultaneously by Biedl and Kraus (7). But the fundamental conception of anaphylaxis as due to cellular location of an antibody, and of the reaction as due to the union of antigen and antibody taking place in the protoplasm, is common to a number of workers who thus differ on details.

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