Synapses of adrenergic fibres

1971 ◽  
Vol 27 (3) ◽  
pp. 280-281 ◽  
Author(s):  
G. Gabella
Keyword(s):  
Adrenergic Fibres

scholarly journals Adrenergic fibres in the human intestine.

Gut ◽  
1968 ◽  
Vol 9 (6) ◽  
pp. 678-682 ◽  
Author(s):  
L Capurso ◽  
C A Friedmann ◽  
A G Parks
Keyword(s):  
Human Intestine ◽  
Adrenergic Fibres

Autonomic Innervation of Pancreas in Egyptian Spiny Mouse (Acomys cahirinus, Desmarest)

2009 ◽  
Vol 78 (4) ◽  
pp. 557-561
Author(s):  
Aleksander Szczurkowski ◽  
Jacek Kuchinka ◽  
Elzbieta Nowak ◽  
Tadeusz Kuder
Keyword(s):  
Pancreatic Duct ◽  
Pancreatic Islets ◽  
Comparative Anatomy ◽  
Glyoxylic Acid ◽  
Autonomic Innervation ◽  
Autonomic Ganglia ◽  
Acomys Cahirinus ◽  
Adrenergic Structures ◽  
Adrenergic Fibres ◽  
Head Of Pancreas

The aim of the study was to obtain details of the morphology of the autonomic innervation of pancreas. Six adult Egyptian spiny mice (Acomys cahirinus, Desmarest) were studied for the presence and location of autonomic fibres and cells in the pancreas. The macromorphological investigations were performed using the thiocholine method adapted for this type of specimens. For processing tissues two histochemical techniques were used: thiocholine method on activity of AChE and the glyoxylic acid method for adrenergic structures. Cholinergic fibres and small autonomic ganglia were found among the secretory sections and along the pancreatic duct and both pancreaticoduodenal arteries, and its branches, reaching the Langerhans islets and forming around them a kind of net. From 24 to 40 AChE-positive ganglions in the whole exocrine part were observed. The highest density of cholinergic fibres was observed in the head of pancreas. Numerous adrenergic fibres that accompanied blood vessels as well as interlobular and intralobular ducts were found inside the exocrine parts of the pancreas. Neither adrenergic cells or adrenergic fibres were observed inside the pancreatic islets. Our results can be used in comparative anatomy studies of pancreas in mammals.

Regulation of the M current: transduction mechanism and role in ganglionic transmission

1992 ◽  
Vol 70 (S1) ◽  
pp. S12-S18 ◽  
Author(s):  
Peter A. Smith ◽  
Hsinyo Chen ◽  
Dmitry E. Kurenny ◽  
Alexander A. Selyanko ◽  
Jeffrey A. Zidichouski
Keyword(s):  
Sympathetic Ganglia ◽  
Cellular Level ◽  
Autonomic Nerve ◽  
Spontaneous Discharge ◽  
Excitatory Postsynaptic Potential ◽  
Parasympathetic Ganglia ◽  
Transduction Mechanism ◽  
M Current ◽  
Adrenergic Fibres ◽  
Paravertebral Sympathetic Ganglia

Slow excitatory postsynaptic potentials in sympathetic ganglia often involve suppression of a voltage-dependent potassium current termed the M current. This current is suppressed by the muscarinic action of acetylcholine, by peptides such as luteinizing hormone releasing hormone, and sometimes by α-adrenoceptor agonists. Activation of β-adrenoceptors sometimes produces weak potentiation. The voltage dependence of the M current is such that its suppression increases the excitability of ganglionic neurones. Since this sometimes leads to spontaneous discharge, activation of the slow excitatory postsynaptic potential mechanism (or modulation of M current) within a sympathetic ganglion produces effects that manifest in the autonomic outflow to the target organ. In frogs, M currents are present in the neurones of both paravertebral sympathetic ganglia and cardiac parasympathetic ganglia. Since the M current is suppressed by adrenaline in the parasympathetic ganglia and these ganglia often receive adrenergic fibres from sympathetic ganglia, this might reflect an important means of interaction between the two branches of the autonomic system. At the cellular level, M-current suppression is little affected by drugs that interfere with membrane phosphorylation–dephosphorylation processes. This observation is discussed in relationship to the current understanding of the transduction mechanism for agonist-induced M-current suppression.Key words: autonomic nerve, K+ channel, G protein, muscarinic mechanism, adrenergic mechanism.

scholarly journals Pharmacology and Nerve-Endings

1935 ◽  
Vol 28 (3) ◽  
pp. 319-332 ◽  
Author(s):  
Henry Dale
Keyword(s):  
Motor Nerve ◽  
Memorial Lecture ◽  
Autonomic Nerves ◽  
Scientific Career ◽  
Nerve Fibres ◽  
Organic Bases ◽  
Release Of Acetylcholine ◽  
Special Mention ◽  
Adrenergic Fibres ◽  
New Evidence

A brief account is given of the scientific career of Walter Ernest Dixon, and of the importance of his work and his influence for the development of Pharmacology in England. It is suggested that the Memorial Lecture may appropriately deal with some matter of new interest, from one of the fields of research in which Dixon himself was active. Special mention is made of his work with Brodie on the physiology and pharmacology of the bronchioles and the pulmonary blood-vessels, as probably showing the beginning of Dixon's interest in the actions of the alkaloids and organic bases which reproduce the effects of autonomic nerves. An account is given of Dixon's early interest in the suggestion, first made by Elliott, that autonomic nerves transmit their effects by releasing, at their endings, specific substances, which reproduce their actions; and of his attempt to obtain experimental support for this conception. After the War it was established by the experiments of O. Loewi; and it is now generally recognized that parasympathetic effects are so transmitted by release of acetylcholine, sympathetic effects by that of a substance related to adrenaline. Very recent evidence indicates that acetylcholine, by virtue of its other (“nicotine-like”) action, also acts as transmitter of activity at synapses in autonomic ganglia, and from motor nerve to voluntary muscle. The terms “cholinergic” and “adrenergic” have been introduced to describe nerve-fibres which transmit their actions by the release at their endings of acetylcholine, and of a substance related to adrenaline, respectively. It is shown that Langley and Anderson's evidence, long available, as to the kinds of peripheral efferent fibres which can replace one another in regeneration, can be summarized by the statement, that cholinergic can replace cholinergic fibres, and that adrenergic can replace adrenergic fibres; but that fibres of different chemical function cannot replace one another. The bearing of this new evidence on conceptions of the mode of action of “neuromimetic” drugs is discussed. The pharmacological problem can now be more clearly defined, and Dixon's participation in further attempts at its solution will be sadly missed.

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