Central hyperglycaemic effect of adrenaline and carbachol

1985 ◽  
Vol 109 (4) ◽  
pp. 440-445 ◽  
Author(s):  
A. Iguchi ◽  
H. Matsunaga ◽  
M. Gotoh ◽  
T. Nomura ◽  
A. Yatomi ◽  
...  
Keyword(s):  
Cholinergic Neurons ◽  
Cerebral Ventricle ◽  
The Third ◽  
Hepatic Glucose ◽  
Anaesthetized Rats ◽  
The Central Nervous System ◽  
Glucagon And Insulin ◽  
Glucose Output ◽  
The Brain ◽  
Stimulation Of

Abstract. The effect of chemical stimulation of the brain on glucoregulation was studied in anaesthetized rats. Adrenaline, noradrenaline, acetylcholine, dopamine and carbachol (5 × 10−8 mol/μl saline) were injected directly into the third cerebral ventricle and changes in hepatic venous plasma glucose, immunoreactive glucagon and insulin concentrations were studied. The injection of adrenaline and carbachol into the third cerebral ventricle resulted in a marked hyperglycaemia associated with increased immunoreactive glucagon. Adrenaline-induced hyperglycaemia was not affected by bilateral adrenalectomy, while carbachol-induced hyperglycaemia was completely inhibited by adrenalectomy. The injection of somatostatin (1 × 10−9 mol) with adrenaline into the third cerebral ventricle did not influence adrenaline-induced hyperglycaemia, while carbachol-induced hyperglycaemia was inhibited by co-administration with somatostatin. These results suggest that adrenergic and cholinergic neurons in the central nervous system may increase hepatic glucose output by different mechanism.

Responses of hepatic glucose output to electro-acupuncture stimulation of the hindlimb in anaesthetized rats

2004 ◽  
Vol 115 (1-2) ◽  
pp. 7-14 ◽  
Author(s):  
Rie Shimoju-Kobayashi ◽  
Hitoshi Maruyama ◽  
Masashi Yoneda ◽  
Mieko Kurosawa
Keyword(s):  
Hepatic Glucose Output ◽  
Acupuncture Stimulation ◽  
Hepatic Glucose ◽  
Anaesthetized Rats ◽  
Glucose Output ◽  
Stimulation Of

scholarly journals III. Contributions to the anatomy of the central nervous system in vertebrated animals. Part I.—Ichthyopsida. Section I.—Pisces. Subsection III.—Dipnoi. On the brain of the Ceratodus forsteri

1888 ◽  
Vol 43 (258-265) ◽  
pp. 420-423
Keyword(s):  
Fourth Ventricle ◽  
Third Ventricle ◽  
Pia Mater ◽  
The Third ◽  
Lateral Ventricles ◽  
Large Size ◽  
General Arrangement ◽  
Tela Choroidea ◽  
The Central Nervous System ◽  
The Brain

The brain of Ceratodus has the following general arrangement:—The membrane which represents the pia mater is of great thickness and toughness; there are two regions where a tela choroidea is developed: one where it covers in the fourth ventricle, and the other where it penetrates through the third ventricle and separates the lateral ventricles from each other. The ventricles are all of large size, and the walls of the lateral ventricles are not completed by nervous tissue. The thalamence-phalon and the mesencephalon are narrow, and the medulla oblongata is wide.

scholarly journals STUDIES IN THE PATHOGENESIS OF EXPERIMENTAL DYSENTERY INTOXICATION

1960 ◽  
Vol 111 (2) ◽  
pp. 145-153 ◽  
Author(s):  
Abraham Penner ◽  
Alice Ida Bernheim
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Intravenous Administration ◽  
Shiga Toxin ◽  
Third Ventricle ◽  
Dosage Level ◽  
Ventricular System ◽  
The Third ◽  
The Central Nervous System ◽  
The Brain

The introduction of Shiga toxin into the ventricular system of the brain with major location in the third ventricle resulted in a response similar to that following the administration of the toxin either intravenously or by cross-circulation. The intravenous administration at the dosage level employed would have elicited no response. These observations lend support to the hypothesis that Shiga toxin activates some mechanisms in the central nervous system which are capable of producing visceral lesions. These mechanisms are those which control the vasomotor components of homeostasis. This hypothesis permits an explanation of the proximo-distal and intramural features of the lesion.

scholarly journals THE INTERACTION BETWEEN THE SYNAPSES OF A SINGLE MOTOR FIBER

1950 ◽  
Vol 34 (2) ◽  
pp. 137-145 ◽  
Author(s):  
C. A. G. Wiersma ◽  
R. S. Turner
Keyword(s):  
Natural Conditions ◽  
Functional Connection ◽  
Block Transmission ◽  
Single Motor ◽  
The Third ◽  
The Brain ◽  
Stimulation Of

It has been shown that stimulation of synapses of the giant motor fibers of the third roots of Cambarus clarkii can block transmission at other synapses located on the same fiber. Peripherally located synapses block most synapses which are more centrally located. The reverse is true in a small number of cases. Possible reasons for this difference are discussed. It was further found that the two medial giant fibers in fresh, carefully dissected, preparations show a functional connection in the brain. It is probable that, under natural conditions, both medial giant fibers are always active at the same time.

The Ferrier Lecture: The nature of central inhibition

1961 ◽  
Vol 153 (953) ◽  
pp. 445-476 ◽  
Keyword(s):  
Scientific Paper ◽  
Nobel Lecture ◽  
Central Inhibition ◽  
The Central Nervous System ◽  
Theoretical Paper ◽  
The Subject ◽  
The Brain ◽  
Synaptic Mechanisms ◽  
Scientific Life ◽  
Stimulation Of

I feel greatly honoured by the invitation to give the Ferrier Lecture. I attended the first Ferrier Lecture, given by Sherrington in 1929, and I learned from Sherrington to value and admire the pioneer contributions of David Ferrier to neurology. In choosing the subject of inhibition for my lecture I was prompted by the peculiar challenge that inhibition has presented to physiologists ever since it was first demonstrated by the Weber brothers in 1846 that stimulation of the vagus nerve could stop the heart and by Setchenov in 1863 that stimulation of areas in the brain could slow or prevent reflex responses of frog limbs. It was Sherrington who greatly extended and organized knowledge of inhibition in the central nervous system; first, by a series of remarkable investigations, and finally by a theoretical paper published by the Royal Society in 1925, in which excitation and inhibition were given equivalent status in the synaptic mechanisms controlling neuronal discharge. His interest in central inhibition continued to the end of his scientific life, and was the subject of his Nobel Lecture in 1932. I might mention that both my first scientific paper and my D.Phil. thesis were concerned with inhibition, and that I have continued to be more interested in the problem of synaptic inhibition than in any other aspect of neurophysiology. In recent years progress has been so rapid that our understanding of the nature of central inhibition is in several respects more complete than that of central excitation. This illumination has followed rather rapidly upon a long period of ingenious theorizing which is now only of historical interest

Hepatic glucose balance in response to direct stimulation of sympathetic nerves in the intact liver of cats

1978 ◽  
Vol 56 (6) ◽  
pp. 1022-1028 ◽  
Author(s):  
W. Wayne Lautt ◽  
Chong Wong
Keyword(s):  
Sympathetic Nerves ◽  
Direct Stimulation ◽  
Blood Flows ◽  
Parasympathetic Nerves ◽  
Hepatic Glucose ◽  
Simultaneous Activation ◽  
Glucose Output ◽  
Hepatic Nerves ◽  
Mixed Nerve ◽  
Stimulation Of

Changes in hepatic glucose balance in response to direct stimulation of the hepatic nerves were measured in cats. Simultaneous measurements were made of glucose concentrations entering and leaving the intact liver; this, combined with measured blood flows, allows calculation of hepatic glucose balance. Stimulation of the hepatic sympathetic nerves (8 Hz, 15 V, 1 ms) produced a rapid increase in hepatic glucose output that was statistically significant after 1 min and reached a peak 3–5 min after onset of stimulation, after which time the output declined somewhat. The half time for deactivation of the response was 1.8–2 min. Variability in the responses was largely accounted for by the variable control base lines measured immediately prior to stimulation. Those animals showing the highest basal output showed the least increase in output in response to the nerves. The response to stimulation of the mixed nerve trunk in the presence and absence of atropine (1 mg/kg, intraportal) was similar. Simultaneous activation of hepatic sympathetic and parasympathetic nerves therefore produces a purely sympathetic type of effect on net glucose balance across the liver. It was also shown that changes in net splanchnic output or simply in arterial – hepatic venous glucose differences are an adequate reflection of liver glucose balance under the currently tested responses.

scholarly journals Deep stimulation in neurosurgery

2019 ◽  
Vol 10 (1) ◽  
pp. 63-71
Author(s):  
Aleksandr A. Kalinkin ◽  
Alexey G. Vinokurov ◽  
Olga N. Kalinkina ◽  
Alexander S. Ilinykh ◽  
Andrey A. Bocharov ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Deep Brain Stimulation ◽  
High Risk ◽  
Brain Stimulation ◽  
Conservative Therapy ◽  
The Central Nervous System ◽  
The Brain ◽  
Deep Brain ◽  
Stimulation Of

The technique of deep brain stimulation is used to treat patients with various diseases of the central nervous system who are not amenable to conservative therapy, while open interventions in them are associated with a high risk of complications. In the review, we evaluate the efficiency of the deep stimulation of different regions of the brain in some pharmacoresistant forms of diseases.

Relative contributions of the nervous system and hormones to CNS-mediated hyperglycemia

1988 ◽  
Vol 255 (6) ◽  
pp. E920-E927 ◽  
Author(s):  
A. Iguchi ◽  
M. Gotoh ◽  
H. Matsunaga ◽  
A. Yatomi ◽  
A. Honmura ◽  
...  
Keyword(s):  
Nervous System ◽  
Insulin Secretion ◽  
Cholinergic Neurons ◽  
Suppressive Effect ◽  
Neural Activation ◽  
Glucose Response ◽  
The Central Nervous System ◽  
Total Glucose ◽  
Glucagon And Insulin ◽  
Intact Rats

We quantitatively determined the relative contributions of hormonal factors and the nervous system to the total glucose response after stimulation of the cholinergic neurons in the central nervous system of fed rats. Hepatic venous plasma glucose, glucagon, insulin, epinephrine, and norepinephrine were measured during 120 min after injection of neostigmine (5 X 10(-8) mol) into the third cerebral ventricle in rats subjected to bilateral adrenodemedullation (ADMX) to prevent epinephrine secretion (observed insulin secretion), with and without intravenous infusion of somatostatin to prevent glucagon and insulin secretion. Injection of neostigmine in intact rats resulted in increases in glucose, glucagon, epinephrine, and norepinephrine. Comparison of glucose areas suggests that 22% of the hyperglycemic response is due to the glucagon effect, that 29% is due to the epinephrine effect, and that an unknown factor other than epinephrine or glucagon, which may include activation through direct neural innervation of the liver via alpha-adrenergic receptor, contributes 49%. The suppressive effect of epinephrine on insulin secretion, which is potentially stimulated by direct neural activation of the pancreas, contributes 18% of the net hyperglycemia.

Gastric inhibitory polypeptide: a gut hormone with anabolic functions

1989 ◽  
Vol 2 (3) ◽  
pp. 169-174 ◽  
Author(s):  
B. Beck
Keyword(s):  
Adipose Tissue ◽  
Intestinal Secretion ◽  
Gastric Inhibitory Polypeptide ◽  
Metabolic Effects ◽  
Gastrointestinal Hormone ◽  
Peripheral Tissues ◽  
Gut Hormone ◽  
Hepatic Glucose ◽  
Glucose Output ◽  
The Brain

Summary The gastrointestinal hormone, gastric inhibitory polypeptide (GIP), has been isolated and characterized because of its enterogastrone-type effects. It is also named glucose-dependent insulinotropic polypeptide and is actually considered to be the main incretin factor of the entero-insular axis. Besides these well-described effects on gastric secretion and pancreatic β cells, it also has direct metabolic effects on other tissues and organs, such as adipose tissue, liver, muscle, gastrointestinal tract and brain. In adipose tissue it is involved in the activation and regulation of lipoprotein lipase (LPL); it also inhibits glucagon-induced lipolysis and potentiates the effect of insulin on incorporation of fatty acids into triglycerides. It may play a role in the development of obesity because of the hypersensitivity of adipose tissue of obese animals to some of these actions. In the liver it does not modify insulin extraction, and its incretin effects are due only to the stimulation of insulin secretion and synthesis. It reduces hepatic glucose output and inhibits glucagon-stimulated glycogenolysis. It might increase glucose utilization in peripheral tissues such as muscle. GIP also has an effect on the volume and/or electrolyte composition of intestinal secretion and saliva. The functional importance of its effect on the hormones of the anterior pituitary lobe remains to be established, as it has never been detected in the brain. Its links with insulin are very close and the presence of insulin is sometimes necessary for the greater efficiency of both hormones. GIP can be considered as a true metabolic hormone, with most of its functions tending to increase anabolism.

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