Hyperglycemia induced by electrical stimulation of lateral part of dorsal parabrachial nucleus

1988 ◽  
Vol 254 (4) ◽  
pp. E468-E475
Author(s):  
T. Fujiwara ◽  
K. Nagai ◽  
S. Takagi ◽  
H. Nakagawa
Keyword(s):  
Electrical Stimulation ◽  
Glucagon Secretion ◽  
Light Period ◽  
Parabrachial Nucleus ◽  
Lateral Part ◽  
Beta Adrenergic ◽  
Adrenergic Mechanism ◽  
Adrenergic Blocker ◽  
Bilateral Lesions ◽  
Stimulation Of

Electrical stimulation of the lateral part of the dorsal parabrachial nucleus (PBD) induces hyperglycemia by enhancing glucagon secretion and suppressing insulin secretion in rats. The mechanism of this effect in the light period was examined by use of blockers of the autonomic nervous system. Hexamethonium, a ganglion blocker, and propranolol, a beta-adrenergic blocker, markedly inhibited the hyperglycemic response to stimulation of the lateral part of the PBD (LPBD). In contrast, phenoxybenzamine, an alpha-adrenergic blocker, and atropine methylnitrate, a muscarinic blocker, had no effect. Because previous studies showed that bilateral lesions of the suprachiasmatic nucleus (SCN) eliminated hyperglycemia induced by intracranial injection of 2-deoxy-D-glucose and that blinding largely suppressed the hyperglycemia, the effects of these two treatments on hyperglycemia induced by electrical stimulation of the LPBD were examined. SCN lesions abolished the hyperglycemic response but did not affect the hyperglucagonemic response. Results 4 wk after orbital enucleation were similar to those after SCN lesions. These findings suggest that the SCN and a beta-adrenergic mechanism are involved in the hyperglycemic response to LPBD stimulation.

scholarly journals Electrical Stimulation of the Lateral Part of the Dorsal Parabrachial Nucleus Causes Hyperglycemia

1987 ◽  
Vol 3 (3) ◽  
pp. 209-216 ◽  
Author(s):  
Hidetoshi INO ◽  
Katsuya NAGAI ◽  
Tsutomu FUJIWARA ◽  
Mariko YAMANO ◽  
Shinobu INAGAKI ◽  
...  
Keyword(s):  
Electrical Stimulation ◽  
Parabrachial Nucleus ◽  
Lateral Part ◽  
Stimulation Of

In vivo stimulation of pancreatic hormone secretion by norepinephrine infusion in the dog

1984 ◽  
Vol 246 (4) ◽  
pp. E339-E343 ◽  
Author(s):  
G. Ribes ◽  
E. R. Trimble ◽  
J. P. Blayac ◽  
C. B. Wollheim ◽  
M. M. Loubatieres-Mariani
Keyword(s):  
Insulin Secretion ◽  
Blood Glucose Concentration ◽  
Hormone Secretion ◽  
Glucagon Secretion ◽  
High Dose ◽  
Venous Blood Flow ◽  
Neural Pathways ◽  
Beta Adrenergic ◽  
Adrenergic Mechanism ◽  
Stimulation Of

Norepinephrine is generally regarded as an inhibitor of insulin release. It has been shown, however, that under hyperglycemic circumstances, norepinephrine infused at a high dose may also stimulate insulin secretion. The goals of this study were, under normoglycemic conditions, to confirm this stimulatory effect and to determine whether a beta-adrenergic mechanism or central neural pathways were involved. Secretion of pancreatic somatostatin and glucagon were also studied. Fasted, anesthetized dogs had norepinephrine (2 micrograms X kg-1 X min-1) infused into a peripheral vein for 60 min; blood was sampled from the pancreaticoduodenal vein. Norepinephrine stimulated insulin, somatostatin, and glucagon secretion without significant changes in either blood glucose concentration or pancreaticoduodenal venous blood flow. The stimulatory effect of norepinephrine on the three hormones was abolished by propranolol pretreatment, thus implicating a beta-adrenergic mechanism. Because bilateral cervical vagotomy prevented stimulation of insulin secretion by norepinephrine, central neural pathways must have been involved in the stimulatory process. However, norepinephrine-induced glucagon secretion was not decreased by vagotomy, showing that the stimulation was due to either a direct action on the pancreatic A cell or of a central pathway not mediated via the vagus nerve. Norepinephrine-induced somatostatin secretion was partly reduced by vagotomy, indicating that several mechanisms could be implicated.

Mechanism of sympathetic neural regulation of insulin, somatostatin, and glucagon secretion

1990 ◽  
Vol 258 (1) ◽  
pp. E220-E227 ◽  
Author(s):  
T. Kurose ◽  
Y. Seino ◽  
S. Nishi ◽  
K. Tsuji ◽  
T. Taminato ◽  
...  
Keyword(s):  
Glucagon Secretion ◽  
Fold Increase ◽  
Splanchnic Nerve ◽  
Stimulatory Action ◽  
Perfused Rat Pancreas ◽  
Rat Pancreas ◽  
Adrenergic Mechanism ◽  
Adrenergic Activation ◽  
Splanchnic Nerve Stimulation ◽  
Stimulation Of

The effects of electrical stimulation of the left splanchnic nerve on insulin, somatostatin, and glucagon secretion from the isolated perfused rat pancreas were investigated. Electrical splanchnic nerve stimulation (SNS), performed by square-wave impulses, produced a 25% decrease in effluent flow and a 10-fold increase in perfusate norepinephrine. Both insulin and somatostatin output in the presence of 16.7 mM glucose were inhibited during SNS by 85 and 56% of the basal value, respectively. Glucagon output in the presence of 5.5 mM glucose was stimulated 20-fold by SNS. Perfusion with 10(-6) M propranolol further decreased insulin and somatostatin output during SNS, when expressed as the total decrement beneath basal during stimulation. The glucagon response to SNS tended to be enhanced, although not significantly, by simultaneous infusion of 10(-6) M propranolol. However, 10(-6) M phentolamine (Phe) attenuated the SNS-induced inhibition of insulin and somatostatin output by 50 and 40%, respectively. However, insulin output remained decreased after SNS with Phe. The SNS-induced glucagon response was completely abolished by 10(-6) M Phe alone or by 10(-6) M Phe plus 10(-6) M propranolol. With 10(-6) M Phe plus 10(-6) M propranolol, insulin and somatostatin output remained decreased after SNS. These results suggest that insulin and somatostatin secretions induced by glucose are inhibited during SNS through the alpha-adrenergic mechanism and also that the beta-adrenergic mechanism exerts a stimulatory action. SNS-induced glucagon secretion occurs mainly through alpha-adrenergic activation.(ABSTRACT TRUNCATED AT 250 WORDS)

Electrical stimulation of the parabrachial nucleus induces reanimation from isoflurane general anesthesia

2016 ◽  
Vol 306 ◽  
pp. 20-25 ◽  
Author(s):  
Fanuel Muindi ◽  
Jonathan D. Kenny ◽  
Norman E. Taylor ◽  
Ken Solt ◽  
Matthew A. Wilson ◽  
...  
Keyword(s):  
Electrical Stimulation ◽  
General Anesthesia ◽  
Parabrachial Nucleus ◽  
Stimulation Of

Mesencephalic mechanisms for integration of female reproductive behavior in the rat

1979 ◽  
Vol 237 (5) ◽  
pp. R285-R290 ◽  
Author(s):  
Y. Sakuma ◽  
D. W. Pfaff
Keyword(s):  
Electrical Stimulation ◽  
Mesencephalic Reticular Formation ◽  
Female Rats ◽  
Motor Systems ◽  
Cuneiform Nucleus ◽  
Electrolytic Lesions ◽  
The Difference ◽  
Central Gray ◽  
Bilateral Lesions ◽  
Stimulation Of

Placement of bilateral electrolytic lesions in the mesencephalic central gray (CG) of estrogen-primed ovariectomized female rats produced an immediate decline in performance of the lordosis reflex. Lesions that destroyed the dorsal half of the CG and the adjacent subtectal region were effective. The decrease in individual animals in terms of the lordosis reflex score ranged from 20 to 100% of the prelesion performance. Such lesions abolished the facilitation of lordosis by electrical stimulation of the ventromedial nucleus of the hypothalamus. Similar abrupt losses of lordosis followed bilateral lesions of either a) the area between CG and the cuneiform nucleus of the mesencephalic reticular formation (NCf); or b) the ventrolateral quadrant of the NCf. The difference between these two lesions was that the effect of the latter could be overridden by electrical stimulation of the CG, whereas that of the former could not. We conclude that the CG is an important supraspinal component of the circuit for lordosis behavior, constituting a link between ascending somatosensory and descending motor systems for lordosis. It probably facilitates lordosis when activated by behaviorally relevant peripheral somatosensory and/or ventromedial hypothalamic inputs.

Widespread reductions in cerebral blood flow and metabolism elicited by electrical stimulation of the parabrachial nucleus in rat

1985 ◽  
Vol 341 (2) ◽  
pp. 283-296 ◽  
Author(s):  
Sima Mraovitch ◽  
Costantino Iadecola ◽  
David A. Ruggiero ◽  
Donald J. Reis
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Electrical Stimulation ◽  
Parabrachial Nucleus ◽  
Stimulation Of

Cocaine-enhanced arrhythmogenesis: neural and nonneural mechanisms

1992 ◽  
Vol 70 (2) ◽  
pp. 240-246 ◽  
Author(s):  
Nicholas S. Gantenberg ◽  
Gilbert R. Hageman
Keyword(s):  
Electrical Stimulation ◽  
Sudden Cardiac Death ◽  
Cardiac Death ◽  
Ventricular Arrhythmias ◽  
Cardiovascular Complications ◽  
Programmed Electrical Stimulation ◽  
Calcium Channel Blockade ◽  
Adrenergic Mechanism ◽  
Cocaine Infusion ◽  
Stimulation Of

Cocaine abuse increases the susceptibility to cardiovascular complications and sudden cardiac death in man. We used programmed electrical stimulation of the heart to examine the arrhythmogenic influence of cocaine. Twenty-three pentobarbital-anesthetized adult dogs underwent programmed electrical stimulation using one to four extrastimuli before and during cocaine infusion. Autonomic decentralization was performed prior to the protocol in eight dogs. Induced ventricular arrhythmias included single premature ventricular depolarizations, doublets, triplets, ventricular tachycardia, and ventricular fibrillation. Intravenous cocaine, and subsequent adrenergic and muscarinic receptor blockade, or calcium channel blockade were evaluated for their influence on arrhythmogenesis. The incidence of induced ventricular arrhythmias was significantly elevated following cocaine and was reduced following propranolol and atropine. Verapamil, however, did not reduce the incidence of induced arrhythmias. In addition, cocaine significantly increased arrhythmia induction in decentralized animals, but propranolol, atropine, and phentolamine failed to reduce the proarrhythmic effects of cocaine in these animals. Thus, cocaine has a proarrhythmic effect on the heart with multiple mechanisms. The adrenergic mechanism appears to be a result of neurotransmitter uptake blockade, whereas the likely ionic mechanism is a neurally independent, direct effect on the heart.Key words: cocaine, programmed electrical stimulation, ventricular arrhythmias, sympathetic nervous system, sudden cardiac death.

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