Experimental Lesions in the Tuber Cinereum of the Dog

Morgan, Lawrence O.

doi:10.1001/archneurpsyc.1930.02220160032004

Arch NeurPsych

1930

DOI: 10.1001/archneurpsyc.1930.02220160032004

|View full text |Cite

Experimental Lesions in the Tuber Cinereum of the Dog

Lawrence O. Morgan¹

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...

Citation Types

Supporting

Mentioning

Contrasting

Year Published

1930

1994

Publication Types

Select...

Article6

Relationship

Self Cite0

Independent6

Authors

Journals

Cited by 16 publications

(1 citation statement)

References 17 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…At that time, they proposed that the enhanced sympathetic activity was likely due to glucopenia "local" to the autonomic nervous system. This position was supported by the earlier work of Claude Bernard (2) and others (3,4), demonstrating that lesions to specific aspects ofthe brain had a profound impact on glucose metabolism. The existence of specific "glucoreceptors" within the hypothalamus was later proposed by Mayer and Marshall (5).…”

mentioning

confidence: 59%

Primacy of liver glucosensors in the sympathetic response to progressive hypoglycemia.

Donovan

Hamilton-Wessler

Halter

et al. 1994

Proc. Natl. Acad. Sci. U.S.A.

View full text Add to dashboard Cite

The impact of hepatic glucose concentration on the sympathetic response to progressive hypoglycemia was examined in chronically cannulated conscious male dogs (n = 6). Graded hypoglycemia was induced via peripheral insulin infusion (30 pmol kg-1-min-1) with either peripheral (PER) or portal (POR) glucose infusion. Over the 260-min experimental period, arterial glycemia was adjusted from 5.2 ± 0.1 to 2.5 ± 0.1 mM in decrements of %0.5 mM every 40 min. Arterial glycemias were not sigfntly different between PER and POR at any measured level. However, hepatic glycemia was signiicantly elevated at all times during POR (8.4 ± 0.8 to 3.4 ± 0.2 mM) when compared to PER (5.2 ± 0.2 to 2.5 ± 0.1 mM). Plasma epinephrine values were significantly greater during PER vs. POR at all arterial glycemias below 4.0 mM. At the lowest level of arterial glycemia studied (2.5 ± 0.2 mM) the epinephrine response above basal was 3-fold greater for PER (8.7 ± 1.7 nM) when compared to POR (2.6 ± 0.6 nM) (P < 0.01). Plasma norepinephrine results were similar for the two protocols, with PER demonstrating a 3-fold greater response above basal when compared to POR at 2.5 mM arterial glycemia (P < 0.05). While the sympathetic response was markedly different between protocols when expressed as a function of arterial glycemia, when expressed as a function of hepatic glycemia this discrepancy was largely eliminated. This latter observation supports the liver as the primary locus for glycemic detection relevant to the sympathoadrenal response when hypoglycemia develops slowly-i.e., over a period of 2-3 h. A comparison of the current findings with our previous observations suggests that the hepatic glucosensors may play a greater role in hypoglycemic counterregulation as the rate of fall in glycemia is less.In 1924 Walter B. Cannon and coworkers (1) provided the first convincing evidence that insulin-induced hypoglycemia resulted in increased sympathetic output. At that time, they proposed that the enhanced sympathetic activity was likely due to glucopenia "local" to the autonomic nervous system. This position was supported by the earlier work of Claude Bernard (2) and others (3, 4), demonstrating that lesions to specific aspects ofthe brain had a profound impact on glucose metabolism. The existence of specific "glucoreceptors" within the hypothalamus was later proposed by Mayer and Marshall (5). Subsequent studies in which direct microinjections were used have now clearly identified glucosensitive neurons within the ventromedial and lateral hypothalamus (6). In addition, substantial evidence has accumulated over the years delineating the efferent capacity of the central nervous system (CNS) to impact upon glucoregulation (6,7). This has led to the prevailing concept that the brain "senses" ambient glycemia and effects the requisite glucoregulatory mechanisms.Evidence for the role of the CNS in glycemic detection has relied largely on nonphysiological stimuli, such as brain lesions, electrical stimulation, glucose analogues, and direct (in th...

show abstract

mentioning

confidence: 59%

Primacy of liver glucosensors in the sympathetic response to progressive hypoglycemia.

Donovan

Hamilton-Wessler

Halter

et al. 1994

Proc. Natl. Acad. Sci. U.S.A.

View full text Add to dashboard Cite

show abstract

Rôle of the Hypothalamus in Regulation of Blood Pressure

Leiter¹,

Grinker²

1934

Arch NeurPsych

View full text Add to dashboard Cite

Neurologic Mechanism Concerned in Epileptic Seizures

Yakovlev¹

1937

Arch NeurPsych

View full text Add to dashboard Cite

scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.

Contact Info

customersupport@researchsolutions.com

10624 S. Eastern Ave., Ste. A-614

Henderson, NV 89052, USA

This site is protected by reCAPTCHA and the Google Privacy Policy and Terms of Service apply.

Blog Terms and Conditions API Terms Privacy Policy Contact Cookie Preferences Do Not Sell or Share My Personal Information

Made with 💙 for researchers

Part of the Research Solutions Family.

Experimental Lesions in the Tuber Cinereum of the Dog

Cited by 16 publications

References 17 publications

Primacy of liver glucosensors in the sympathetic response to progressive hypoglycemia.

Primacy of liver glucosensors in the sympathetic response to progressive hypoglycemia.

Rôle of the Hypothalamus in Regulation of Blood Pressure

Neurologic Mechanism Concerned in Epileptic Seizures

Contact Info

Product

Resources

About