Evidence for ascending noradrenergic mediation of hypothalamic hyperphagia

Kapatos, Gregory; Gold, Richard M.

doi:10.1016/0091-3057(73)90060-9

Cited by 62 publications

(30 citation statements)

References 20 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Since the P-animals did not show hyperphagia, anterior parts of the VMH are more involved in Feeding than posterior ones. This is compatible with the finding that damage to the Ventral Noradrenergic Bundle (VNB) is responsible for the hyperphagia (Gold, 1973;Kapatos and Gold, 1973). According to Gold, this VNB ascends from the lower brainstem, follows a longitudinal course ventrolateral of the VMH, and gives off fibers and/or terminalia around the rostra1 tip of the VMH.…”

Section: Discussionsupporting

confidence: 83%

The ventromedial hypothalamus and aggressive behaviour in rats

Olivier

1977

Aggr. Behav.

View full text Add to dashboard Cite

Male rats were given bilateral lesions in either the anterior or posterior ventromedial hypothalamus (VMH). The intermale aggressive behaviour of these animals within their own territory was observed before and after the surgical procedure and compared with the behaviour of sham‐operated animals. The effects of anterior VMH lesions include an increased tendency to respond with frontal threatening upon approach of a conspecific male. This behaviour closely resembles the aggressive responses described in “shock‐induced aggression” tests. Posterior VMH lesions facilitate territorial aggressive behaviour characterized by approaching the opponent followed by lateral threatening and fighting. It is suggested that 2 distinct neural substrates exist, which serve to inhibit defensive (anterior‐VMH) and offensive (posterior‐VMH) intermale aggression, respectively.

show abstract

Section: Discussionsupporting

confidence: 83%

The ventromedial hypothalamus and aggressive behaviour in rats

Olivier

1977

Aggr. Behav.

View full text Add to dashboard Cite

show abstract

“…Electrolytic lesions of the LHA suppresses feeding 14 , and drinking 15 while lesioning of the nearby VMH promotes feeding and body weight gain 16 . Later studies that utilized chemical lesions to destroy catecholaminergic fibers containing either norepinephrine 17 or dopamine 18 demonstrated that these fibers of passage contained within the median forebrain bundle are important components controlling feeding and drinking. Anand and Brobeck 14 suggested that fibers of passage, but also fibers of origin from somata distributed throughout the LHA are also important for controlling feeding.…”

Section: Classic Experiments On Lha Functionmentioning

confidence: 99%

Lateral hypothalamic circuits for feeding and reward

2016

View full text Add to dashboard Cite

In experiments conducted over 60 years ago, the lateral hypothalamic area (LHA) was identified as a critical neuroanatomical substrate for motivated behavior. Electrical stimulation of the LHA induces voracious feeding even in non-restricted animals. In the absence of food, animals will work tirelessly, often lever-pressing 1000’s of times per hour, for electrical stimulation at the same site that provokes feeding, drinking, and other species-typical motivated behaviors. Here we review the classic findings from electrical stimulation studies and integrate them with more recent work that has utilized contemporary circuit-based approaches to study the LHA. We identify specific anatomically and molecularly defined LHA elements that integrate diverse information arising from cortical, extended amygdala, and basal forebrain networks to ultimately generate a highly specified and invigorated behavioral state conveyed via LHA projections to downstream reward and feeding specific circuits.

show abstract

“…The intracerebral application of exogenous NE has been reported to both elicit {Grossman, 1960) and suppress {Margides, 1969) eating in the rat. Other studies indicate the acquired obesity that results from damage to the ventromedial nucleus of the hypothalamus may be due to damage to the ventral noradrenergic bundle (Ahlskogand Hoebel, 1973;Kapatos and Gold, 1973;Gold. 1973).…”

Section: Introductionmentioning

confidence: 99%

Elevated Hypothalamic Norepinephrine Content in Mice with the Hereditary Obese-Hyperglycemic Syndrome

Feldman¹,

Blalock²,

Zern³

1979

Horm Res

View full text Add to dashboard Cite

There is evidence that hypothalamic norepinephrine (NE) plays a role in the control of appetite in the rat. Using specific and sensitive radioenzymatic assays, we determined if there was a difference in the tissue (hypothalamus, cerebral cortex and kidney) concentration of NE or of dopamine (DA) in mice with the hereditary obese-hyperglycemic syndrome (ob/ob) and their normal weight littermates. Obese mice had a higher concentration of hypothalamic NE than their normal weight littermates, both when they were in the rapid growth phase (2-3 months of age) and when they were mature (6-7 months of age). The concentration of NE was similar in the cerebral cortex of obese and normal mice and in the kidneys of obese and normal mice. The concentration of DA was similar in the hypothalamus of obese and normal mice and in the cerebral cortex of obese and normal mice. These observations support the concept that alterations in hypothalamic NE may play a role in the obesity of ob/ob mice.

show abstract

Evidence for ascending noradrenergic mediation of hypothalamic hyperphagia

Cited by 62 publications

References 20 publications

The ventromedial hypothalamus and aggressive behaviour in rats

The ventromedial hypothalamus and aggressive behaviour in rats

Lateral hypothalamic circuits for feeding and reward

Elevated Hypothalamic Norepinephrine Content in Mice with the Hereditary Obese-Hyperglycemic Syndrome

Contact Info

Product

Resources

About