World Library  
Flag as Inappropriate
Email this Article

Ventromedial nucleus of the hypothalamus

Article Id: WHEBN0003013546
Reproduction Date:

Title: Ventromedial nucleus of the hypothalamus  
Author: World Heritage Encyclopedia
Language: English
Subject: Hypothalamus, Neuroendocrinology
Collection: Hypothalamus, Neuroendocrinology
Publisher: World Heritage Encyclopedia

Ventromedial nucleus of the hypothalamus

Ventromedial nucleus of the hypothalamus
Ventromedial nucleus is 'VM', at center, in green.
Latin nucleus ventromedialis hypothalami
Part of Hypothalamus
MeSH A08.186.211.730.385.357.352.953
NeuroNames hier-381
NeuroLex ID Ventromedial nucleus of hypothalamus
Anatomical terms of neuroanatomy

The ventromedial nucleus of the hypothalamus (VMN, also sometimes referred to as the ventromedial hypothalamus, VMH) is a nucleus of the hypothalamus. "The ventromedial hypothalamus (VMH) is a distinct morphological nucleus involved in feeding, fear, thermoregulation, and sexual activity."[1] This nuclear region is involved with the recognition of the feeling of fullness.


  • Structure 1
  • Function 2
  • References 3
  • Further References 4
  • External links 5


It has four subdivisions:

  • anterior (VMHa)
  • dorsomedial (VMHdm)
  • ventrolateral (VMHvl)
  • central (VMHc).

These subdivisions differ anatomically, neurochemically, and behaviorally.


The ventromedial nucleus (VMN) is most commonly associated with satiety. Early studies showed that VMN lesions caused over-eating and obesity in rats. However, the interpretation of these experiments was summarily discredited when Gold's research demonstrated that precision lesioning of the VMN did not result in hyperphagia.[2] Nevertheless, numerous studies have shown that the immediacy of hyperphagia and obesity syndrome are a consequence of VMN lesions or procaine injections, and point to the VMN's role in satiety.[3][4][5][6][7][8][9] A major review of the subject in 2006 concluded that, "anatomical studies done both before and after Gold's study did not replicate his results with lesions, and in nearly every published direct comparison of VMH lesions vs. PVN or VNAB lesions, the group with VMH lesions ate substantially more food and gained twice as much weight."[10] This strongly substantiates the classification of VMN as the primary satiety center in the hypothalamus.

It has also been found that lesions to the VMH in rats caused increased plasma insulin levels. Rats with a VMH lesion compared to normal rats overproduce a circulating satiety factor, to which the control rats can respond and rats with a VMH lesion cannot respond. A lesion to the VMH makes rats overproduce leptin, which they cannot respond to causing them to over eat, leading to obesity.[11]

Two researchers, Heterington and Ranson, looked at series of twenty-one animals of various degrees of adiposity, with respect to growth appearance, fat distribution, general physical condition, and the correlation between the level of adiposity attained and the correlation of the hypothalamic lesion. Lesions in the hypothalamic area, particularly the region of the ventromedial hypothalamus interrupts a large number of the descending fibers from the hypothalamic cell groups that were found to contribute to obesity in rats.[12]

Taylor and Jamshi found that there seems to be a higher concentration of cannabinoid receptor mRNA within the VMH in comparison to other nuclei within the hypothalamus. The cannabinoid ingestion has been linked to rewarding processes, and also with the release of dopamine in the brain.[13]

VMH is also important in mammal play behaviour. Lesions to VMH along with the hippocampus, amygdala, the cerebellum, and the lateral hypothalamus are all linked to reduced play [14]

The VMHdm has a role in the male vocalizations and scent marking behaviors.[15][16][17]

The VMHvl plays a role in sexual behaviors in females (lordosis), thus stimulating their sexual arousal.[18][19][20][21]

Bilateral FOS expression in the VMH after repeated seizures is associated with alteration in the severity of flurothyl induced seizures in C57BL/6J mice that are not present in DBA/2J mice. [22]


  1. ^ Kurrasch, D., & Cheung, C. (2007). The neonatal ventromedial hypothalamus transcriptome reveals novel markers with spatially distinct patterning" The Journal of Neuroscience 27(50), Retrieved from
  2. ^
  3. ^
  4. ^
  5. ^
  6. ^
  7. ^
  8. ^
  9. ^
  10. ^
  11. ^
  12. ^
  13. ^
  14. ^
  15. ^ Yahr and Green, 1992
  16. ^ Flanagan-Cato et al. 2001
  17. ^ Harding and McGinnis, 2005
  18. ^ Kow and Pfaff, 1998
  19. ^ Christensen et al., 1977
  20. ^ Pfaff and Sakuma, 1979
  21. ^ Matsumoto and Yamanouchi, 2000
  22. ^ Kadiyala et al.

Further References

  • Dugger, et al. (2007). Androgen receptors are required for full masculinization of the ventromedial hypothalamus (VMH) in rats.
  • Storlien, L., & Albert, D. (1972). The effect of vmh lesions, lateral cuts and anterior cuts on food intake, activity level, food motivation, and reactivity to taste . Physiology & Behavior, 9(2), 191–192. Retrieved from
  • Carlson, N. (2010). Physiology of behavior. (10 ed., pp. 355–357). Boston: Allyn and Bacon.

External links

  • Diagram of Ventromedial motor tract at
  • New Scientist: Seat of female libido revealed (June 26, 2006)
This article was sourced from Creative Commons Attribution-ShareAlike License; additional terms may apply. World Heritage Encyclopedia content is assembled from numerous content providers, Open Access Publishing, and in compliance with The Fair Access to Science and Technology Research Act (FASTR), Wikimedia Foundation, Inc., Public Library of Science, The Encyclopedia of Life, Open Book Publishers (OBP), PubMed, U.S. National Library of Medicine, National Center for Biotechnology Information, U.S. National Library of Medicine, National Institutes of Health (NIH), U.S. Department of Health & Human Services, and, which sources content from all federal, state, local, tribal, and territorial government publication portals (.gov, .mil, .edu). Funding for and content contributors is made possible from the U.S. Congress, E-Government Act of 2002.
Crowd sourced content that is contributed to World Heritage Encyclopedia is peer reviewed and edited by our editorial staff to ensure quality scholarly research articles.
By using this site, you agree to the Terms of Use and Privacy Policy. World Heritage Encyclopedia™ is a registered trademark of the World Public Library Association, a non-profit organization.

Copyright © World Library Foundation. All rights reserved. eBooks from Project Gutenberg are sponsored by the World Library Foundation,
a 501c(4) Member's Support Non-Profit Organization, and is NOT affiliated with any governmental agency or department.