Ventromedial nucleus of the hypothalamus

Ventromedial nucleus of the hypothalamus

Ventromedial nucleus is 'VM', at center, in green.
Details
Part of Hypothalamus
Artery Basilar
Identifiers
Latin nucleus ventromedialis hypothalami
MeSH A08.186.211.730.385.357.352.953
NeuroNames hier-381
NeuroLex ID Ventromedial nucleus of hypothalamus
Dorlands
/Elsevier		 n_11/12584102
TA A14.1.08.928
FMA 62332

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

It has four subdivisions:

These subdivisions differ anatomically, neurochemically, and behaviorally.

Function

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]

Researchers looked at a 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]

Another study 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] Moreover, bilateral lesions of the VMH are able to block the propagation of seizure discharge to enter the brainstem seizure system. [23]


References

  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 http://www.jneurosci.org/content/27/50/13624.full.pdf
  2. ↑ Gold, R.M. (1973). "Hypothalamic Obesity: The myth of the ventromedial nucleus". Science. 182: 488–490. doi:10.1126/science.182.4111.488.
  3. ↑ Balagura, S.; Devenport, L.D. (1970). "Feeding patterns of normal and ventromedial hypothalamic lesioned male and female rats". J. Comp Physiol Psychol. 71: 357–364. doi:10.1037/h0029118.
  4. ↑ Becker, E.E.; Kissileff, H.R. (1974). "Inhibitory controls of feeding by the ventromedial hypothalamus". Am J Physiol. 226: 383–396.
  5. ↑ Berthoud, H.R.; Jeanrenaud, B. (1979). "Changes in insulinemia, glycemia and feeding behavior induced by VMH-procainization in the rat". Brain Res. 174: 184–187. doi:10.1016/0006-8993(79)90816-3.
  6. ↑ Brooks, C.M.; Lockwood, R.A.; Wiggins, M.L. (1946). "A study of the effects of hypothalamic lesions on the eating habits of the albino rat". Am J Physiol. 147: 735–741.
  7. ↑ Epstein, A.N. (1960). "Reciprocal changes in feeding behavior produced by intrahypothalamic chemical injections". Am J Physiol. 199: 969–974.
  8. ↑ Larkin, R.P. (1975). "Effect of ventromedial hypothalamic procaine injections on feeding, lever pressing, and other behavior in the rat". J Comp Physiol Psychol. 89: 1100–1108. doi:10.1037/h0077192.
  9. ↑ Maes, H. (1980). "Time course of feeding induced by pentobarbital-injections into the rat's VMH". Physiol Behav. 24: 1107–1114. doi:10.1016/0031-9384(80)90055-4.
  10. ↑ King, Bruce M. (February 2006). "The rise, fall and resurrection of the ventromedial hypothalamus in the regulation of feeding behavior and body weight". J Physiol Behav. 87 (2): 221–244. doi:10.1016/j.physbeh.2005.10.007.
  11. ↑ {{SATOH, N., & OGAWA, Y. (1997). Pathophysiological significance of the obese gene product, leptin, in ventromedial hypothalamus (vmh)- lesioned rats: Evidence for loss of its satiety effect in vmh-lesioned rats*. Department of Medicine and Clinical Science, 138(3), 847-150. Retrieved from http://endo.endojournals.org/content/138/3/947.full.pdf html}}
  12. ↑ {{Hetherinton , A., & Ranson, S. (n.d.). The relation of various hypothalamic lesions to adiposity in the rat. Institute of Neurology, Northwestern University Medical School, 477-481. Retrieved from https://wiki.brown.edu/confluence/download/attachments/74844947/rathypothalamus.pdf }}
  13. ↑ Jamshidi, N; Taylor, DA (2001). "Anandamide administration into the ventromedial hypothalamus stimulates appetite in rats". Br. J. Pharmacol. 134: 1151–4. PMC 1573067 Freely accessible. PMID 11704633. doi:10.1038/sj.bjp.0704379.
  14. ↑ "The psychobiology of play: Theoretical and methodological perspectives". Neuroscience. 8: 465–492. doi:10.1016/0149-7634(84)90005-8.
  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., 2015; Kadiyala and Ferland, 2017
  23. ↑ Ferland and Applegate, 1998

Further References

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