Ventromedial nucleus of the hypothalamus

Ventromedial nucleus of the hypothalamus
Ventromedial nucleus is 'VM', at center, in green.
Details
Part ofHypothalamus
ArteryBasilar
Identifiers
Latinnucleus ventromedialis hypothalami
MeSHD014697
NeuroNames398
NeuroLex IDbirnlex_1572
TA98A14.1.08.928
TA25729
FMA62332
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 terminating hunger, fear, thermoregulation, and sexual activity."[1] This nuclear region is involved in the recognition of the feeling of fullness.

Structure

It has four subdivisions:

  • Anterior (VMHa)
  • Dorsomedial (VMHdm)
  • Ventrolateral (VMHvl)
  • Central (VMHc)

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]

The VMHvl contains many distinct neuronal populations that contribute to varying, often distinct, functions.[17] Notably, this region plays a role in sexual behaviors in females (lordosis), thus stimulating their sexual arousal.[18][19][20][21] The VMHvl has also been found to play a role in estrogen-mediated movement [22] and energy expenditure/thermogenesis.[23]

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.[24][25] Moreover, bilateral lesions of the VMH are able to block the propagation of seizure discharge to enter the brainstem seizure system.[26]

References

  1. ↑ Kurrasch DM, Cheung CC, Lee FY, Tran PV, Hata K, Ingraham HA (December 2007). "The neonatal ventromedial hypothalamus transcriptome reveals novel markers with spatially distinct patterning". The Journal of Neuroscience. 27 (50): 13624–34. doi:10.1523/JNEUROSCI.2858-07.2007. PMC 6673626. PMID 18077674.
  2. ↑ Gold RM (November 1973). "Hypothalamic obesity: the myth of the ventromedial nucleus". Science. 182 (4111): 488–90. Bibcode:1973Sci...182..488G. doi:10.1126/science.182.4111.488. PMID 4795550. S2CID 3011420.
  3. ↑ Balagura S, Devenport LD (June 1970). "Feeding patterns of normal and ventromedial hypothalamic lesioned male and female rats". Journal of Comparative and Physiological Psychology. 71 (3): 357–64. doi:10.1037/h0029118. PMID 5480868.
  4. ↑ Becker EE, Kissileff HR (February 1974). "Inhibitory controls of feeding by the ventromedial hypothalamus". The American Journal of Physiology. 226 (2): 383–96. doi:10.1152/ajplegacy.1974.226.2.383. PMID 4811195.
  5. ↑ Berthoud HR, Jeanrenaud B (September 1979). "Changes of insulinemia, glycemia and feeding behavior induced by VMH-procainization in the rat". Brain Research. 174 (1): 184–7. doi:10.1016/0006-8993(79)90816-3. PMID 487120. S2CID 39015121.
  6. ↑ Brooks CM, Lockwood RA, Wiggins ML (December 1946). "A study of the effect of hypothalamic lesions on the eating habits of the albino rat". The American Journal of Physiology. 147 (4): 735–41. doi:10.1152/ajplegacy.1946.147.4.735. PMID 20277066.
  7. ↑ Epstein AN (December 1960). "Reciprocal changes in feeding behavior produced by intrahypothalamic chemical injections". The American Journal of Physiology. 199 (6): 969–74. doi:10.1152/ajplegacy.1960.199.6.969. PMID 13697000.
  8. ↑ Larkin RP (November 1975). "Effect of ventromedial hypothalamic procaine injections on feeding, lever pressing, and other behavior in rats". Journal of Comparative and Physiological Psychology. 89 (9): 1100–8. doi:10.1037/h0077192. PMID 1202103.
  9. ↑ Maes H (June 1980). "Time course of feeding induced by pentobarbital-injections into the rat's VMH". Physiology & Behavior. 24 (6): 1107–14. doi:10.1016/0031-9384(80)90055-4. PMID 7413790. S2CID 43051882.
  10. ↑ King BM (February 2006). "The rise, fall, and resurrection of the ventromedial hypothalamus in the regulation of feeding behavior and body weight". Physiology & Behavior. 87 (2): 221–44. doi:10.1016/j.physbeh.2005.10.007. PMID 16412483. S2CID 40880350.
  11. ↑ Satoh N, Ogawa Y, Katsuura G, Tsuji T, Masuzaki H, Hiraoka J, Okazaki T, Tamaki M, Hayase M, Yoshimasa Y, Nishi S, Hosoda K, Nakao K (March 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". Endocrinology. 138 (3): 947–54. doi:10.1210/endo.138.3.4989. PMID 9048594.
  12. ↑ Hetherington AW, Ranson SW (June 1942). "The relation of various hypothalamic lesions to adiposity in the rat" (PDF). Journal of Comparative Neurology. 76 (3): 475–99. doi:10.1002/cne.900760308. S2CID 85715802.
  13. ↑ Jamshidi N, Taylor DA (November 2001). "Anandamide administration into the ventromedial hypothalamus stimulates appetite in rats". British Journal of Pharmacology. 134 (6): 1151–4. doi:10.1038/sj.bjp.0704379. PMC 1573067. PMID 11704633.
  14. ↑ Panksepp J, Siviy S, Normansell L (1984). "The psychobiology of play: theoretical and methodological perspectives". Neuroscience and Biobehavioral Reviews. 8 (4): 465–92. doi:10.1016/0149-7634(84)90005-8. PMID 6392950. S2CID 26810046.
  15. ↑ Flanagan-Cato LM, Lee BJ, Calizo LH (June 2006). "Co-localization of midbrain projections, progestin receptors, and mating-induced fos in the hypothalamic ventromedial nucleus of the female rat". Hormones and Behavior. 50 (1): 52–60. doi:10.1016/j.yhbeh.2006.01.012. PMID 16546183. S2CID 36201218.
  16. ↑ Harding SM, McGinnis MY (October 2005). "Microlesions of the ventromedial nucleus of the hypothalamus: effects on sociosexual behaviors in male rats". Behavioral Neuroscience. 119 (5): 1227–34. doi:10.1037/0735-7044.119.5.1227. PMID 16300430.
  17. ↑ Kammel LG, Correa SM (January 2020). "Selective sexual differentiation of neurone populations may contribute to sex-specific outputs of the ventromedial nucleus of the hypothalamus". Journal of Neuroendocrinology. 32 (1): e12801. doi:10.1111/jne.12801. PMC 6982598. PMID 31605642.
  18. ↑ Kow LM, Pfaff DW (May 1998). "Mapping of neural and signal transduction pathways for lordosis in the search for estrogen actions on the central nervous system". Behavioural Brain Research. 92 (2): 169–80. doi:10.1016/S0166-4328(97)00189-7. PMID 9638959. S2CID 28276218.
  19. ↑ Christensen LW, Nance DM, Gorski RA (1977). "Effects of hypothalamic and preoptic lesions on reproductive behavior in male rats". Brain Research Bulletin. 2 (2): 137–41. doi:10.1016/0361-9230(77)90010-7. PMID 880486. S2CID 4700161.
  20. ↑ Pfaff DW, Sakuma Y (March 1979). "Facilitation of the lordosis reflex of female rats from the ventromedial nucleus of the hypothalamus". The Journal of Physiology. 288: 189–202. doi:10.1113/jphysiol.1979.sp012690 (inactive 31 October 2021). PMC 1281421. PMID 469715.{{cite journal}}: CS1 maint: DOI inactive as of October 2021 (link)
  21. ↑ Matsumoto T, Yamanouchi K (September 2000). "Acceleration of mounting behaviors in female rats by ibotenic acid lesions in the ventromedial hypothalamic nucleus". Neuroscience Letters. 291 (3): 143–6. doi:10.1016/S0304-3940(00)01388-4. PMID 10984627. S2CID 10334038.
  22. ↑ Correa SM, Newstrom DW, Warne JP, Flandin P, Cheung CC, Lin-Moore AT, Pierce AA, Xu AW, Rubenstein JL, Ingraham HA (January 2015). "An Estrogen-Responsive Module in the Ventromedial Hypothalamus Selectively Drives Sex-Specific Activity in Females". Cell Reports. 10 (1): 62–74. doi:10.1016/j.celrep.2014.12.011. PMC 4324838. PMID 25543145.
  23. ↑ van Veen JE, Kammel LG, Bunda PC, Shum M, Reid MS, Massa MG, Arneson D, Park JW, Zhang Z, Joseph AM, Hrncir H, Liesa M, Arnold AP, Yang X, Correa SM (April 2020). "Hypothalamic estrogen receptor alpha establishes a sexually dimorphic regulatory node of energy expenditure". Nature Metabolism. 2 (4): 351–63. doi:10.1038/s42255-020-0189-6. PMC 7202561. PMID 32377634.
  24. ↑ Kadiyala SB, Papandrea D, Tuz K, Anderson TM, Jayakumar S, Herron BJ, Ferland RJ (January 2015). "Spatiotemporal differences in the c-fos pathway between C57BL/6J and DBA/2J mice following flurothyl-induced seizures: A dissociation of hippocampal Fos from seizure activity". Epilepsy Research. 109: 183–96. doi:10.1016/j.eplepsyres.2014.11.009. PMC 4272448. PMID 25524858.
  25. ↑ Kadiyala SB, Ferland RJ (March 2017). "Dissociation of spontaneous seizures and brainstem seizure thresholds in mice exposed to eight flurothyl-induced generalized seizures". Epilepsia Open. 2 (1): 48–58. doi:10.1002/epi4.12031. PMC 5560332. PMID 28825051.
  26. ↑ Ferland RJ, Applegate CD (November 1998). "The role of the ventromedial nucleus of the hypothalamus in epileptogenesis". NeuroReport. 9 (16): 3623–9. doi:10.1097/00001756-199811160-00013. PMID 9858370. S2CID 29713035.

Further reading

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