Status
Please wait ...

Details for anatomical structure: ventromedial nucleus of hypothalamus

EndoNet ID: ENC00582

To link to the content of EndoNet use the EndoNet ID that is given on the detail pages in the format ENX0000, where X is a place holder for the type of the component (e. g. R for receptor or C for anatomical structure).
As URL for the linking append this ID to the detail page for this type of component.
For an hormone that would be:

http://endonet.bioinf.med.uni-goettingen.de/hormone/ENH00000

It is also possible to use the search of EndoNet to link to the right detail page. The URL should look like

http://endonet.bioinf.med.uni-goettingen.de/search/ENC00000
If the search pattern is unambigious the user is directed to the corresponding detail page.

Synonyms

ventromedial nucleus of hypothalamus, ventromedial hypothalamic nucleus, Nucleus ventromedialis hypothalami

General information

A circumscript ovoid group of small neurons in the medial zone of the tuberal region of the hypothalamus

Links to other resources

Cytomer cy0006472

Larger structures

    Substructures

      Secreted hormones

        Receptors

        • Receptor: CRF-R2

          Induced phenotype:

          • hyperactivity of HPA axis
            • Levels of the CRF-R2 mRNA in the VMH were significantly lower in diabetic rats. Expression of CRF-R2 is mostly related to the insulin, but not to the corticosterone, status. Alterations in the brain CRF system due to insulin deficiency may contribute to the hyperdipsia in diabetes. [1]
            • Basal HPA axis may also be affected by magnocellular CRF that directly stimulates the AVP secretion through a paracrine mechanism at the level of neurohemal zone of the neurohypophysis. [1]
          • hyperphagia
            • Levels of the CRF-R2 mRNA in the VMH were significantly lower in diabetic rats. Expression of CRF-R2 is mostly related to the insulin, but not to the corticosterone, status. Alterations in the brain CRF system due to insulin deficiency may contribute to the hyperphagia in diabetes. [1]
          • hyperdipsia
            • Levels of the CRF-R2 mRNA in the VMH were significantly lower in diabetic rats. Expression of CRF-R2 is mostly related to the insulin, but not to the corticosterone, status. Alterations in the brain CRF system due to insulin deficiency may contribute to the hyperdipsia in diabetes. [1]

          Influences:

          • insulin
            • The VMH is a brain region seemingly involved in the modulation of insulin secretion as ablation of the VMH led to increase in the parasympathetic tone to the pancreas and insulin oversecretion. [2]
            • There is evidence that the CRF-R2 in the VMH mediates the anorectic effects of CRF. [3]
            • A part of insulin central effects may be mediated through its regulation of CRF-R2 VMH expression. [1]
        • Receptor: NPY6-R

        Reference