Details for anatomical structure: arcuate nucleus of hypothalamus
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- Hormones
- Receptors
-
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- Related structures
- Hormones
- Receptors
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Click to access the toolbox
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Synonyms
arcuate nucleus of hypothalamus, infundibular nucleus, arcuate nucleus-2, arcuate periventricular nucleus, infundibular periventricular nucleus, Nucleus arcuatus hypothalamusLinks to other resources
Cytomer | cy0006467 |
Related structures
Larger structures
Substructures
Secreted hormones
-
Hormone: GHRH
Influenced by:
-
Hormone: GnRH-I
- Estrogen directly respresses GnRH. [1]
Influenced by:
- ER-beta in arcuate_nucleus_of_hypothalamus
- unspecified testosterone receptor 1 in arcuate_nucleus_of_hypothalamus
- progesterone receptor A in arcuate_nucleus_of_hypothalamus
- NPY5-R in arcuate_nucleus_of_hypothalamus
- leptin receptor
in
arcuate_nucleus_of_hypothalamus
- Decrease in Leptin causes inhibition of GnRH/LH secretion in rats during lactation [2]
-
Hormone: AGRP
Influenced by:
-
Hormone: alpha-MSH
Influenced by:
-
Hormone: galanin
-
Hormone: NPY
- NPY neurons coexpress ghrelin receptors and the orexigens, agouti-related peptide (AgrP) and {gamma}-aminobutyric acid (GABA). [6]
- The orexigenic neuropeptides that are downregulated by leptin are NPY (neuropeptide Y), MCH (melanin-concentrating hormone), orexins, and AGRP (agouti-related peptide). [4]
- Neuropeptide Y (NPY) and agouti-related protein (AgRP) are potent food-stimulating neuropeptides that are highly co-localised in arcuate nucleus neurons of the hypothalamus. [3]
Influenced by:
- insulin receptor in arcuate_nucleus_of_hypothalamus
- leptin receptor
in
arcuate_nucleus_of_hypothalamus
- Decrease in Leptin causes increase in NPY secretion in rats during lactation [2]
- GHS-R1 in arcuate_nucleus_of_hypothalamus
- NPY2-R in arcuate_nucleus_of_hypothalamus
- NPY2-R
in
hypothalamus
- PYY(3-36) binding to NPY2-R inhibits orexigenic NPY in hypothalamus causing short-term inhibition of food intake [7]
-
Hormone: dopamine
Influenced by:
-
Hormone: metastin
- Kisspeptin is expressed abundantly in the arcuate nucleus (Arc) and the anteroventral periventricular nucleus (AVPV) of the forebrain. [8]
Influenced by:
- ER-alpha
in
arcuate_nucleus_of_hypothalamus
- Estradiol and testosterone down-regulate Kiss1 mRNA in the Arc. [8]
- ER-beta
in
arcuate_nucleus_of_hypothalamus
- Estradiol and testosterone down-regulate Kiss1 mRNA in the Arc. [8]
- unspecified testosterone receptor 1
in
arcuate_nucleus_of_hypothalamus
- Estradiol and testosterone down-regulate Kiss1 mRNA in the Arc. [8]
-
Hormone: galanin-like peptide Isoform 1
- GALP expression is positively regulated by the adipose tissue hormone leptin. [9]
-
Hormone: insulin
Influenced by:
- insulin receptor
in
arcuate_nucleus_of_hypothalamus
- insulin stimulates phosphorylation of signalling proteins in ARC [10]
- insulin receptor
in
arcuate_nucleus_of_hypothalamus
-
Hormone: POMC
Influenced by:
- leptin receptor in arcuate_nucleus_of_hypothalamus
- GHS-R1
in
arcuate_nucleus_of_hypothalamus
- Ghrelin inhibits POMC neurons of the Hypothalamus
-
Hormone: APOE
-
Hormone: dynorphin A
Receptors
-
Receptor: leptin receptor
Induced phenotype:
- regulation of synapse organization
- Leptin induces a fast rewiring of POMC and Npy/Agrp cells in the ARC - peripheral leptin treatment rapidly restored the synaptic inputs in these groups of cells. [11]
Influences:
- regulation of synapse organization
-
Receptor: unspecified testosterone receptor 1
Influences:
-
Receptor: NPY5-R
Induced phenotype:
- positive regulation of appetite
- The injection of neuropeptide-Y into either the cerebral ventricles or directly into the hypothalamic paraventricular nucleus promoted a robust increase in food intake. [12]
Influences:
- positive regulation of appetite
-
Receptor: sst2
-
Receptor: progesterone receptor A
Influences:
-
Receptor: ER-beta
Induced phenotype:
Influences:
-
Receptor: ER-alpha
Induced phenotype:
Influences:
-
Receptor: GHS-R1
Induced phenotype:
- positive regulation of appetite
- regulation of feeding behavior
- Ghrelin activates feeding through fatty acid oxidation and free radical buffering in the NPY/Agrp neurons of the ARC. Ghrelin induces feeding by the activation of its receptor, the G-protein-coupled growth hormone secretagogue receptor, in the NPY/Agrp neurons, which induces a rapid increase in the firing rate of these cells. [12]
- Short stature
Influences:
-
Receptor: PRLR
Influences:
-
Receptor: insulin receptor
Influences:
-
Receptor: NPY2-R
Induced phenotype:
- negative regulation of appetite
- The short form of peptide YY (PYY3-36) is cleaved from the long form (PYY1-36) by the enzyme dipeptidyl peptidase IV, and decreases food intake when administered peripherally. [17]
- The anorectic effect of PYY3-36 requires Y2 receptors because it fails to inhibit food intake in Y2 receptor-knockout mice. PYY3-36 decreased NPY mRNA in the ARC and its direct delivery into the ARC was sufficient to decrease food intake, highlighting the probable importance of NPY cells in the anorectic effect of PYY3-36. [12]
- The effects of PYY3-36 in decreasing food intake are are due to a combination of various mechanisms involving different brain areas (independent of the melanocortin system. [12]
- positive regulation of appetite
- The injection of neuropeptide-Y into either the cerebral ventricles or directly into the hypothalamic paraventricular nucleus promoted a robust increase in food intake. [12]
Influences:
- negative regulation of appetite
-
Receptor: melanocortin-4 receptor
Induced phenotype:
- negative regulation of appetite
- Both alpha-Melanocyte-stimulating hormone (alpha-MSH) and agouti-related protein (AGRP) exert effects on energy balance by signaling through melanocortin receptor 4 and that induced an inhibitory influence on appetite and body weight. Alpha-MSH acts as an agonist to the receptor and suppresses feeding, and AGRP conversely stimulates food intake by antagonizing the alpha-MSH signaling.g. . [18]
- negative regulation of appetite
-
Receptor: melanocortin receptor 3
Induced phenotype:
- negative regulation of appetite
- Both alpha-Melanocyte-stimulating hormone (alpha-MSH) and agouti-related protein (AGRP) exert effects on energy balance by signaling through melanocortin receptor 3 and that induced an inhibitory influence on appetite and body weight. Alpha-MSH acts as an agonist to the receptor and suppresses feeding, and AGRP conversely stimulates food intake by antagonizing the alpha-MSH signaling. [18]
- negative regulation of appetite
-
Receptor: NPY1-R
Induced phenotype:
- positive regulation of appetite
- The injection of neuropeptide-Y into either the cerebral ventricles or directly into the hypothalamic paraventricular nucleus promoted a robust increase in food intake. [12]
- positive regulation of appetite
-
Receptor: NPY6-R
Induced phenotype:
- positive regulation of appetite
- The injection of neuropeptide-Y into either the cerebral ventricles or directly into the hypothalamic paraventricular nucleus promoted a robust increase in food intake. [12]
- positive regulation of appetite
-
Receptor: GHSR
Induced phenotype:
- regulation of synapse organization
- The orexigenic hormone ghrelin has an inhibitory effect on the synaptic arrangement/rewiring of the POMC and Npy/Agrp cells in the ARC. [12]
- positive regulation of appetite
- Ghrelin has been shown to exert its orexigenic effect by activating NPY/Agrp neurons while inhibiting the anorexigenic POMC neurons.However, similar to leptin, ghrelin also acts in other brain regions to modulate food intake [19]
- Ghrelin binds to neurons in the ventral tegmental area (VTA), where it increases dopamine neuronal activity and dopamine turnover in the nucleus accumbens. Direct VTA administration of ghrelin was sufficient to induce food intake, while the blockage of ghrelin's action in the VTA by infusion of a ghrelin antagonist blocked the orexigenic effect of circulating ghrelin. [20]
- regulation of synapse organization
-
Receptor: NPY4-R
Induced phenotype:
- positive regulation of appetite
- The injection of neuropeptide-Y into either the cerebral ventricles or directly into the hypothalamic paraventricular nucleus promoted a robust increase in food intake. [12]
- positive regulation of appetite