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Details for anatomical structure: arcuate nucleus of hypothalamus

EndoNet ID: ENC00189

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Synonyms

arcuate nucleus of hypothalamus, infundibular nucleus, arcuate nucleus-2, arcuate periventricular nucleus, infundibular periventricular nucleus, Nucleus arcuatus hypothalamus

Links to other resources

Cytomer cy0006467

Larger structures

    Substructures

      Secreted hormones

      • Hormone: GHRH

        Influenced by:

        • PRLR
          in arcuate_nucleus_of_hypothalamus
      • 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

        • 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]
        • The orexigenic neuropeptides that are downregulated by leptin are NPY, MCH, orexins, and AGRP. [4]

        Influenced by:

        • leptin receptor
          in arcuate_nucleus_of_hypothalamus
        • insulin receptor
          in arcuate_nucleus_of_hypothalamus
        • GHS-R1
          in arcuate_nucleus_of_hypothalamus
        • NPY2-R
          in arcuate_nucleus_of_hypothalamus
      • Hormone: alpha-MSH

        • In the human hypothalamus, cell bodies containing alpha-MSH were exclusively located in the infundibular (arcuate) nucleus. [5]
        • Alpha-MSH is upregulated by Leptin. [4]

        Influenced by:

        • leptin receptor
          in arcuate_nucleus_of_hypothalamus
        • insulin receptor
          in arcuate_nucleus_of_hypothalamus
      • 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:

        • PRLR
          in arcuate_nucleus_of_hypothalamus
      • 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]
      • 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:

        • alpha-MSH
        • AGRP
        • NPY
          • Decrease in Leptin causes increase in NPY secretion in rats during lactation [2]
        • POMC
        • GnRH-I
          • Decrease in Leptin causes inhibition of GnRH/LH secretion in rats during lactation [2]
      • Receptor: unspecified testosterone receptor 1

        Influences:

        • GnRH-I
        • metastin
          • Estradiol and testosterone down-regulate Kiss1 mRNA in the Arc. [8]
      • 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:

        • GnRH-I
      • Receptor: sst2

      • Receptor: progesterone receptor A

        Influences:

        • GnRH-I
      • Receptor: ER-beta

        Induced phenotype:

        • regulation of synapse organization
          • Estrogen has a facilitatory effect on the formation of new spine synapses in the arcuate neurons, reflecting a circuit remodeling in the ARC after estrogen treatment. [13]
          • 17ß-estradiol administration lead to changes in the neuronal membrane ultrastructure within the ARC. [14]

        Influences:

        • GnRH-I
        • metastin
          • Estradiol and testosterone down-regulate Kiss1 mRNA in the Arc. [8]
      • Receptor: ER-alpha

        Induced phenotype:

        • regulation of synapse organization
          • Estrogen has a facilitatory effect on the formation of new spine synapses in the arcuate neurons, reflecting a circuit remodeling in the ARC after estrogen treatment. [13]
          • 17ß-estradiol administration lead to changes in the neuronal membrane ultrastructure within the ARC. [14]

        Influences:

        • metastin
          • Estradiol and testosterone down-regulate Kiss1 mRNA in the Arc. [8]
      • Receptor: GHS-R1

        Induced phenotype:

        • positive regulation of appetite
          • Ghrelin transduces an appetite-stimulatory signal from peripheral tissues to central nervous system [15]
          • Ghrelin acts in harmony with appetite-stimulating signals from peripheral organs and stimulate food intake [16]
        • 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:

        • AGRP
        • NPY
        • POMC
          • Ghrelin inhibits POMC neurons of the Hypothalamus
      • Receptor: PRLR

        Influences:

        • GHRH
        • dopamine
      • Receptor: insulin receptor

        Influences:

        • NPY
        • AGRP
        • alpha-MSH
        • insulin
          • insulin stimulates phosphorylation of signalling proteins in ARC [10]
      • 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:

        • NPY
        • AGRP
      • 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]
      • 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]
      • 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]
      • 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]
      • 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]
      • 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]
      Reference