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Details for anatomical structure: paraventricular nucleus of hypothalamus

EndoNet ID: ENC00025

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Synonyms

paraventricular nucleus of hypothalamus, filiform nucleus, paraventricular hypothalamic nucleus, Nucleus paraventricularis hypothalami

General information

A triangular group of large magnocellular neurons in the periventricular zone of the anterior half of the hypothalamus

Links to other resources

Cytomer cy0006454

Larger structures

    Substructures

      Secreted hormones

      • Hormone: TRH

        • S.101 [1]
        • Many TRH-containing neurons were present in the paraventricular nucleus (PVN), especially in the dorsocaudal part of this nucleus. [2]

        Influenced by:

        • THRB1
          in paraventricular_nucleus_of_hypothalamus
        • THRA1
          in paraventricular_nucleus_of_hypothalamus
        • thyroid hormone receptor beta 2
          in paraventricular_nucleus_of_hypothalamus
        • leptin receptor
          in paraventricular_nucleus_of_hypothalamus
          • Leptin stimulates TRH mRNA production and releases TRH but only from hypothalamic neurons of the PVN. S.138 [3]
      • Hormone: antidiuretic hormone

        • Expression of vasopressin (VP) mRNA in the human paraventricular nuclei. [4]
        • Is stored in the neurohypophysis. [5]
      • Hormone: Oxytocin-Neurophysin 1

        • Is stored in the neurohypophysis. [5]
        • Oxytocin neurons in the human PVN have a role in food regulation as satiety neurons. [6]

        Influenced by:

        • thyroid hormone receptor beta 2
          in paraventricular_nucleus_of_hypothalamus
          • TRH inhibits oxytocin biosynthesis in adult rats [7]
      • Hormone: CRH

        • CRH neurons in the PVN decrease food intake. [6]

        Influenced by:

        • leptin receptor
          in paraventricular_nucleus_of_hypothalamus
          • after leptin administration CRH genexpression have been noted after 6h and 5d [8]
        • glucocorticoid receptor
          in hypothalamus
          • Glucocorticoid/Cortisol binding to GR in the hypothalamus inhibits secretion of CRH [9]
        • CRF-R1
          in paraventricular_nucleus_of_hypothalamus
          • CRF may modulate its own biosynthesis as well as that of its type-1 receptor through an ultra-short positive feedback loop. [10]
        • glucocorticoid receptor
          in hypothalamus
          • The reduction in CRF mRNA expression in the parvocellular PVN in uncontrolled diabetes most probably depends on the levels of plasma corticosterone. Increased corticosterone levels were accompanied with a decrease in parvocellular CRF expression. [11]
      • Hormone: somatostatin

      • Hormone: galanin-like peptide Isoform 1

      • Hormone: APOE

      • Hormone: FGF-23

      Receptors

      • Receptor: melanin-concentrating hormone receptor 1

      • Receptor: THRA1

        Influences:

        • TRH
      • Receptor: thyroid hormone receptor beta 2

        Influences:

        • TRH
        • Oxytocin-Neurophysin 1
          • TRH inhibits oxytocin biosynthesis in adult rats [7]
        • antidiuretic hormone
          • TRH is colocalized with vasopressin in the supraoptic and paraventricular nuclei and can participate in the regulation og biosynthesis and secretion of vasopressin [12]
          • TRH stimulates vasopressin biosynthesis in young rats [12]
      • Receptor: THRB1

        Influences:

        • TRH
      • Receptor: melanocortin-4 receptor

        Induced phenotype:

        • promotion of positive energy balance
          • A component of the melanocortin system within the arcuate nucleus of hypothalamus consists of a neuronal population that produces proopiomelanocortin (POMC)-derived peptides, such as alpha-melanocyte stimulating hormone, and cocaine- and amphetamine-regulated transcript (CART) peptides, which promote positive energy balance. [13]
          • In the PVN, the peptides derived from the breakdown of POMC (mainly alpha-MSH)are endogeneous agonists of MC4R. [14]
        • negative regulation of appetite
          • A component of the melanocortin system within the arcuate nucleus of hypothalamus consists of a neuronal population that produces proopiomelanocortin (POMC)-derived peptides, such as alpha-melanocyte stimulating hormone, and cocaine- and amphetamine-regulated transcript (CART) peptides, which promote satiety. [13]
          • In the PVN, the peptides derived from the breakdown of POMC (mainly alpha-MSH)are endogeneous agonists of MC4R. [14]
        • obesity
          • Dominant mutations in the agouti peptide were known to cause an obese phenotype in mice and this has been proved to be due to the antagonism of melanocortin receptors located in the PVN [15]
      • Receptor: leptin receptor

        Influences:

        • TRH
          • Leptin stimulates TRH mRNA production and releases TRH but only from hypothalamic neurons of the PVN. S.138 [3]
        • CRH
          • after leptin administration CRH genexpression have been noted after 6h and 5d [8]
        • norepinephrine
          • Leptin lowers noradrenalin concentration in PNV [16]
      • Receptor: CRF-R1

        Induced phenotype:

        • hyperactvity of HPA axis
          • Systemic deficit in insulin and corticosterone results in opposite effects on the central expression of CRF and CRF-R1. Uncontrolled diabetes led to a decrease in CRF expression in parvocellular PVN. Insulin and corticosterone deficiency have the opposite effects on the hypophysiotropic CRF and CRF-R1. Alterations in the brain CRF system due to insulin deficiency may contribute to the hyperactivity of the HPA axis in diabetes. [17]
          • 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. [17]
        • hyperdipsia
          • Systemic deficit in insulin and corticosterone results in opposite effects on the central expression of CRF and CRF-R1. Uncontrolled diabetes led to a decrease in CRF expression in parvocellular PVN. Insulin and corticosterone deficiency have the opposite effects on the hypophysiotropic CRF and CRF-R1. Alterations in the brain CRF system due to insulin deficiency may contribute to the hyperdipsia in diabetes. [17]
        • hyperphagia
          • Systemic deficit in insulin and corticosterone results in opposite effects on the central expression of CRF and CRF-R1. Uncontrolled diabetes led to a decrease in CRF expression in parvocellular PVN. Insulin and corticosterone deficiency have the opposite effects on the hypophysiotropic CRF and CRF-R1. Alterations in the brain CRF system due to insulin deficiency may contribute to the hyperphagia in diabetes. [17]

        Influences:

        • CRH
          • CRF may modulate its own biosynthesis as well as that of its type-1 receptor through an ultra-short positive feedback loop. [10]
      • Receptor: melanocortin receptor 3

        Induced phenotype:

        • promotion of positive energy balance
          • A component of the melanocortin system within the arcuate nucleus of hypothalamus consists of a neuronal population that produces proopiomelanocortin (POMC)-derived peptides, such as alpha-melanocyte stimulating hormone, and cocaine- and amphetamine-regulated transcript (CART) peptides, which promote positive energy balance. [13]
          • In the PVN, the peptides derived from the breakdown of POMC (mainly alpha-MSH)are endogeneous agonists of MC3R. [14]
        • negative regulation of appetite
          • A component of the melanocortin system within the arcuate nucleus of hypothalamus consists of a neuronal population that produces proopiomelanocortin (POMC)-derived peptides, such as alpha-melanocyte stimulating hormone, and cocaine- and amphetamine-regulated transcript (CART) peptides, which promote satiety. [13]
          • In the PVN, the peptides derived from the breakdown of POMC (mainly alpha-MSH)are endogeneous agonists of MC3R. [14]
        • obesity
          • Dominant mutations in the agouti peptide were known to cause an obese phenotype in mice and this has been proved to be due to the antagonism of melanocortin receptors located in the PVN [15]
      • Receptor: galanin receptor 2

      • Receptor: apelin receptor

      Reference