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Details for anatomical structure: hypothalamus

EndoNet ID: ENC00361

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Synonyms

hypothalamus, preoptico-hypothalamic area, preoptico-hypothalamic region, Hypothalamus

General information

The part of the diencephalon below the thalamus forming the floor and the lateral walls of the 3rd ventricle below the hypothalamic sulcus; lying medial to the internal capsule and subthalamus, continuous with the precommissural septum anteriorly and with the mesencephalic tegmentum and central gray substance posteriorly

Links to other resources

Cytomer cy0032121

Larger structures

    Substructures

      Secreted hormones

      • Hormone: neuromedin B

      • Hormone: NPB23

      • Hormone: NPB29

      • Hormone: apelin-13

      • Hormone: apelin-28

      • Hormone: apelin-31

      • Hormone: apelin-36

      • Hormone: CGRP1

      • Hormone: dynorphin B

      • Hormone: NPW23

      • Hormone: NPW30

      • Hormone: PrRP20

      • Hormone: cortistatin

      • Hormone: GnRH-I

        Influenced by:

        • progesterone receptor
          in hypothalamus
          • ovairan progesterione is essential for the secretion of GnRH, mediated by interaction with cognate intracellular progesterone receptor. [1]
      • Hormone: antidiuretic hormone

        Influenced by:

        • CXCR4
          in hypothalamus
          • In acute stimulation conditions, such as an increase in osmolarity or Angiotensin II, SDF-1/CXCL12 co-localized with AVP can be somatodendritically released and inhibit AVP release by an autoregulatory mechanism involving its receptor CXCR4. In conditions in which AVP is chronically stimulated, such as dehydration, SDF-1/CXCL12 is strongly released, resulting in a down-regulation of CXCR4. Such down-regulation of the receptor blocks the inhibitory effect of SDF-1/CXCL12 on AVP release, allowing a sustained increase in AVP secretion. [2]
      • Hormone: NT

      • Hormone: GH

        Influenced by:

        • GHS-R1a
          in hypothalamus
          • Ghrelin is an endogenous ligand for the growth hormone secretagogue type 1a receptor (GHS-R1a), the functionally active form of GHS-R, and stimulates feeding and growth hormone secretion. [3]
          • Ghrelin stimulates GH release by activating both AC and PLC pathways, either by binding to distinct binding pockets of GHS-R, and/or enabling dimeric GHS-R forms, or by binding and activating an alternate, different receptor. [4]
        • GHSR
          in hypothalamus
          • GHS-R in the hypothalamus is involved in the regulation of GH secretion, food intake, and adiposity. [5]
      • Hormone: insulin-like peptide INSL5

      • Hormone: nociceptin

      • Hormone: cocaine- and amphetamine-regulated transcript protein

      • Hormone: orexin-A

      • Hormone: RFRP-1

        • Neuropeptides RFRP-1 and NPVF are detected in the hypothalamus. [6]

        Influenced by:

        • melatonin 1 receptor
          in hypothalamus
          • Melatonin stimulates the expression and release of GnIH via melatonin receptors expressed by GnIH neurons. [7]
      • Hormone: angiopoietin-like protein 4

        • Angptl4 was ubiquitously expressed in hypothalamus, cerebrum, and cerebellum. [8]
      • Hormone: secretoneurin

        • The highest concentrations of this peptide were present in the hypothalamus, in particular, in the median eminence and are comparable to those of the most highly concentrated neuropeptides. [9]

      Receptors

      • Receptor: CaSR

      • Receptor: leptin receptor isoform b

        Influences:

        • orexin-B
          • Leptin inhibts the secretion of orexin
        • orexin-A
          • Leptin inhibits the secretion of orexin [10]
      • Receptor: NPY2-R

        Influences:

        • NPY
          • PYY(3-36) binding to NPY2-R inhibits orexigenic NPY in hypothalamus causing short-term inhibition of food intake [11]
      • Receptor: mGluR4

      • Receptor: melatonin 1 receptor

        Influences:

        • GnRH-I
          • Potential signal transduction mechanisms involved in the control of GnRH gene expression and secretion by melatonin. [12]
        • MSH
        • RFRP-1
          • Melatonin stimulates the expression and release of GnIH via melatonin receptors expressed by GnIH neurons. [7]
      • Receptor: GHS-R1a

        Influences:

        • GH
          • Ghrelin is an endogenous ligand for the growth hormone secretagogue type 1a receptor (GHS-R1a), the functionally active form of GHS-R, and stimulates feeding and growth hormone secretion. [3]
          • Ghrelin stimulates GH release by activating both AC and PLC pathways, either by binding to distinct binding pockets of GHS-R, and/or enabling dimeric GHS-R forms, or by binding and activating an alternate, different receptor. [4]
        • orexin-A
          • Ghrelin stimulates the secretion of orexin [10]
      • Receptor: glucocorticoid receptor

        Influences:

        • CRH
          • Glucocorticoid/Cortisol binding to GR in the hypothalamus inhibits secretion of CRH [13]
        • orexin-A
          • Glucose inhibits the orexin neurons in the hypothalamus
        • CRH
          • 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. [14]
      • Receptor: progesterone receptor

        Influences:

        • GnRH-I
          • ovairan progesterione is essential for the secretion of GnRH, mediated by interaction with cognate intracellular progesterone receptor. [1]
      • Receptor: CXCR4

        Influences:

        • antidiuretic hormone
          • In acute stimulation conditions, such as an increase in osmolarity or Angiotensin II, SDF-1/CXCL12 co-localized with AVP can be somatodendritically released and inhibit AVP release by an autoregulatory mechanism involving its receptor CXCR4. In conditions in which AVP is chronically stimulated, such as dehydration, SDF-1/CXCL12 is strongly released, resulting in a down-regulation of CXCR4. Such down-regulation of the receptor blocks the inhibitory effect of SDF-1/CXCL12 on AVP release, allowing a sustained increase in AVP secretion. [2]
      • Receptor: NPY5-R

      • Receptor: NPY6-R

      • Receptor: CCK-1

        Induced phenotype:

        • negative regulation of appetite
          • Cholecystokinin is released by the gastrointestinal system during meals and induces an anorexigenic response. [15]
          • This physiological pathway is believed to be an essential component of postprandial satiety. [16]
          • CCK activates POMC cells in the nucleus of the solitary tract (NTS), which is located in the brainstem. This effect of peripheral CCK is dependent upon melanocortin signaling, because in the absence of MC4R or by pharmacological inhibition of MC4R in the NTS, the anorexigenic effects of CCK are blocked. [17]
      • Receptor: CCK-2

        Induced phenotype:

        • negative regulation of appetite
          • Cholecystokinin is released by the gastrointestinal system during meals and induces an anorexigenic response. [15]
          • This physiological pathway is believed to be an essential component of postprandial satiety. [16]
          • CCK activates POMC cells in the nucleus of the solitary tract (NTS), which is located in the brainstem. This effect of peripheral CCK is dependent upon melanocortin signaling, because in the absence of MC4R or by pharmacological inhibition of MC4R in the NTS, the anorexigenic effects of CCK are blocked. [17]
      • Receptor: GHSR

        Influences:

        • GH
          • GHS-R in the hypothalamus is involved in the regulation of GH secretion, food intake, and adiposity. [5]
      • Receptor: PRLR

        Induced phenotype:

        • tuberoinfundibular hypothalamic development
          • Prolactin induces tuberoinfundibular hypothalamic dopamine development. [18]
        • organ maturation
          • In the hypothalamus, prolactin has been suggested to be important for maturation of the neonatal neuroendocrine system. [19]
      • Receptor: CNTFR

        Induced phenotype:

        • positive regulation of neurogenesis
          • CNTF treatment increases the expression of anorexigenetic nueuons in the hypothalamus [20]
      • Receptor: GLP-1R

        Induced phenotype:

        • reduction of food intake
          • Such data indicate that hypothalamic GLP-1 receptors is likely to participate in the ability of GLP-1 to reduce food intake. [21]
      • Receptor: 5-HT-1D

      • Receptor: dopamine receptor D5

      • Receptor: OPRL1

      • Receptor: GPR10

      • Receptor: steroidogenic factor 1

      • Receptor: GHS-R1

        Induced phenotype:

        • memory performance
          • Ghrelin is involved in memory performance. [22]
        • positive regulation of appetite
          • High ghrelin levels lead on the level of the hypothlamus to increased food intake [23]
        • Short stature

        Influences:

        • GH
          • GHS-R 1a mediates the classical GH-releasing effect [24]
      • Receptor: NPFF-R1

        • GnIH acts on the pituitary and on GnRH neurons in the hypothalamus via a novel G protein-coupled receptor (GPR147) [7]

        Influences:

        • GnRH-I
          • Thus, GnIH/RFRP may also inhibit gonadotropin synthesis and release by inhibiting GnRH neurons [25]
      • Receptor: NPSR1

      Reference