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Details for anatomical structure: pituitary gland of diencephalon

EndoNet ID: ENC00053

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Synonyms

pituitary gland of diencephalon, hypophysis of diencephalon, pituitary gland of central nervous system, Glandula pituitaria diencephali

General information

A small oval shaped unpaired endocrine gland suspended from the base of the hypothalamus by a short extension of the infundibulum, the infundibular or pituitary stalk, it consists of two major subdivisions, the neurohypohysis and the adenohypophysis

Links to other resources

Cytomer cy0038475

Larger structures

  • brain
  • central_nerve_system_element

Substructures

  • glial_cell_of_central_nervous_system
  • microglial_cell_in_central_nervous_system
  • oligodendrocyte
  • acidophil_somatotroph_cell_of_anterior_pituitary
  • cell_of_intermediate_pituitary
  • adenohypophysis
  • bergmann_glia
  • gonadotropin_releasing_hormone_neuron
  • astrocyte
  • basophil_gonadotroph_cell_of_anterior_pituitary_FSH
  • acidophil_mammotroph_cell_of_anterior_pituitary
  • basophil_corticotroph_cell_of_anterior_pituitary
  • macrophage
  • folliculostellate_cell
  • fibroblast
  • basophil_thyrotroph_cell_of_anterior_pituitary

Secreted hormones

  • Hormone: alpha-MSH

  • Hormone: uteroglobin

  • Hormone: melanotropin beta

  • Hormone: melanotropin gamma

  • Hormone: ACTH

    Influenced by:

    • sst2
      in pituitary_gland_of_diencephalon
      • Selective sst5 activation regulates sst2 signaling resulting in an inhibition of ACTH secretion from pituitary tumor cells. [1]
    • sst5
      in pituitary_gland_of_diencephalon
      • Selective sst5 activation regulates sst2 signaling resulting in an inhibition of ACTH secretion from pituitary tumor cells. [1]
    • FTS receptor
      in pituitary_gland_of_diencephalon
      • Thymulin modulates the secretion of ACTH by the anterior pituitary gland and that its actions are associated with increased cyclic nucleotide formation. [2]

  • Hormone: GnRH-I

  • Hormone: GH

    Influenced by:

    • TRH-R
      in pituitary_gland_of_diencephalon
      • Tri-iodothyronine-induced downregulation of thyrotropin-releasing hormone-binding sites o pituitary membranes (meaning down-regulation of pituitary TRH receptors) inhibits GH secretion. [3]
    • CXCR4
      in pituitary_gland_of_diencephalon
      • SDF-1-alpha /CXCL12 causes both proliferation and growth hormone release, suggesting that the activation of CXCR4 may represent a novel regulatory mechanism for growth hormone secretion and pituitary cell proliferation, which may contribute to pituitary adenoma development. [4]

  • Hormone: PRL

    Influenced by:

    • sst5
      in pituitary_gland_of_diencephalon
      • PRL secretion was inhibited in sst5-expressing tumors [5]
    • FTS receptor
      in pituitary_gland_of_diencephalon
      • Thymulin appears to exert an inhibitory influence on immunoreactive-PRL release. [2]

  • Hormone: LH

    Influenced by:

    • FTS receptor
      in pituitary_gland_of_diencephalon
      • Thymulin modulates possibly the secretion of LH by the anterior pituitary gland and that its actions are associated with increased cyclic nucleotide formation. [2]
    • ER-alpha:ER-beta
      in pituitary_gland_of_diencephalon
      • In female ER alpha knock out mice, disruption of the negative feedback actions of estradiol in the hypothalamic-pituitary axisresults in elevated levels of the gonadotropin subunit mRNAs in the pituitary and in serum LH. [6]

  • Hormone: chemerin

  • Hormone: big dynorphin

    • Big Dyn was identified in the pituitary gland and brain as an abundant prodynorphin-derived peptide. [7]

Receptors

  • Receptor: sst1

  • Receptor: CRF-R1

  • Receptor: GHRH-R

    Induced phenotype:

    • dwarfism

  • Receptor: glucocorticoid receptor

  • Receptor: sst2

    Influences:

    • ACTH
      • Selective sst5 activation regulates sst2 signaling resulting in an inhibition of ACTH secretion from pituitary tumor cells. [1]

  • Receptor: sst5

    Influences:

    • PRL
      • PRL secretion was inhibited in sst5-expressing tumors [5]
    • ACTH
      • Selective sst5 activation regulates sst2 signaling resulting in an inhibition of ACTH secretion from pituitary tumor cells. [1]

  • Receptor: sst3

  • Receptor: THRB1

    • THRB expression pattern is more restricted, and is developmentally regulated. Its main expression sites are the liver, pituitary, inner ear, retina and several brain areas. [8]

  • Receptor: CRF-R2

    Influences:

    • ACTH
      • Inihibition of CRH in the hypothalamus inhibts secretion of ACTH in pituritary gland [9]

  • Receptor: TRH-R

    Influences:

    • GH
      • Tri-iodothyronine-induced downregulation of thyrotropin-releasing hormone-binding sites o pituitary membranes (meaning down-regulation of pituitary TRH receptors) inhibits GH secretion. [3]

  • Receptor: CXCR4

    Influences:

    • GH
      • SDF-1-alpha /CXCL12 causes both proliferation and growth hormone release, suggesting that the activation of CXCR4 may represent a novel regulatory mechanism for growth hormone secretion and pituitary cell proliferation, which may contribute to pituitary adenoma development. [4]

  • Receptor: ER-alpha:ER-beta

    Influences:

    • LH
      • In female ER alpha knock out mice, disruption of the negative feedback actions of estradiol in the hypothalamic-pituitary axisresults in elevated levels of the gonadotropin subunit mRNAs in the pituitary and in serum LH. [6]

  • Receptor: growth hormone receptor

    Induced phenotype:

    • dwarfism
      • In humans, that lack GH or not have a functional GHR, dwarfism is always observed. [10]
      • Laron-like dwarfism [11]
    • Acromegaly due to pituitary adenoma
      • Dysregulated growth hormone hypersecretion is usually caused by a GH-secreting pituitary adenoma and leads to acromegaly. [12]

  • Receptor: FTS receptor

    Induced phenotype:

    • gonadotropin hormone-releasing hormone activity
      • In an in vitro study using pituitary cells obtained from female rats in different days of the estrous cycle, it was observed that thymulin modulates the stimulatory activity of gonadotropin-releasing hormone on LH and follicle-stimulating hormone (FSH) release. [13]
    • neuroendocrine cell differentiation
      • Recent immunoneutralization studies have strengthened the hypothesis that thymulin is a physiological mediator of the perinatal influence of the thymus on neuroendocrine maturation. Thus, neonatal immunoneutralization of circulating thymulin in otherwise normal C57BL/6 mice induced significant morphologic alterations in most anterior pituitary endocrine cell populations when the animals reached puberty. [14]
      • Thymulin immunoneutralization from birth to puberty in normal mice also induced serum gonadotropin and serum TSH, PRL, and GH reduction when the animals reached puberty. [15]
    • regulation of steroid biosynthetic process
      • Thymulin also modulates gonadotropin-induced testicular steroidogenesis. [16]
      • There is in vitro and in vivo evidence suggesting that thymulin plays a role in the regulation of female spontaneous puberty, possibly through effects on pituitary gonadotropin release and ovarian steroidogenesis. [17]

    Influences:

    • ACTH
      • Thymulin modulates the secretion of ACTH by the anterior pituitary gland and that its actions are associated with increased cyclic nucleotide formation. [2]
    • PRL
      • Thymulin appears to exert an inhibitory influence on immunoreactive-PRL release. [2]
    • LH
      • Thymulin modulates possibly the secretion of LH by the anterior pituitary gland and that its actions are associated with increased cyclic nucleotide formation. [2]

  • Receptor: melatonin 1 receptor

    Induced phenotype:

    • inhibition of adenylate cyclase activity by G-protein signaling pathway
      • Inhibition of adenylate cyclase at level of pituitary. [18]

  • Receptor: GHS-R1

    Induced phenotype:

    • Short stature

    Influences:

    • PRL
      • ...stimulatory effect of CST on PRL release is exerted through a receptor not shared by SST...it has been reported that CST(...)binds with high affinity to GHS-R1a(...) which in turn is known to stimulate PRL secretion [19]

  • Receptor: NPFF-R1

    • GnIH acts on the pituitary and on GnRH neurons in the hypothalamus via a novel G protein-coupled receptor (GPR147) [20]

    Influences:

    • FSH
      • Thus, GnIH/RFRP may inhibit gonadotropin synthesis and release by direct actions on the pituitary gland. [21]
    • LH
      • Thus, GnIH/RFRP may inhibit gonadotropin synthesis and release by direct actions on the pituitary gland. [21]
Reference