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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

    Substructures

      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