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Details for anatomical structure: brain

EndoNet ID: ENC00020

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Synonyms

brain, encephalon, suprasegmental structures, suprasegmental levels of nervous system, Encephalon

General information

One of the two components of the central nervous system, contained within the cranium; the brain is the centre of thought and emotion, it is responsible for the coordination and control of bodily activities and the interpretation of information from the senses (sight, hearing, smell)

Links to other resources

Cytomer cy0051792

Larger structures

  • central_nerve_system_element

Substructures

  • area_postrema_of_pons
  • isocortex
  • acidophil_somatotroph_cell_of_anterior_pituitary
  • epiphysis
  • pituitary_gland_of_diencephalon
  • arcuate_nucleus_of_hypothalamus
  • subthalamic_nucleus
  • hippocampus
  • tegmentum_of_mesencephalon
  • cerebral_cortex
  • astrocyte
  • glial_cell_of_peripheral_nervous_system
  • amygdaloid_body
  • suprachiasmatic_nucleus_of_hypothalamus
  • mesenchyme_cell
  • macrophage
  • basket_cell
  • paraventricular_nucleus_of_hypothalamus
  • oligodendrocyte
  • microglial_cell_in_central_nervous_system
  • neuromuscular_junction
  • cerebellum
  • corpus_callosum
  • pallidum
  • substantia_nigra
  • medulla_oblongata
  • putamen
  • lateral_hypothalamic_area
  • bergmann_glia
  • endothelial_cell
  • olfactory_bulb
  • basophil_gonadotroph_cell_of_anterior_pituitary_FSH
  • folliculostellate_cell
  • basophil_thyrotroph_cell_of_anterior_pituitary
  • glial_cell_of_central_nervous_system
  • dentate_gyrus_of_hippocampus
  • cell_of_intermediate_pituitary
  • adenohypophysis
  • Müllers_radial_cell_of_retina
  • choroid_plexus_of_telencephalon
  • Golgi_cell
  • osteoblast
  • gonadotropin_releasing_hormone_neuron
  • compact_part_of_substantia_nigra
  • basophil_corticotroph_cell_of_anterior_pituitary
  • posterior_raphe_nucleus_of_midbrain
  • cerebellar_cortex
  • fibroblast
  • Schwann_cell
  • bed_nucleus_of_stria_terminalis
  • brain_stem
  • periventricular_nucleus_of_hypothalamus
  • caudate_nucleus
  • thalamus
  • granular_layer_of_cerebellar_cortex
  • Purkinje_cell
  • corpus_striatum
  • supra-optic_nucleus
  • reticular_part_of_substantia_nigra
  • smooth_muscle_cell
  • pyramidal_layer_of_hippocampus
  • red_nucleus
  • hypothalamus
  • nucleus_accumbens
  • ventromedial_nucleus_of_hypothalamus
  • acidophil_mammotroph_cell_of_anterior_pituitary
  • white_matter
  • neuron
  • osteocyte

Secreted hormones

  • Hormone: C-C motif chemokine 2

    • The pro-inflammatory chemokine MCP-1 is both released by and stimulates astrocytes. [1]

  • Hormone: CLC

  • Hormone: MCP-2

  • Hormone: abeta42

    Influenced by:

    • thrombin receptor
      in brain
      • The amyloid beta-protein (A beta) and protease nexin-2/amyloid beta-protein precursor (PN-2/A beta PP) are major constituents of senile plaques and cerebrovascular deposits in individuals with Alzheimer's disease and related disorders. It has been suggested that the coagulation protease thrombin may process A beta PP in a manner leading to the formation of A beta. [2]
      • Effects of thrombin on the secretion and processing of PN-2/A beta PP and the production of A beta in a cellular system. [2]
      • thrombin does not directly contribute to A beta formation, its proteolysis of secreted PN-2/A beta PP may disrupt regions near the carboxyl terminus of the secreted proteins that account for their neuroprotective and cell adhesive properties. [2]
      • Thrombin was found to proteolyze secreted forms of A beta PP proteins and, through activation of its cell surface receptor, induce secretion of PN-2/A beta PP in certain cell types resulting in decreased levels of soluble A beta. These findings demonstrate that thrombin causes nonamyloidogenic processing of ApPP in cultured cells. [2]

  • Hormone: abeta40

    Influenced by:

    • thrombin receptor
      in brain
      • The amyloid beta-protein (A beta) and protease nexin-2/amyloid beta-protein precursor (PN-2/A beta PP) are major constituents of senile plaques and cerebrovascular deposits in individuals with Alzheimer's disease and related disorders. It has been suggested that the coagulation protease thrombin may process A beta PP in a manner leading to the formation of A beta. [2]
      • Effects of thrombin on the secretion and processing of PN-2/A beta PP and the production of A beta in a cellular system. [2]
      • Thrombin does not directly contribute to A beta formation, its proteolysis of secreted PN-2/A beta PP may disrupt regions near the carboxyl terminus of the secreted proteins that account for their neuroprotective and cell adhesive properties. [2]
      • Thrombin was found to proteolyze secreted forms of A beta PP proteins and, through activation of its cell surface receptor, induce secretion of PN-2/A beta PP in certain cell types resulting in decreased levels of soluble A beta. These findings demonstrate that thrombin causes nonamyloidogenic processing of ApPP in cultured cells. [2]

  • Hormone: neuregulin-2

    • NRG-2 was identified on the basis of its homology to NRG-1 and, like NRG-1, is expressed predominantly by neurons in the central nervous system. [3]

  • Hormone: hepcidin

  • Hormone: BMP2

  • Hormone: BMP7

  • Hormone: neuregulin 1 isoform GGF2

  • Hormone: MCH

  • Hormone: osteomodulin

  • Hormone: laminin-5B

  • Hormone: nocistatin

  • Hormone: WNT3A

  • Hormone: Dkk2

  • Hormone: Dkk1

  • Hormone: Dkk2

  • Hormone: SFRP1

  • Hormone: sFRP-2

  • Hormone: sFRP-3

  • Hormone: sFRP-5

  • Hormone: twisted gastrulation

  • Hormone: crossveinless-2

  • Hormone: gremlin-1

  • Hormone: laminin alpha-5 chain

  • Hormone: semaphorin 3B

  • Hormone: semaphorin 3F

  • Hormone: semaphorin 3E

  • Hormone: QRFP

  • Hormone: humanin

  • Hormone: CTGF

  • Hormone: SEMA4D

  • Hormone: IL-17D

  • Hormone: apelin-28

  • Hormone: apelin-31

  • Hormone: apelin-36

  • Hormone: CYR61

  • Hormone: laminin alpha-1 chain

  • Hormone: neudesin

  • Hormone: NT

  • Hormone: CGRP2

  • Hormone: Cystatin-C

  • Hormone: laminin alpha-2 chain

  • Hormone: leumorphin

  • Hormone: dynorphin B

  • Hormone: beta-neoendorphin

  • Hormone: laminin gamma-3 chain

  • Hormone: tomoregulin-2 ectodomain

  • Hormone: VCAM1 soluble form

  • Hormone: slit-1

    • SLIT1 expression is neuronal specific. [4]

  • Hormone: slit-3 isoform 1

  • Hormone: vasorin

  • Hormone: TIP39

  • Hormone: IL-28A

  • Hormone: IL-28B

  • Hormone: IL-29

  • Hormone: FAM3A

  • Hormone: VIP

  • Hormone: NPS

    • Prepro-NPS mRNA is expressed discretely in a few brain areas, with strongest expression in the peri-locus ceruleus, principle sensory 5 nucleus, and the lateral parabrachial nucleus of the brainstem. [5]

  • Hormone: big dynorphin

    • Dynorphins are produced in several brain areas, including the basal ganglia, striatum, hippocampus, cerebral cortex, and spinal cord. [6]
    • Big Dyn was identified in the pituitary gland and brain as an abundant prodynorphin-derived peptide. [6]

  • Hormone: C-type natriuretic peptide

    • CNP is the most highly expressed natriuretic peptide in the brain and is found in high concentrations in chondrocytes and cytokine-exposed endothelial cells. [7]

Receptors

  • Receptor: sst1

  • Receptor: sst2

  • Receptor: sst5

  • Receptor: sst3

  • Receptor: sst4

  • Receptor: glucocorticoid receptor

  • Receptor: THRA1

  • Receptor: GR-beta

  • Receptor: PPARgamma1

    • PPARγ1 has a broader expression pattern that extends to settings such as the gut, brain, vascular cell and specific kinds of immune and inflammatory cells. [8]

  • Receptor: Tie2

  • Receptor: EP4

  • Receptor: TLR7

  • Receptor: angiotensin II type 1 receptor

    Induced phenotype:

    • regulation of blood pressure
      • In the brain, intraventricular injection of angiotensin II causes a dramatic pressor response mediated by AT1 receptors. [9]
      • AT1 receptors outside the kidney also make a unique contribution to blood pressure homeostasis that is virtually equivalent to and independent of the intrarenal actions of angiotensin II. [10]
      • AT1 receptors in the CNS and/or in the vasculature are more likely to mediate the component of blood pressure regulation that is independent of the kidney. [10]

  • Receptor: RXR-alpha

  • Receptor: laminin receptor

  • Receptor: B-CAM

  • Receptor: frizzled 9

  • Receptor: frizzled 10

  • Receptor: kremen 2

  • Receptor: PTC1

  • Receptor: neuropilin 1

    Induced phenotype:

    • axon guidance
      • Semaphorin 3a is a chemorepellent with multiple guidance functions, including axon pathfinding. [11]

  • Receptor: PLXND1

    Induced phenotype:

    • CHARGE syndrome
      • Mutations in Sema3e are associated with CHARGE syndrome. [12]

  • Receptor: PLXNA2

  • Receptor: Vascular endothelial growth factor receptor 1

  • Receptor: sVEGF-R1

  • Receptor: renin receptor

    • High levels found in the heart, brain, placenta, and lower levels in the kidney and liver. [13]

  • Receptor: PACAP-R-1

    Induced phenotype:

    • negative regulation of neuron apoptosis
      • PACAP-38 has an antiapoptotic effect on neurons, it increases survival of cerebellar neurons in a dose-dependent manner by decreasing the extent of apoptosis estimated by DNA fragmentation. PACAP-38 induced activation of the extracellular signal-regulated kinase (ERK)-type of mitogen-activated protein (MAP) kinase through a cAMP-dependent pathway. [14]

  • Receptor: VPAC1

    Induced phenotype:

    • regulation of immune system process
      • Vasoactive intestinal peptide contributes ot homeostasis of the immune system. [15]
    • regulation of circadian rhythm
      • Vasoactive intestinal peptide regulates mammalian circadian clock. [16]
    • regulation of exocrine and endocrine secretion
      • Vasoactive intestinal peptide is a neuropeptide that contributes to regulation of intestinal secretion and motility, and of exocrine and endocrine secretions. [15]
    • sensory perception of pain
      • Vasoactive intestinal peptide participatse in pain perception. [17]
    • suppression of inflammation
      • Vasoactive intestinal peptide is important for suppression of inflammation. [18]

  • Receptor: LTB4-R1

  • Receptor: basigin

    Influences:

    • MMP-3
      • CD147/Basigin induces matrix metalloproteinase expression in neighbouring fibroblasts, leading to tumor cell invasion [19]

  • Receptor: IL-10R-alpha

  • Receptor: mGluR2

  • Receptor: GluR-3

  • Receptor: GluR-2

  • Receptor: GluR delta-1

    Induced phenotype:

    • high frequency hearing

  • Receptor: GFR-alpha-2

    Induced phenotype:

    • regulates noxious heat transduction

  • Receptor: ADAM17

  • Receptor: ALCAM

  • Receptor: neogenin

  • Receptor: Putative tumor suppressor protein EXTL3

    • However, EXTL3 is also expressed in other tissues, such as brain. [20]

  • Receptor: EphA6

  • Receptor: vasorin

  • Receptor: ephrin-A5

  • Receptor: ROBO1

  • Receptor: ROBO2

  • Receptor: CHRNA1-2

  • Receptor: MRC2

  • Receptor: thrombin receptor

    Influences:

    • FSH
    • abeta40
      • The amyloid beta-protein (A beta) and protease nexin-2/amyloid beta-protein precursor (PN-2/A beta PP) are major constituents of senile plaques and cerebrovascular deposits in individuals with Alzheimer's disease and related disorders. It has been suggested that the coagulation protease thrombin may process A beta PP in a manner leading to the formation of A beta. [2]
      • Effects of thrombin on the secretion and processing of PN-2/A beta PP and the production of A beta in a cellular system. [2]
      • Thrombin does not directly contribute to A beta formation, its proteolysis of secreted PN-2/A beta PP may disrupt regions near the carboxyl terminus of the secreted proteins that account for their neuroprotective and cell adhesive properties. [2]
      • Thrombin was found to proteolyze secreted forms of A beta PP proteins and, through activation of its cell surface receptor, induce secretion of PN-2/A beta PP in certain cell types resulting in decreased levels of soluble A beta. These findings demonstrate that thrombin causes nonamyloidogenic processing of ApPP in cultured cells. [2]
    • abeta42
      • The amyloid beta-protein (A beta) and protease nexin-2/amyloid beta-protein precursor (PN-2/A beta PP) are major constituents of senile plaques and cerebrovascular deposits in individuals with Alzheimer's disease and related disorders. It has been suggested that the coagulation protease thrombin may process A beta PP in a manner leading to the formation of A beta. [2]
      • Effects of thrombin on the secretion and processing of PN-2/A beta PP and the production of A beta in a cellular system. [2]
      • thrombin does not directly contribute to A beta formation, its proteolysis of secreted PN-2/A beta PP may disrupt regions near the carboxyl terminus of the secreted proteins that account for their neuroprotective and cell adhesive properties. [2]
      • Thrombin was found to proteolyze secreted forms of A beta PP proteins and, through activation of its cell surface receptor, induce secretion of PN-2/A beta PP in certain cell types resulting in decreased levels of soluble A beta. These findings demonstrate that thrombin causes nonamyloidogenic processing of ApPP in cultured cells. [2]

  • Receptor: neurotensin receptor type 1

    Induced phenotype:

    • eating behavior
      • NTR1 is involved in control of food consumption and body weight, but not in Neurotensin-induced analgesia. [21]

  • Receptor: PLXNB1

    Induced phenotype:

    • axon guidance
      • Binding of CD100/Sema4D to plexin-B1 (plexin-B1 associates with active Rac) leads to subsequent RhoA activation, this is responsible for CD100/Sema4D-induced growth cone collapse and neurite retraction, demonstrating a requirement for Rho guanine nuclear exchange factors (RhoGEFs) and RhoA activation in CD100/Sema4D-mediated cytoskeletal changes. [22]

  • Receptor: CRF-R1

    Influences:

    • antidiuretic hormone
      • Basal HPA axis may be affected by magnocellular CRF that directly stimulates the AVP secretion through a paracrine mechanism at the level of neurohemal zone of the neurohypophysis. [23]

  • Receptor: PRLR

    Induced phenotype:

    • hyperphagia
      • Increased Food intake (hyperphagia) can be observed in mammals in response to prolactin. Elevated prolactin levels stimulate food intake in a dose-dependent manner. [24]
    • decrease in libido
      • Elevated circulating prolactin is also thought to be responsible libido. [25]
    • modulation of ATPase activity
      • Prolactin has specific effect on different ATPases, in different regions of the brain. PRL has been shown to effect energy metabolism by modulating ATPase activity in monkey brain: Na+-K+-dependent ATPase was stimulated while Mg2+ and Ca2+-dependent ATPases were reduced in neural as well as glial cells. [26]
    • regulation of sensory perception of pain
      • Prolactin has been shown to have analgesic effects that can be mimicked by a number of central nervous system neurotransmitters. [27]
    • alteration of sleep-wake-cycle
      • Elevated circulating prolactin is thought to be responsible for and alteration of the sleep-wake-cycle. [28]
    • increase in REM sleep
      • Elevated circulating prolactin is thought to be responsible for increased rapid eye movement sleep. [29]
    • adaptive stress response
      • One set of behavioral responses that are induced by prolactin are adaptive stress responses. PRL plays a protective role against stress-induced biological modifications in animals. [30]
    • modulation of carbohydrate metabolism
      • PRL affects carbohydrate metabolism in several vertebrate classes, including hyperglycemic/diabetogenic actions. PRL has a differential effect on the activities of enzymes involved in the Embden-Meyerhoff pathway and the hexose monophosphate shunt in neural and glial cells of male monkeys. [31]
    • induction of excessive grooming
      • PRL is considered to be responsible for inducing excessive grooming in rats. [32]
    • pseudopregnancy
      • In women, elevated levels of prolactin are associated with some phsychosomatic reactions, including a form of pseudopregnancy. [33]

  • Receptor: Lysophosphatidic acid receptor 1

    Induced phenotype:

    • cerebral cortex development
      • LPA1 was identified initially in studies of genes that are involved in the development of the cerebral cortex. [34]
    • positive regulation of cytoskeleton organization
      • EDG2 overexpression in a neuronal-like cell exaggerated LPA-stimulated cytoskeletal changes (Rho-mediated). [35]
    • regulation of actin filament bundle assembly
      • In Xenopus LPA1 and LPA2 homologs were reported to regulate normal cortical actin assembly. [36]
    • brain development
      • LPA1 deficiency resulted in defects in cortical development, including reduced proliferative populations and increased cortical apoptosis. [37]
    • inhibition of adenylate cyclase activity by G-protein signaling pathway
      • EDG2 overexpression in a neuronal-like cell exaggerated LPA-stimulated inhibition of adenylate cyclase. [35]

  • Receptor: Sphingosine 1-phosphate receptor 5

    Induced phenotype:

    • proliferation of radial glia cells
      • S1PR5 may play a regulatory role in the transformation of radial glial cells into astrocytes and may affect proliferative activity of these cells. [38]
    • astrocyte development
      • S1PR5 is the receptor for the lysosphingolipid sphingosine 1-phosphate (S1P). S1P is a bioactive lysophospholipid that elicits diverse physiological effect on most types of cells and tissues. S1PR5 may play a regulatory role in the transformation of radial glial cells into astrocytes [38]

  • Receptor: Lysophosphatidic acid receptor 3

  • Receptor: Lysophosphatidic acid receptor 4

  • Receptor: Ovarian cancer G-protein coupled receptor 1

    Induced phenotype:

    • positive regulation of neuron projection development
      • OGR1 is expressed in the brain. SPC induced a neurite outgrowth in the different neuroblastoma cell lines. [39]

  • Receptor: G-protein coupled receptor 12

    Induced phenotype:

    • positive regulation of neuron differentiation
      • SPC stimulates cell proliferation and clustering in hippocampal HT22 cell lines, and it increases amounts of synaptophysin (a neuronal differentiation marker) in primary rat cortical cells that could be mediated by GPR12, suggesting roles for SPC–GPR12 signaling in neuronal differentiation. [40]

  • Receptor: Sphingosine 1-phosphate receptor 1

    Induced phenotype:

    • positive regulation of neurogenesis
      • Embryos lacking S1P exhibit severely disturbed neurogenesis, including neural tube closure, and angiogenesis. [41]
      • S1P1 receptor-null mice also showed severe defects in neurogenesis. [42]

  • Receptor: Sphingosine 1-phosphate receptor 2

    Induced phenotype:

    • neuron projection morphogenesis
      • In neuronal cell culture, SP1 acts through S1P2 and S1P5 to regulate neurite retraction and soma rounding. [43]

  • Receptor: Sphingosine 1-phosphate receptor 3

  • Receptor: G-protein coupled receptor 4

  • Receptor: Psychosine receptor

    Induced phenotype:

    • Krabbe disease
      • Globoid cell leukodystrophy (GLD; also known as Krabbe's disease) is a hereditary metabolic disorder of infants, characterized morphologically by almost total absence of myelin, severe gliosis, and the presence of characteristic, multinucleated globoid cells in the white matter. [44]
      • The deficiency of the catabolic enzyme galatosyl ceramidase results in accumulation of psychosine (PSY; d-galactosyl-β-1,1′-sphingosine) in the brain. [44]
      • This accumulation of PSY in the white matter of children with GLD correlates temporally with apoptosis of oligodendrocytes and globoid cell formation by microglia. [45]
      • The PSY/TDAG8 pair evokes a multinuclear phenotype in cultured cells reminiscent of the globoid cell formation that is the neurohistoligic fingerprint of Krabbe's disease. [46]
    • negative regulation of cytokinesis
      • Psy inhibits cytokinesis and induces the formation of multinuclear globular giant cells. Psy-induced formation of multinuclear cells was not due to cell–cell fusion but to inhibition of cytokinesis. [47]

  • Receptor: FGFR-1

    Induced phenotype:

    • Kallmann syndrome 2
      • Mutations in FGFR1 or FGF8, encoding fibroblast growth factor receptor-1 and fibroblast growth factor-8, respectively, underlie an autosomal dominant form Kallmann syndrome 2 with incomplete penetrance. [48]
    • olfactory bulb morphogenesis
      • FGF signaling through FGFR1 is required for olfactory bulb morphogenesis. [49]
      • A striking defect caused by loss of Fgfr1 in the telencephalon is a failure of normal olfactory bulb (OB) formation. [49]

  • Receptor: relaxin receptor 2

  • Receptor: parathyroid hormone 2 receptor

    • The PTH2 receptor is most likely to function in the brain and the pancreas. [50]
    • Independent demonstration of the presence of PTH2R mRNA and immunoreactivity supports the specific expression of the PTH2R in the human brainstem [51]
    • Northern blots show that PTH2R mRNA is most abundant in the brain. [52]

  • Receptor: glypican 1

    • Glypican 1 is localized in special membrane domains called detergent-insoluble, glycoshingolipid-enriched (DIG) domains. [53]

  • Receptor: PPAR beta/delta

    • Of the three isotypes, PPAR/ has the broadest expression pattern, and the levels of expression in certain tissues depend on the extent of cell proliferation and differentiation. Important functions have been assigned to this isotype in the skin, gut, placenta, skeletal muscle, adipose tissue, and brain [8]

  • 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. [54]
Reference