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Details for anatomical structure: central nerve system element

EndoNet ID: ENC00027

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Synonyms

central nerve system element, , Systema nervosum centrale

General information

Pertaining to the brain, cranial nerves and spinal cord; it does not include muscles or peripheral nerves

Links to other resources

Cytomer cy0043783

Larger structures

    Substructures

      Secreted hormones

      • Hormone: norepinephrine

        Influenced by:

        • alpha-2A adrenoreceptor
          in cerebellar_cortex
          • Alpha 2 adrenergic receptors mediate synaptic transmission in pre- and postsynaptic nerve terminals by decreasing the release of norepinephrine (due to the inhibition of the norepinephrine system in the brain) and acetylcholine. [1]
        • alpha-2B adrenoreceptor
          in cerebellar_cortex
          • Alpha 2 adrenergic receptors mediate synaptic transmission in pre- and postsynaptic nerve terminals by decreasing the release of norepinephrine (due to the inhibition of the norepinephrine system in the brain) and acetylcholine. [1]
        • alpha-2C adrenoreceptor
          in cerebellar_cortex
          • Alpha 2 adrenergic receptors mediate synaptic transmission in pre- and postsynaptic nerve terminals by decreasing the release of norepinephrine (due to the inhibition of the norepinephrine system in the brain) and acetylcholine. [1]
      • Hormone: NOV

      • Hormone: cholecystokinin

      • Hormone: REG1A

      • Hormone: slit-1

      • Hormone: CNTF

        • CNTF ia expressed in glia cells within the CNS [2]
      • Hormone: metallothionein 3

      • Hormone: FABP5

      • Hormone: FABP7

      • Hormone: PTN

        • During mouse embryogenesis, PTN is highly expressed in the central and peripheral nervous systems, in organs undergoing branching morphogenesis including the salivary glands, lung and kidney, digestive and skeletal systems, sense organs and facial processes, and limbs. [3]
        • In the adult stage, PTN expression is mainly restricted to the central nervous system. [3]
      • Hormone: cholecystokinin 39

      Receptors

      • Receptor: galanin receptor 2

      • Receptor: complement receptor 3

      • Receptor: 5-ht-5 receptor

      • Receptor: Gamma-aminobutyric acid receptor C

      • Receptor: Gamma-aminobutyric acid receptor A

      • Receptor: Gamma-aminobutyric acid receptor B

      • Receptor: neurotensin receptor type 1

        Induced phenotype:

        • modulation of dopaminergic transmission
        • pituitary hormone release
          • Central administration for Neurotensin: modulation of pituitary hormone release. [4]
        • eating behavior
          • inhibition of food intake
      • Receptor: CRF-R1

        Induced phenotype:

        • regulation of HPA axis
          • Corticotropin-releasing hormone is secreted under stress and regulates the hypothalamic-pituitary-adrenal (HPA) axis. [5]
      • Receptor: PRLR

        Induced phenotype:

        • experimental allergic encephalomyelitis
          • Prolactin has been shown to be increases and to effect a number of autoimmune states, such as acute experimental allergic encephalomyelitis. [6]
          • Prolactin levels are elevated after immunization and before the onset of experimental allergic encephalomyelitis, bromocriptine inhibits both prolactin secretion and the severity of acute experimental allergic encephalomyelitis, and inhibition is also present when treatment is begun after sensitization, suggesting an effect of prolactin on the effector limb of the immune response during experimental allergic encephalomyelitis. [6]
        • Systemic lupus erythematosus
          • Prolactin has been shown to be increases and to effect a number of autoimmune states, such as systemic lupus erythematosus. [7]
      • Receptor: Lysophosphatidic acid receptor 1

        Induced phenotype:

        • schizophrenia
          • An intriguing link may exist between LPA signaling and neurological diseases such as schizophrenia, on the basis of phenotypic and molecular similarities. Craniofacial dysmorphism, defects in prepulse inhibition, and widespread brain alterations in serotonin neurotransmitter levels are present in both Lpar1-deficient mice and patients suffering from schizophrenia. [8]
      • Receptor: FTS receptor

        Induced phenotype:

        • neuroprotection
          • The neuroprotective role of thymulin in the CNS becomes evident during inflammatory states. [9]
          • Thymulin appears to play a protective role against inflammation in the CNS. This protective effect appears to be exerted directly at the level of the CNS. [9]
        • regulation of sensory perception of pain
          • A series of experiments showing the hyperalgesic actions of thymulin in the nervous system. [9]
          • Thymulin may be acting directly or indirectly on nerve terminals of the CNS. PGE2 might be a key mediator in these actions. [9]
          • The attenuation of hyperalgesia by high doses of thymulin involve the downregulation of proinflammatory cytokines. [9]
      • Receptor: 5-ht-6R

      • Receptor: neuromedin B receptor

      • Receptor: PTPRB

        • PTPζ/RPTPβ1 is a receptor-like protein-tyrosine phosphatase, which is abundantly expressed in the central nervous system as a chondroitin sulfate proteoglycan. [10]

        Induced phenotype:

        • neuronal migration
          • We further demonstrated that pleiotrophin-induced neurite outgrowth and neuronal migration were suppressed by chondroitin sulfate, polyclonal antibodies against the extracellular domain of PTPζ, and sodium vanadate, a protein-tyrosine phosphatase inhibitor. [10]
      Reference