PubMed · 4326409
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T Fujita. 1971. [Hypoparathyroidism].. https://pubmed.ncbi.nlm.nih.gov/4326409/
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Corticotropin-releasing factor (CRF), a peptide first isolated from mammalian brain, is critical in the regulation of the pituitary-adrenal axis, and in complementary stress-related endocrine, autonomic and behavioural responses. Fish urotensin I and amphibian sauvagine were considered to be homologues of CRF until peptides even more closely related to CRF were identified in these same vertebrate classes. We have characterized another mammalian member of the CRF family and have localized its urotensin-like immunoreactivity to, and cloned related complementary DNAs from, a discrete rat midbrain region. The deduced protein encodes a peptide that we name urocortin, which is related to urotensin (63% sequence identity) and CRF (45% sequence identity). Synthetic urocortin evokes secretion of adrenocorticotropic hormone (ACTH) both in vitro and in vivo and binds and activates transfected type-1 CRF receptors, the subtype expressed by pituitary corticotropes. The coincidence of urotensin-like immunoreactivity with type-2 CRF receptors in brain, and our observation that urocortin is more potent than CRF at binding and activating type-2 CRF receptors, as well as at inducing c-Fos (an index of cellular activation) in regions enriched in type-2 CRF receptors, indicate that this new peptide could be an endogenous ligand for type-2 CRF receptors.
We have investigated the effects of a chronic inflammatory stress on substance P (SP) levels in the hypothalami of rats given adjuvant-induced arthritis (AA). Fourteen days after injection of Mycobacterium butyricum, substance P concentrations in the paraventricular nucleus (PVN) and median eminence/arcuate nucleus were significantly increased. In AA rats injected intraperitoneally with the specific neurokinin-1 receptor antagonist RP67580, plasma ACTH and corticosterone concentrations were significantly elevated, and corticotropin-releasing hormone (CRH) mRNA in the PVN was increased compared to the AA group which received saline alone. The increases in hypothalamic SP in AA, together with the data demonstrating that HPA axis activity is enhanced in AA following injection of a SP antagonist, are consistent with the hypothesis that SP is acting as an inhibitor of CRH expression in this model of chronic inflammatory stress.
ACTH-related peptides are promising neurotrophic and neuroprotective agents, as demonstrated in many in vivo and in vitro studies. They accelerate nerve repair after injury, improving both sensor and motor function. Furthermore, ACTH-related peptides have neuroprotective properties against cisplatin- and taxol-induced neurotoxicity, they improve neuronal function in animals with neuropathy due to experimental diabetes, and they prevent degeneration of myelinated axons in rats suffering from experimental allergic neuritis, a model of peripheral demyelinating neuropathy. Studies in neuronal cultures have corroborated these clinical observations and serve to investigate the mechanism of action of the ACTH-related peptide effects. This paper reviews both in vitro and in vivo effects and emphasizes the mechanism of action. Recent data on melanotrophic receptors and signal transduction systems will be discussed in this context.