Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.4.37 (CNPase)
 539 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To determine whether somatomedin has a direct action on cerebral development instead of an indirect action of a growth hormone, we examined the central nervous system of the pygmy mouse (pg), a mutant with normal somatomedin activity. Our findings are: (A) the weights of the pg/pg cerebrum and cerebellum weighted were significantly less than those of the normal controls (pg/+), 14 and 15% less, respectively; (B) the total DNA content was reduced by 17% in the cerebrum and cerebellum of the pg/pg mouse; (C) the total RNA content was reduced in the cerebrum and cerebellum, proportional to the reduction in DNA; (D) CNPase activity was reduced selectively in the cerebrum of the pg/pg mouse by 25%; and (E) the pg/pg mice exhibited a strikingly reduced level of activity with an indistinct diurnal periodicity. Therefore, the present findings suggest that the action of somatomedin on the proliferation and maturation of glial cells might be a necessary precondition to myelin formation.
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PMID:Microcephalic cerebrum with hypomyelination in the pygmy mouse (pg). 128 86

We administered bovine growth hormone to the Little (lit), a promising model of isolated growth hormone deficiency, during the first and second 20 days after birth. Positive results were obtained only when bovine growth hormone was given during the first 20 days of postnatal life. We observed a distinct increase in cerebral weight, DNA content, and 2',3'-cyclic nucleotide 3'-phosphohydrolase activity. The latter administration of bovine growth hormone was ineffective. These data prove that growth hormone has an independent action on cerebral development, apart from the complementary or synergistic action of thyroid hormones, and that the administration of exogenous growth hormone led to increased myelinogenesis through its stimulatory effects on glial proliferation, as evidenced by the increase in cerebral DNA content.
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PMID:Restoration of microcephalic cerebrum with hypomyelination in the growth hormone-deficient mouse (lit): stimulatory effects of GH restricted to the first 20 days of postnatal life. 283 65

In comparison with normal controls, hydrocortisone-intoxicated rats (HC rats) had smaller cerebra, lowered 2',3'-cyclic nucleotide 3'-phosphohydrolase (CNPase) activity, and greatly reduced learning ability. The reduction in cerebral weight and DNA content was considered to be caused by a decrease in the number of proliferating glial cells, because the usual postnatal elevation of thymidine kinase (TK) activity was found to be suppressed in the cerebra from the HC rats. Electron microscopic observation of the pituitary gland revealed that the 5-day-old HC rat contained growth hormone (GH) secretory cells which were fully packed with GH granules, suggesting a disorder in the system which releases GH. In an attempt to promote cerebral development in the HC rats, we administered bovine GH (bGH) to some of the HC rats daily from the day of birth until weaning (HC + bGH rats). In the HC + bGH rats, the cerebral DNA was restored to normal levels and a concomitant increase in TK and CNPase activity was noted. Furthermore, in the brightness discrimination test, whereas the HC + bGH rats attained the learning ability of the normal controls after only 10 sessions, the HC rats were unable to reach an equivalent level even after 25 sessions.
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PMID:Effects of bovine growth hormone on the retarded cerebral development induced by neonatal hydrocortisone intoxication. 612 66

Conventional histological examination of the pituitary does not distinguish Snell dwarf mutants (dw/dw) from their normal littermates (+/?) in the neonatal stage. However, immunohistochemical examination of pituitaries of litters born to heterozygous Snell parents revealed that in approximately 25% of the glands examined, the number of positive cells was very low in the neonatal stage. We attempted to delineate the events resulting in the poor myelination in the brain of the Snell dwarf mouse, and to devise an immunohistochemical method for identifying the mutant neonate. Differences in the brain weights of the dw/dw and +/? mice first became apparent on the 10th day of age, and from this time on no further increase in the weight of the dwarf mouse brain was recorded. Increase in CNPase activity was found to be suppressed in the cerebrum and brain stem throughout the developmental stage, but not in the other parts of the brain. The yield of isolated myelin decreased by 58% in the mutant mouse, but CNPase activity was equivalent to that of control myelin. Differences in DNA content per cerebrum from the dw/dw and +/? mice first became apparent on the 10th day of age. Henceforth, the dw/dw mice showed no further increase, although the +/? mice continued to increase. [3H]Thymidine incorporation into the DNA fraction in vivo on the 7th day of age, when glial cell proliferation in the cerebrum is most active, was suppressed to about 50% of the control level in all parts of the dwarf brain. These findings indicate that the poor myelination found in the mutant cerebrum is a hypomyelination due to reduce oligodendroglial proliferation caused by lack of circulating growth hormone.
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PMID:Factors contributing to the poor myelination in the brain of the Snell dwarf mouse. 629 67

Brain composition and developmental changes were investigated in mice homozygous for the locus "dwarf," and characterized by a reduced level of growth hormone, thyroid stimulating hormone, and prolactin, and by secondary hypothyroidism. The difference in adult brain weight (-32%) between the dwarf and the normal mice was not found to parallel the difference in body weight (-71%), whereas the differences in the weight of the liver (-79%) and that of the kidney (-75%) did. Several biochemical parameters of brain development were assayed in dwarf and normal mice between the ages of 15 and 210 days. Levels of cerebrosides, sulfatides, gangliosides, phospholipids, cholesterol, protein, and RNA (per gram wet weight) were the same for the dwarf and the controls, but the net difference in total brain DNA was less than the net total brain RNA difference (-11% vs. -27%). Total brain lipids (absolute quantities) were the same at 15 days. The difference was -37% by the 50th day, and remained constant thereafter. No change in the specific activity of 2',3'-cyclic nucleotide 3'-phosphohydrolase or 3'-phosphoadenosine-5'-phosphosulfate: galactocerebroside sulfotransferase was observed. These data suggest that the regulation of the development of brain structures is maintained, but the level of the synthesis of the various brain constituents is reduced in proportion to the brain weight. The development of the dwarf brain seems to proceed harmoniously.
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PMID:Changes in brain components during the development of mice homozygous for the locus "dwarf" (dw)(1,5.). 2427 46