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Biomedical subjects

T Sugisaki

Publications and source records attributed to T Sugisaki.

At least 91 records · Page 5Linked to original sources
PubMed1985

Cerebral myelinogenesis in the Snell dwarf mouse: stimulatory effects of GH and T4 restricted to the first 20 days of postnatal life.

We attempted to define the critical time period during early postnatal life when GH and T4 are essential for myelination. We administered bGH and T4 to Snell dwarf mice during the first and second 20 days after birth. Positive results were obtained only when hormones were given during the first 20 days of postnatal life. We observed a distinct increase in brain weight, DNA content, CNPase activity and a remarkably increased level of spontaneous locomotion activity with a diurnal periodicity. Morphological observations of brain sections stained for myelin basic protein (MBP) correlated the biochemical findings. The later administration of hormones was ineffective. Our interpretation is that the administration of exogenous hormones led to increased myelinogenesis through their stimulatory effects on glial proliferation, as evidenced by the increase in cerebral DNA content.

2',3'-Cyclic Nucleotide 3'-Phosphodiesterase↗
PubMed1985

Abnormal neuronal growth in the little (lit) cerebrum.

Mice genetically deficient in growth hormone were compared with normal littermates for evidence of altered neuronal development. In the lit/lit motor cortex, area 6 of Caviness, cell number, stratification of neurons, and the proportionate layer widths were identical to those of the controls (lit/+). Examined by the Golgi-Cox method modified by Ramon-Moliner, however, the pyramidal neuron was found to have short primary dendrites with sparse branchings. This result was confirmed in sections stained for neuron-specific enolase. Therefore, we conclude that growth hormone has an independent action on neuronal development.

Animals↗
PubMed1985

Partial restoration of cerebral myelination of the congenitally hypothyroid mouse by parenteral or breast milk administration of thyroxine.

We attempted to define whether thyroid hormone can ameliorate the cerebral hypomyelination present in the congenitally hypothyroid (hyt) neonatal mouse, and to define the critical time period during early postnatal life when thyroxine (T4) is essential for myelin formation. We administered T4 to the hyt mouse by breast milk during the first 20 days of postnatal life, and through the diet during the second 20 days of postnatal life. Positive results were obtained only when hormone was given during the first 20 days of postnatal life. A distinct increase in cerebral 2',3'-cyclic nucleotide 3'-phosphohydrolase activity was noted, and brain sections stained for myelin basic protein correlated with the biochemical findings. The later administration of hormone through diet was ineffective.

Administration, Oral↗
PubMed1984

Stimulation of Snell dwarf mouse neuronal growth by GH and T4.

An investigation of the Snell dwarf motor cortex, area 6 of Caviness, was carried out by means of a modified Golgi silver impregnation method. The pyramidal neurons located in layer V were found to have small perikarya, short primary dendrites with sparse branchings. Following administration of bovine growth hormone (bGH) and thyroxine (T4) during the first 20 d of postnatal life, this retarded neuronal growth was restored to normal: neuronal perikarya were enlarged, and the dentrites were thicker with denser branchings. These results were confirmed in the sections stained for neuron specific enolase (NSE). These findings demonstrate that exogenous GH and T4, will enhance neuronal growth in the Snell dwarf cerebrum, and restore neuronal arborization to normal.

Animals↗
PubMed1984

Hypomyelination in the cerebrum of the congenitally hypothyroid mouse (hyt).

2',3'-Cyclic nucleotide 3'-phosphohydrolase activity in the cerebrum of the inherited primary hypothyroid mouse (hyt/hyt) is reduced in comparison with the normal heterozygate (hyt/+). No differences were observed with regard to DNA and RNA content and the RNA/DNA ratio. The results of this study indicate that hypomyelination in the hypothyroid mouse is restricted to the cerebrum, and is not related to arrested glial proliferation.

2',3'-Cyclic-Nucleotide Phosphodiesterases↗
PubMed1983

Poor myelination in the central nervous system of "dilute-lethal mutant mice" (d1/d1).

The activity of 2',3'-cyclic nucleotide 3'-phosphohydrolase (CNPase), as a marker for myelinogenesis, was measured in different parts of the nervous system of dilute-lethal mutant mice (d1/d1). The activity in terms of micromoles of 2'-AMP formed per milligram of protein of homogenate per minute was found to be exceedingly reduced in the cerebrum, brain stem, and medulla oblongata, slightly reduced in the cerebellum and cervical spinal cord, but not reduced in the thoracic spinal cord and the optic and sciatic nerves. These results clearly indicate that dilute-lethal mutant mice show poor myelination in the cerebrum, brain stem, and medulla oblongata.

2',3'-Cyclic Nucleotide 3'-Phosphodiesterase↗
PubMed1983

Faulty development of cortical neurons in the Snell dwarf cerebrum.

In the Snell dwarf motor cortex, area 6 of Caviness, the cell number, the stratification of neurons and the portion of layer-widths were absolutely identical to those of the controls. By means of the Golgi-Cox method modified by Ramon-Moliner, however, the pyramidal neuron was found to have small perikarya, short primary dendrites with sparse branchings, and a low spine density on the dendrites. The corpus callosum of the dwarf contained a reduced number of fibers compared to that of the controls, and the staining for myelin basic protein revealed a considerable reduction of positive-fibers of radiation in this area. The content of Thy-1 antigen in the cerebrum, cerebellum and brainstem, was significantly lower than that of controls, but the monoamine content was normal in the cerebrum and brainstem. From these results, it appears that the Snell dwarf cerebrum shows retarded neuronal growth; a reduction in size of neurons, an underdevelopment of axons and dendrites, and a retarded maturation of spine, in addition to arrested glial proliferation. At present, it is unclear which hormone deficient in these mutants, growth hormone or thyroxine, is the essential potentiator for neuronal growth.

Animals↗
PubMed1982

Factors contributing to the poor myelination in the brain of the Snell dwarf mouse.

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.

2',3'-Cyclic-Nucleotide Phosphodiesterases↗
PubMed1982

Effects of bovine growth hormone on the retarded cerebral development induced by neonatal hydrocortisone intoxication.

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.

Animals↗
PubMed1982

Postnatal action of growth and thyroid hormones on the retarded cerebral myelinogenesis of Snell dwarf mice (dw).

Snell dwarf mice (dw) showed a lower CNPase activity (59% of the normal controls) only in the cerebrum among different parts of the CNS, and a strikingly reduced level of spontaneous locomotion activity with an indistinct diurnal periodicity in a 24-h record at 40 days of age. Daily administration of bGH and T4 to the dwarfs during the first 40 days of postnatal life restored CNPase activity to the level of the normal controls, and was accompanied by normalization of the pattern of spontaneous locomotion activity. Daily administration of bGH alone also restored CNPase activity and spontaneous locomotion, but to a lesser extent. The daily administration of thyroid stimulating hormone (TSH) alone, however, failed to restore CNPase activity, in spite of the fact that the thyroid glands of the TSH-treated dwarfs were indistinguishable from the normal controls in organization and appearance. These results indicate that the restoration of both the retarded myelinogenesis and abnormal behavior of the Snell dwarf mice might essentially depend upon GH levels and the synergistic effects of T4.

2',3'-Cyclic-Nucleotide Phosphodiesterases↗