Effects of immunologically induced growth hormone deficiency on myelinogenesis in developing rat cerebrum

Pelton, Elaine; Grindeland, R. E.; Young, Elizabeth H.; Bass, Norman H.

doi:10.1212/wnl.27.3.282

Cited by 42 publications

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“…In addition to their effect on enzyme activity, glucocorticoids also regulate the synthesis of GH (Martial et al, 1977;Brattin and Portanova, 1979), and decreased GH levels are known to result in decreased brain weight, DNA content, and amount of myelin (Pelton et al, 1977;Noguchi et al, 1982~). However, in these latter studies, GH levels…”

Section: Discussionmentioning

confidence: 99%

“…The factors that act on the oligodendrocyte to regulate myelination are largely unknown. Certain hormones, including thyroxine and growth hormone (GH), are known to play a role in controlling CNS myelin formation (Hamburgh, 1969;Matthieu et al, 1975;Pelton et al, 1977). Another class of hormones, glucocorticoids, has been shown to regulate the specific activity of various oligodendroglial enzymes believed to be involved in myelination (de Vellis and Inglish, 1968;Dawson and Kernes, 1979;Sapirstein et al, 1980), but the extent to which that control affects myelination has not been investigated.…”

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confidence: 99%

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Adrenalectomy of Rats Results in Hypomyelination of the Central Nervous System

Preston

McMorris

1984

Journal of Neurochemistry

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The effect of adrenalectomy on CNS myelin accumulation was investigated to determine whether glucocorticoids play a role in regulating myelination. When 14-day-old rats were adrenalectomized and sacrificed 7-8 days later, the amount of bulk-isolated myelin in whole brain, as expressed per gram wet weight of brain or per milligram DNA-phosphate, was reduced to about 75% that of sham-operated controls. Both brain weight and DNA content were unchanged by adrenalectomy. Examination of individual brain regions also revealed decreased amounts of myelin in adrenalectomized animals. Brain glycerol 3-phosphate dehydrogenase specific activity was reduced in adrenalectomized animals to 40-60% that of controls, and serum corticosterone levels were less than 0.6% of control levels. The amount of cerebral myelin in animals adrenalectomized on day 21 and sacrificed 9 days later was not significantly reduced. This suggests a possible role of glucocorticoids during the early period of rapid myelination.

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

Adrenalectomy of Rats Results in Hypomyelination of the Central Nervous System

Preston

McMorris

1984

Journal of Neurochemistry

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“…GH deficiency has been associated with more severe deficits in memory, attention, executive function, mood, and sleep, as well as being associated with fatigue, many of which are often reported as postconcussive symptoms. [3][4][5][6][7][8][9][10] GH also may play a critical role in recovery, as it is involved in both myelin formation [11][12][13] and neuronal plasticity. [14][15][16][17] A number of potential pathophysiological mechanisms have been suggested as to how the pituitary gland is damaged.…”

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confidence: 99%

The Effects of Repeat Traumatic Brain Injury on the Pituitary in Adolescent Rats

Greco¹,

Hovda²,

Prins³

2013

Journal of Neurotrauma

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Adolescents are one of the highest groups at risk for sustaining both traumatic brain injury (TBI) and repeat TBI (RTBI). Consequences of endocrine dysfunction following TBI have been routinely explored in adults, but studies in adolescents are limited, and show an incidence rate of endocrine dysfunction in 16-61% in patients, 1-5 years after injury. Similar to in adults, the most commonly affected axis is growth hormone (GH) and insulin-like growth hormone 1 (IGF-1). Despite TBI being the primary cause of morbidity and mortality among the pediatric population, there are currently no experimental studies specifically addressing the occurrence of pituitary dysfunction in adolescents. The present study investigated whether a sham, single injury or four repeat injuries (24 h interval) delivered to adolescent rats resulted in disruption of the GH/IGF-1 axis. Circulating levels of basal GH and IGF-1 were measured at baseline, 24 h, 72 h, 1 week, and 1 month after injury, and vascular permeability of the pituitary gland was quantified via Evans Blue dye extravasation. Changes in weight and length of animals were measured as a potential consequence of GH and IGF-1 disruption. The results from the current study demonstrate that RTBI results in significant acute and chronic decreases in circulation of GH and IGF-1, reduction in weight gain and growth, and an increase in Evans Blue dye extravasation in the pituitary compared with sham and single injury animals. RTBI causes significant disruption of the GH/IGF-1 axis that may ultimately affect normal cognitive and physical development during adolescence.

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“…Previous studies have shown that growth hormone affects myelination in rats and mice. When newborn rats are made growth hormone-deficient by injection of antiserum against growth hormone, CNS myelination is reduced by 70-90%, possibly because of a deficit in the number of oligodendrocytes (28). Secondly, Snell dwarf mice, which are genetically deficient in growth hormone and several other pituitary hormones, myelinate poorly, and the defect is reversible by growth hormone (29,30).…”

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Insulin-like growth factor I/somatomedin C: a potent inducer of oligodendrocyte development.

McMorris¹,

Smith²,

DeSalvo³

et al. 1986

Proc. Natl. Acad. Sci. U.S.A.

345

191

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Cell cultures established from cerebrum of 1-day-old rats were used to investigate hormonal regulation of the development of oligodendrocytes, which synthesize myelin in the central nervous system. The number of oligodendrocytes that developed was preferentially increased by insulin, or by insulin-like growth factor I (IGF-I), also known as somatomedin C. High concentrations (5 Pg/ml) of insulin were required for substantial induction of oligodendrocyte development, whereas only 3.3 ng of IGF-I per ml was needed for a 2-fold increase in oligodendrocyte numbers. At an IGF-I concentration of 100 ng/ml, oligodendrocyte numbers were increased 6-fold in cultures grown in the presence of 10% fetal bovine serum, or up to 60-fold in cultures maintained in serum-free medium. IGF-I produced less than a 2-fold increase in the number of nonoligodendroglial cells in the same cultures. Type I IGF receptors were identified on oligodendrocytes and on a putative oligodendrocyte precursor cell population identified by using mouse monoclonal antibody A2B5. These results indicate that IGF-I is a potent inducer of oligodendrocyte development and suggest a possible mechanism based on IGF deficiency for the hypomyelination that results from early postnatal malnutrition.Oligodendrocytes play a critical role in nervous system function by synthesizing and maintaining myelin in the central nervous system (CNS) (1). Very little is known about the stimuli or regulatory signals that promote the development of oligodendrocytes, but such information might provide the basis for approaches to promote repair in demyelinating disorders.We studied tissue cultures established from cerebrum of MATERIALS AND METHODS Cell Explantation and Culture. Cells were explanted by mechanical dissociation of cerebrum of 1-day-old strain LEC rats as described (3, 4) and were inoculated into polystyrene tissue culture dishes, glass microscope slide chambers, or dishes containing glass coverslips. Glass surfaces were previously treated with D-polylysine (10-50 pug/ml) or polylysine followed by fibronectin (1 Atg/cm2; purified by method B of ref. 9). Cells were maintained as mixed cultures without separation of individual cell types. Unless otherwise noted, culture medium was Eagle's minimum essential medium supplemented with glucose to a total of 6 g/liter, 0.1 mM of each nonessential amino acid, antibiotics, and 10% fetal bovine serum. For serum-free culture, cells were maintained in the presence of 10%6 fetal bovine serum for the first 16-24 hr of culture to allow the cells to attach (10, 11), and the cells were then rinsed and refed with serum-free culture medium. Serum-free medium (modified from ref. 10) consisted ofequal parts of Dulbecco's modified Eagle's medium (high-glucose formula) and Ham's F-12 medium, supplemented with glucose to a total of 6 g/liter/15 nM triiodothyronine/30 nM sodium selenite/transferrin (50 pug/ml). Insulin was absent except where noted. In all cases, medium was changed on the fourth day after explantation and every second da...

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Effects of immunologically induced growth hormone deficiency on myelinogenesis in developing rat cerebrum

Cited by 42 publications

References 0 publications

Adrenalectomy of Rats Results in Hypomyelination of the Central Nervous System

Adrenalectomy of Rats Results in Hypomyelination of the Central Nervous System

The Effects of Repeat Traumatic Brain Injury on the Pituitary in Adolescent Rats

Insulin-like growth factor I/somatomedin C: a potent inducer of oligodendrocyte development.

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