Response of the Adrenal Cortex of the Neonatal Rat after Subjection to Stress

Haltmeyer, Gary C.; Denenberg, Victor H.; Thatcher, J.; Zarrow, M. X.

doi:10.1038/2121371a0

Cited by 110 publications

(38 citation statements)

References 14 publications

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“…However the problem with this supposition has been that the majority of the reported values for plasma corticosterone during development are uniformly high from the second through the third postnatal week (66)(67)(68)(69)(70). We raised the question of why the high concentrations of endogenous corticosterone did not elicit intestinal changes during the second week of life and proposed (57,71) that the timing of glucocorticoid action in this system must reflect increased responsiveness of the target cells at the beginning of the third postnatal week.…”

Section: Role Of Hormonesmentioning

confidence: 99%

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Biochemistry of Intestinal Development

Henning¹

1979

Environmental Health Perspectives

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In biochemical terms, the rat small intestine is relatively immature at birth and for the first two postnatal weeks. Then during the third week a dramatic array ofenzymic changes begins, and by the end ofthe fourth week the intestine has the digestive and absorptive properties of the adult. Selective examples of these changes are discussed with emphasis on their implications for toxicological studies. The review also includes a detailed consideration of the roles of the dietary change of weaning and of glucocorticoid and thyroid hormones in the regulation of intestinal development.My aim in this paper is to use the rat as a model system for a discussion of the postnatal development of small intestinal function. Factors which affect the developmental process will be reviewed in terms of their implications for toxicological studies. Morphologic Development of the IntestineBy the time of birth, the intestinal mucosa of the rat displays a high level of structural development characterized by villi lined with a single layer of columnar epithelial cells which have well-defined microvilli at their absorptive surface (1-3). After birth, continuous proliferation of epithelial cells occurs only in the lower regions of the crypts (4, 5), and cells migrate from there onto and along the villi, eventually being extruded from the tips into the lumen of the intestine. In adult rats and mice the generation time for the crypt cells is 10-14 hr (6), and the transit time along the length of the villus is approximately 48 hr (7). The characteristics of proliferation and migration of enterocytes in adult animals are dealt with in detail in the review by Lipkin (8). In neonatal rats, generation and migration of the cells is much slower than in adults. Despite the fact that the neonatal villi are shorter, the transit time is at least % hr (7, 9). During the third postnatal week there are significant changes in both cell kinetics and mor-

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Section: Role Of Hormonesmentioning

confidence: 99%

“…Although the hypothalamus-pituitary-adrenal axis is quiescent from day 3 through day 10 (67,68,70), between days 11 and 18, stress-induced elevation of plasma corticosterone can be expected to cause precocious maturation of intestinal function. The stress effect of administering nutrient by gastrostomy has already been mentioned (41).…”

Section: Role Of Hormonesmentioning

confidence: 99%

Biochemistry of Intestinal Development

Henning¹

1979

Environmental Health Perspectives

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“…Stress responses in neonatal rats appear during the third postnatal week (Haltmeyer et al, 1966;Kakihana et al, 1974), but there are no studies in the literature pertaining to opioid control of stress responses during development. Accordingly we have studied the ontogeny of opioid modulation of corticosterone responses to stress from day 10 to adulthood.…”

Section: Introductionmentioning

confidence: 99%

Developmental responses to opioids reveals a lack of effect on stress‐induced corticosterone levels in neonatal rats

Bailey

Kitchen

1987

British J Pharmacology

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1 The neonate has an unusual capacity for survival and the possibility exists that mechanisms for controlling stress responses may differ in the developing animal. In adults both endogenous and exogenous opioids can modulate the corticosterone responses to stress. We have studied this effect in neonatal rats and found that opioid modulation is absent in early postnatal development.2 Neonatal rats ofeither sex were injected with morphine (5-50mg kg-'), fentanyl (10-100 .tLg kg-'), buprenorphine (O.1-30 mg kg') or naloxone (O.1-Omg kg-') and plasma corticosterone measured fluorimetrically 15 or 20 min later. In addition naloxone reversibility studies (1 mg kg-', co-administered) were carried out for the opioid agonists. 3 In adult rats, elevations in plasma corticosterone caused by injection stress were potentiated by morphine, fentanyl and buprenorphine. In neonates, though injection stress-induced rises in plasma corticosterone were absent at 10 days, elevations were observed at 21 days and later. However, significant potentiation of this corticosterone response by fentanyl was absent at 21 days and at later ages (30 and 40 days) for morphine and buprenorphine. The potentiating effect of all three agonists did not become fully effective until day 45. In addition, in animals acclimatized to injection stress by 7 day injection pretreatment, fentanyl did not significantly alter corticosterone levels in 30 day old neonates.4 High doses ofnaloxone (10mg kg-')significantly increased the corticosterone response to injection stress in adult rats but this effect was absent in 30 day old animals. A dose of naloxone (I mg kg-') which had no significant effect on the corticosterone response inhibited the effects of morphine, fentanyl and buprenorphine in 45 day old and adult rats. 5 This late development of opioid action is unusual in comparison with the maturation of endogenous peptides, receptors and antinociceptive responses and suggests that alternative mechanisms may be involved in stress-control in the neonate.

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“…Jamdar and Greengard [3] reported that administration of hydrocortisone and glucose induced glucokinase activity as early as the 10th postnatal day. They concluded that the change to solid food and the flux in glucocorticoid secretion that occurs around the 10th postnatal day [5,6] were the physiological stimuli for normal development of this enzyme. Administration of corticotropin or insulin has been reported by Adelman and Freeman [7] to induce glucokinase activity at the 4th postnatal day.…”

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confidence: 99%

Premature Induction of Glucokinase in the Neonatal Rat by Thyroid Hormone

Partridge

Hoh

Weaver

et al. 1975

European Journal of Biochemistry

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It was shown that the development of liver glucokinase in the rat coincided with a peak in the levels of circulating thyroid hormone at about the 16th postnatal day. Administration of thyroid inhibitors blocked the development of the enzyme and administration of thyroid hormone restored activity to normal levels. Glucokinase could be induced prematurely as early as the 2nd postnatal day by the administration of thyroid hormone followed by daily injection of glucose (10 mg/g body weight). Glucocorticoids and corticotropin failed to induce glucokinase activity prematurely. The postnatal increase in circulating thyroid hormone levels together with increased intake of carbohydrate at weaning may be the normal physiological stimulus for induction of this enzyme.

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Response of the Adrenal Cortex of the Neonatal Rat after Subjection to Stress

Cited by 110 publications

References 14 publications

Biochemistry of Intestinal Development

Biochemistry of Intestinal Development

Developmental responses to opioids reveals a lack of effect on stress‐induced corticosterone levels in neonatal rats

Premature Induction of Glucokinase in the Neonatal Rat by Thyroid Hormone

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