Postnatal handling alters glucocorticoid, but not mineralocorticoid messenger RNA expression in the hippocampus of adult rats

O’Donnell, Dajan; Larocque, Sylvie; Seckl, Jonathan R.; Meaney, Michael J.

doi:10.1016/0169-328x(94)90096-5

Cited by 120 publications

(73 citation statements)

References 28 publications

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“…MDep-induced reduction of cortical GR-mRNA, shown here, is consistent with studies implicating cortical-GR expression in long-term influences of neonatal manipulations on HPA tone [7]. Thus, enhancement of GR-mRNA levels has led to decreased HPA tone [7], whereas reduced expression (reported here) should enhance HPA sensitivity.…”

supporting

confidence: 89%

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Differential regulation of glucocorticoid receptor messenger RNA (GR-mRNA) by maternal deprivation in immature rat hypothalamus and limbic regions

Avishai-Eliner

Hatalski

Tabachnik

et al. 1999

Developmental Brain Research

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Maternal deprivation (MDep) of neonatal rats significantly influences the hypothalamic-pituitaryadrenal (HPA) axis. This study hypothesized that GR-mRNA modulation constituted an early, critical mechanism for the acute effects of MDep on neuroendocrine stress-responses. GR-mRNA hybridization signal in hippocampal CA1, hypothalamic paraventricular nucleus (PVN) and frontal cortex was significantly reduced immediately following 24 h MDep. In amygdala, cingulate cortex, PVN and CA1, apparent gender-dependent MDep effects on GR-mRNA expression were observed, without significant differences in absolute levels. Thus, rapid, regionspecific MDep effects on GR-mRNA expression in HPA-regulating areas are shown, consistent with involvement of GR-expression in mechanisms of MDep influence on HPA tone.

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supporting

confidence: 89%

“…Thus, enhancement of GR-mRNA levels has led to decreased HPA tone [7], whereas reduced expression (reported here) should enhance HPA sensitivity.…”

mentioning

confidence: 60%

Differential regulation of glucocorticoid receptor messenger RNA (GR-mRNA) by maternal deprivation in immature rat hypothalamus and limbic regions

Avishai-Eliner

Hatalski

Tabachnik

et al. 1999

Developmental Brain Research

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“…Sensory input derived from altered maternal behavior is generally believed to influence the pup's HPA-axis at the molecular level, leading eventually to significantly reduced responses to subsequent stress (4,6). Thus, enhanced GR expression in hippocampus and frontal cortex (29,30) and decreased levels of hypothalamic CRH expression (10, 11) of adult rats handled early in life have been considered to underlie their diminished stress response compared with that of those raised undisturbed.…”

Section: Early-life Experience Influences the Stress Response Profounmentioning

confidence: 99%

Down-Regulation of Hypothalamic Corticotropin-Releasing Hormone Messenger Ribonucleic Acid (mRNA) Precedes Early-Life Experience-Induced Changes in Hippocampal Glucocorticoid Receptor mRNA**This work was supported by NIH Grants NS-28912 and NS-39307.

et al. 2001

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Early-life experiences, including maternal interaction, profoundly influence hormonal stress responses during adulthood. In rats, daily handling during a critical neonatal period leads to a significant and permanent modulation of key molecules that govern hormonal secretion in response to stress. Thus, hippocampal glucocorticoid receptor (GR) expression is increased, whereas hypothalamic CRH-messenger RNA (mRNA) levels and stress-induced glucocorticoid release are reduced in adult rats handled early in life. Recent studies have highlighted the role of augmented maternal sensory input to handled rats as a key determinant of these changes. However, the molecular mechanisms, and particularly the critical, early events leading from enhanced sensory experience to long-lasting modulation of GR and CRH gene expression, remain largely unresolved.To elucidate the critical primary genes governing this molecular cascade, we determined the sequence of changes in GR-mRNA levels and in hypothalamic and amygdala CRH-mRNA expression at three developmental ages, and the temporal relationship between each of these changes and the emergence of reduced hormonal stress-responses. Down-regulation of hypothalamic CRH-mRNA levels in daily-handled rats was evident already by postnatal day 9, and was sustained through postnatal days 23 and 45, i.e. beyond puberty. In contrast, handling-related up-regulation of hippocampal GR-mRNA expression emerged subsequent to the 23rd postnatal day, i.e. much later than changes in hypothalamic CRH expression. The hormonal stress response of handled rats was reduced starting before postnatal day 23. These findings indicate that early, rapid, and persistent changes of hypothalamic CRH gene expression may play a critical role in the mechanism(s) by which early-life experience influences the hormonal stress-response long-term.EARLY-LIFE EXPERIENCE influences both hormonal and behavioral responses to stress throughout life (1-5). In the human, early-life experiences may modulate stress-responses and coping, with long-term implications for emotional health and cognitive function (5). In rats, daily handling during a critical neonatal period leads to a significantly reduced stress response (compared with animals raised without any disturbance) that persists throughout

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“…These effects appear to be mediated by changes in hippocampal glucocorticoid receptor gene expression (14) which can either permanently increase or decrease sensitivity to feedback, depending on subtle differences in perinatal experience (15). Further support for a role of glucocorticoids in maintaining high blood pressure following fetal undernutrition comes from the observation that adrenalectomy in rats exposed to a low-protein diet in utero lowered blood pressure, and that subsequent replacement of corticosterone increased blood pressure (16).…”

Section: Intrauterine Programming Mechanismsmentioning

confidence: 98%

Perinatal development and adult blood pressure

Ashton

2000

Braz J Med Biol Res

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A growing body of evidence supports the concept of fetal programming in cardiovascular disease in man, which asserts that an insult experienced in utero exerts a long-term influence on cardiovascular function, leading to disease in adulthood. However, this hypothesis is not universally accepted, hence animal models may be of value in determining potential physiological mechanisms which could explain how fetal undernutrition results in cardiovascular disease in later life. This review describes two major animal models of cardiovascular programming, the in utero protein-restricted rat and the cross-fostered spontaneously hypertensive rat. In the former model, moderate maternal protein restriction during pregnancy induces an increase in offspring blood pressure of 20-30 mmHg. This hypertensive effect is mediated, in part, by fetal exposure to excess maternal glucocorticoids as a result of a deficiency in placental 11-ß hydroxysteroid dehydrogenase type 2. Furthermore, nephrogenesis is impaired in this model which, coupled with increased activity of the renin-angiotensin system, could also contribute to the greater blood pressure displayed by these animals. The second model discussed is the cross-fostered spontaneously hypertensive rat. Spontaneously hypertensive rats develop severe hypertension without external intervention; however, their adult blood pressure may be lowered by 20-30 mmHg by crossfostering pups to a normotensive dam within the first two weeks of lactation. The mechanisms responsible for this antihypertensive effect are less clear, but may also involve altered renal function and downregulation of the renin-angiotensin system. These two models clearly show that adult blood pressure is influenced by exposure to one of a number of stimuli during critical stages of perinatal development. Correspondence

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Postnatal handling alters glucocorticoid, but not mineralocorticoid messenger RNA expression in the hippocampus of adult rats

Cited by 120 publications

References 28 publications

Differential regulation of glucocorticoid receptor messenger RNA (GR-mRNA) by maternal deprivation in immature rat hypothalamus and limbic regions

Differential regulation of glucocorticoid receptor messenger RNA (GR-mRNA) by maternal deprivation in immature rat hypothalamus and limbic regions

Down-Regulation of Hypothalamic Corticotropin-Releasing Hormone Messenger Ribonucleic Acid (mRNA) Precedes Early-Life Experience-Induced Changes in Hippocampal Glucocorticoid Receptor mRNA**This work was supported by NIH Grants NS-28912 and NS-39307.

Perinatal development and adult blood pressure

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