Development of Pituitary Pro-Opiomelanocortin Gene and Peptide Expression: Characterization and Effect of Repeated Intermittent Maternal Isolation

Vázquez, Delia M.; Akil, Huda

doi:10.1159/000126245

Cited by 21 publications

(4 citation statements)

References 41 publications

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“…The elevation of basal corticosterone and the increased corticosterone response to novelty directly after deprivation are in line with results of other maternal deprivation studies in rats and mice (Cirulli et al, 1994; Levine et al, 1991; Rosenfeld et al, 1991; Schmidt et al, 2002; Stanton et al, 1988; van Oers et al, 1998). Also the lower expression of CRH and GR mRNA in the PVN corresponds to other data (Dent et al, 2000; Schmidt et al, 2002, 2003b; Vazquez and Akil, 1992). However, basal and stress‐induced ACTH were apparently not affected by 24 h maternal deprivation at pnd 4, which is in contradiction to the results of previous maternal deprivation on pnd 9 (Schmidt et al, 2002).…”

Section: Discussionsupporting

confidence: 88%

Ontogeny of the HPA axis of the CD1 mouse following 24 h maternal deprivation at pnd 3

Enthoven

Schmidt

Cheung

et al. 2009

Intl J of Devlp Neuroscience

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One of the striking characteristics of the developing neuroendocrine system of rats and mice is the stress hypo-responsive period (SHRP), i.e. low basal corticosterone secretion and the inability to increase corticosterone in response to mild stressors during the first 2 weeks of life. However, immediately after 24 h of deprivation from maternal care the response of the hypothalamic-pituitary-adrenal (HPA) axis to mild stressors is enhanced. This study examines in CD1 mouse pups the recovery pattern of markers of HPA axis (re)activity from maternal deprivation (once for 24 h from postnatal days (pnds) 3 to 4). As expected, deprivation induced a profound corticosterone response to novelty immediately after deprivation. In contrast, 1 day after reunion with the mother (pnd 5), this effect was abolished, lasting for at least 3 days. Basal corticosterone remained even below control levels. Corticotropin-releasing hormone (CRH) mRNA expression in the hypothalamic paraventricular nucleus (PVN) was suppressed for 2 days, exceeded control levels at pnds 7 and 8, and subsequently followed the gradual decline observed in controls until pnd 12. Delayed and rather short-lasting changes were found for adrenocorticotropic hormone (low at pnd 5), and glucocorticoid receptor mRNA expression (decreased in the PVN at pnd 4, and in the hippocampal CA1 area at pnd 5). Hippocampal mineralocorticoid receptor mRNA expression was unaffected. From pnds 9 to 13, both deprived and control pups gradually emerged from the SHRP in a similar temporal pattern. In conclusion, maternal deprivation at pnd 3 augments hypo-responsiveness of corticosterone secretion to mild stress for several days, but does not affect the duration of the SHRP. Whether CRH and glucocorticoid receptor changes are cause or consequence remains to be established.

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Section: Discussionsupporting

confidence: 88%

Ontogeny of the HPA axis of the CD1 mouse following 24 h maternal deprivation at pnd 3

Enthoven

Schmidt

Cheung

et al. 2009

Intl J of Devlp Neuroscience

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“…CORT was assayed with all groups represented using a RIA as previously described (Vázquez and Akil, 1992). The antibody crossreacts 2.2% with cortisol and less than 1% with other endogenous steroids.…”

Section: Riamentioning

confidence: 99%

Impact of Maternal Deprivation on Brain Corticotropin-Releasing Hormone Circuits: Prevention of CRH Receptor-2 mRNA Changes by Desipramine Treatment

Vázquez

Eskandari

Phelka

et al. 2002

Neuropsychopharmacol

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Corticotropin-releasing hormone (CRH) acts within the brain and pituitary to coordinate the overall endocrinological and behavioral stress response. From postnatal day (PND) 4 to 14, the infant rat displays minimal adrenal response to mild stress. However, maternal deprivation alters the pituitary-adrenal system such that the infants become responsive to specific stimuli. We hypothesized that maternal deprivation would also affect CRH brain circuits. Since tricyclic antidepressants have been shown to decrease the adrenal response to stress in adult rats, we hypothesized that CRH-related changes induced by maternal deprivation would be prevented by this treatment. Thus, we investigated CRH-related molecules on animals that were maternally deprived on PND 13 compared with nondeprived animals. We found that maternal deprivation caused alterations in the gene expression of both CRH receptors (CRHr) 1 and 2 in specific brain regions, and that some of these effects were augmented by chronic isotonic saline injections. There was a significant increase in CRH, CRHr1, and r2 mRNA in the cortex. In amygdala, CRHr1 and r2 mRNAs were decreased. CRHr2 mRNA was also decreased in the ventromedial nucleus of the hypothalamus, whereas an increase was detected in the hippocampal pyramidal cells. One week of desipramine (DES) administration preceding the maternal deprivation event prevented all the deprivation-induced changes in CRHr2 mRNA, regardless of the direction of the original change. We also found that chronic injection treatments enhanced the adrenocortical response and improved the efficiency of negative feedback in maternal deprivation animals. These results demonstrate that maternal deprivation elicits modifications of CRH brain circuits in a site-specific manner, and that the regulation of CRHr2 gene expression is mediated by mechanisms different from those involved with the modulation of CRHr1 in the infant rat.

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“…It is known that stress, and activation of the neuroendocrine stress system, can have important consequences for a developing organism. Studies in rodents show that the developing brain may be more sensitive to changes in circulating corticosteroids than teh adult brian, 100–102 and therefore activation of the HPA axis could have a more negative impact on the brain systems that participate in the modulation of mood, cognitions, and behaviorl control.…”

Section: Early Life Stress and Hpa Regulationmentioning

confidence: 99%

Regulation of 5‐HT Receptors and the Hypothalamic‐Pituitary‐Adrenal Axis

López

Vázquez

Chalmers

et al. 1997

Annals of the New York Academy of Sciences

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Disturbances in the serotonin (5-HT) system is the neurobiological abnormality most consistently associated with suicide. Hyperactivity of the hypothalamic-pituitary-adrenal (HPA) axis is also described in suicide victims. The HPA axis is the classical neuroendocrine system that responds to stress and whose final product, corticosteroids, targets components of the limbic system, particularly the hippocampus. We will review results from animal studies that point to the possibility that many of the 5-HT receptor changes observed in suicide brains may be a result of, or may be worsened by, the HPA overactivity that may be present in some suicide victims. The results of these studies can be summarized as follows: (1) chronic unpredictable stress produces high corticosteroid levels in rats; (2) chronic stress also results in changes in specific 5-HT receptors (increases in cortical 5-HT2A and decreases in hipocampal 5-HT1A and 5-HT1B); (3) chronic antidepressant administration prevents many of the 5-HT receptor changes observed after stress; and (4) chronic antidepressant administration reverses the overactivity of the HPA axis. If indeed 5-HT receptors have a partial role in controlling affective states, then their modulation by corticosteroids provides a potential mechanism by which these hormones may regulate mood. These data may also provide a biological understanding of how stressful events may increase the risk for suicide in vulnerable individuals and may help us elucidate the neurobiological underpinnings of treatment resistance.

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Development of Pituitary Pro-Opiomelanocortin Gene and Peptide Expression: Characterization and Effect of Repeated Intermittent Maternal Isolation

Cited by 21 publications

References 41 publications

Ontogeny of the HPA axis of the CD1 mouse following 24 h maternal deprivation at pnd 3

Ontogeny of the HPA axis of the CD1 mouse following 24 h maternal deprivation at pnd 3

Impact of Maternal Deprivation on Brain Corticotropin-Releasing Hormone Circuits: Prevention of CRH Receptor-2 mRNA Changes by Desipramine Treatment

Regulation of 5‐HT Receptors and the Hypothalamic‐Pituitary‐Adrenal Axis

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