Neuroendocrine Responses to Ethanol in the Prepubertal Female Rat

Dees, W. Les; Nyberg, Christopher L.; Hiney, Jill K.

doi:10.1007/978-1-4612-0243-1_3

Cited by 5 publications

(2 citation statements)

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“…It is now well established that EtOH acts within the hypothalamus to cause suppressed release of LHRH in both prepubertal and adult rats (Ching and Negro-Villar, 1988; Dees et al, 1983; 1990; 1995; 2005; 2009; Hiney and Dees, 1991; Ogilive and Rivier, 1997) and primates (Dissen et al, 2004). Studies to discern the mechanism of this EtOH action are important for understanding how this drug disrupts puberty and reproductive function.…”

Section: Discussionmentioning

confidence: 99%

“…Previous studies have shown that chronic ethanol (EtOH) exposure to females alters puberty-related hormones (for review see Dees et al, 1995; 2009) and delays sexual maturation in both rodents (Bo et al, 1982; Dees and Skelley, 1990, Emanuele et al, 2002) and primates (Dees et al, 2000). These effects in both species are due to the hypothalamic action of EtOH to diminish LHRH secretion (Dees et al, 2005; Hiney and Dees, 1991; Hiney et al, 2003; Dissen et al, 2004; Ogilvie and Rivier, 1997).…”

Section: Introductionmentioning

confidence: 99%

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Prepubertal ethanol exposure alters hypothalamic transforming growth factor-α and erbB1 receptor signaling in the female rat

Srivastava

Hiney

Dees

2011

Alcohol

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Glial derived transforming growth factor-α (TGFα) activates the erbB1/erbB2 receptor complex on adjacent glial cells in the medial basal hypothalamus (MBH). This receptor activation stimulates the synthesis and release of prostaglandin-E 2 (PGE 2 ) from the glial cells, which then induces the release of prepubertal luteinizing hormone releasing hormone (LHRH) secretion from nearby nerve terminals; thus, showing the importance of glial-neuronal communications at the time of puberty. Ethanol (EtOH) is known to cause depressed prepubertal LHRH secretion and delayed pubertal development. In this study, we assessed whether short-term EtOH exposure could alter the hypothalamic glial to glial signaling components involved in prepubertal PGE 2 secretion. Immature female rats began receiving control or EtOH diets beginning when 27 days old. The animals were killed by decapitation after 4 and 6 days of treatment and confirmed to be in the late juvenile stage of development. Blood and brain tissues were collected for gene, protein and hormonal assessments. Real-time PCR analysis demonstrated that EtOH did not affect basal levels of erbB1 gene expression in the MBH. Expression of total erbB1 protein was also unaffected; however, the EtOH caused suppressed phosphorylation of erbB1 protein in the MBH at both 4 and 6 days (p<0.01) as revealed by Western blotting. Phosphorylation and totaql protein levels of erbB2 receptor were not affected by EtOH exposure. Because this receptor is critical for PGE 2 synthesis/release, which mediates the secretion of LHRH, we assessed whether in vivo EtOH exposure could affect the release of PGE 2 . EtOH exposure for 6 days suppressed (p<0.01) basal levels of PGE 2 released into the medium. The effects of 4 and 6 day EtOH exposure on gene and protein expressions of TGFα, an upstream component in the activation of erbB1/erbB2, were also studied. The levels of TGFα mRNA were increased markedly at 4 days (p<0.001), but declined to near basal levels by 6 days in the EtOH-treated animals. The EtOH caused increases in TGFα protein expression at both 4 (p<0.001) and 6 (p<0.01) days; hence, suggesting that the EtOH inhibited release of the peptide. We confirmed this inhibition by showing decreased (p<0.01) TGFα released from MBHs incubated in vitro following 6 days of EtOH exposure in vivo. Thus, these results demonstrate that EtOH is capable of interfering with hypothalamic glial to glial signaling processes involved in prepubertal PGE 2 secretion.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Prepubertal ethanol exposure alters hypothalamic transforming growth factor-α and erbB1 receptor signaling in the female rat

Srivastava

Hiney

Dees

2011

Alcohol

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Ethanol Blocks the Central Action of Igf-1 to Induce Luteinizing Hormone Secretion in the Prepubertal Female Rat

et al. 1997

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Alcohol Consumption by Young Actively Growing Rats: A Histomorphometric Study of Cancellous Bone

Sampson

Chaffin

Lange

et al. 1997

Alcoholism Clin & Exp Res

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Alcohol consumption by young actively growing rats has been previously demonstrated to decrease bone density. This study addresses the mechanism of alcohol action on the early phases of bone growth and development using histomorphometric techniques. Four-week-old, female Sprague-Dawley rats were divided into three groups. Alcohol-treated animals were fed a modified Lieber-DeCarli diet ad libitum containing 35% ethanol-derived calories, whereas the pair-fed animals (weight-matched to ethanol rats) received an isocaloric liquid diet in which maltose-dextrin-substituted calories were supplied by ethanol. Chow animals were fed a standard rat chow ad libitum. Proximal tibiae, including epiphyseal growth plate, were removed for analysis after 2, 4, 6, or 8 weeks on the diets. Trabecular volume and number were greatly reduced in the alcohol-fed animals; however, bone formation rates and mineralization rates were normal. Epiphyseal growth rate and proliferation rate were essentially stopped in the alcohol-fed animals.

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Neuroendocrine Responses to Ethanol in the Prepubertal Female Rat

Cited by 5 publications

References 74 publications

Prepubertal ethanol exposure alters hypothalamic transforming growth factor-α and erbB1 receptor signaling in the female rat

Prepubertal ethanol exposure alters hypothalamic transforming growth factor-α and erbB1 receptor signaling in the female rat

Ethanol Blocks the Central Action of Igf-1 to Induce Luteinizing Hormone Secretion in the Prepubertal Female Rat

Alcohol Consumption by Young Actively Growing Rats: A Histomorphometric Study of Cancellous Bone

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