In Utero Ethanol Exposure Increases Proenkephalin, a Precursor of a Neuropeptide That Is Inhibitory to Neuronal Growth

Druse, Mary J.; Hao, Hong‐Lin; Eriksen, Jason L.

doi:10.1097/00000374-199909000-00015

Cited by 1 publication

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“…This study provides the first evidence that prenatal exposure to ethanol, at 1 or 3 g/kg/day, stimulates expression of ENK specifically in the PVN and NAcC, but not the NAcSh, of postnatal offspring, consistent with studies showing a higher dose of ethanol (4.5 g/kg) to increase ENK levels in whole hypothalamus and accumbens of adolescent or adult offspring (Druse et al, 1999; Lugo et al, 2006). It additionally shows a similar increase in mRNA levels of GAL in the PVN and OX in the PFLH and reveals these effects both at birth and P15.…”

Section: Discussionsupporting

confidence: 84%

“…This evidence, suggesting the existence of a positive feedback loop in these brain sites (Morganstern et al, 2011), contrasts with that obtained in the arcuate nucleus (ARC), where GAL is unaffected by ethanol and neuropeptide Y (NPY) is negatively affected by ethanol (Barson et al, 2011). Whereas there are few studies of these peptide systems in offspring exposed in utero to ethanol, the evidence obtained so far shows that prenatal ethanol can stimulate the expression and levels of ENK in whole hypothalamus and NAc, as shown in preweanling and pubertal offspring (Druse et al, 1999; Lugo et al, 2006) but has little impact on NPY in whole hypothalamus (Dembele et al, 2006). These findings give some indication that the effects of prenatal ethanol on peptide expression in the offspring may be similar to those produced by ethanol intake in adult animals, raising the possibility that ethanol may alter in utero development of neurons expressing these orexigenic peptides known to stimulate ethanol drinking.…”

Section: Introductionmentioning

confidence: 99%

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Prenatal ethanol exposure stimulates neurogenesis in hypothalamic and limbic peptide systems: Possible mechanism for offspring ethanol overconsumption

et al. 2012

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Exposure to ethanol during the prenatal period contributes to increased alcohol consumption and preference in rodents and increased risk for alcoholism in humans. With studies in adult animals showing the orexigenic peptides, enkephalin (ENK), galanin (GAL) and orexin (OX), to stimulate ethanol consumption, the question addressed here is whether prenatal ethanol alters the development in utero of specific neurons that express these peptides. With reports describing suppressive effects of high doses of ethanol, we examined the offspring of dams gavaged from embryonic day 9 to parturition with a control solution or lower ethanol doses, 1 and 3 g/kg/day, known to promote ethanol consumption in the offspring. To understand underlying mechanisms, measurements were taken in postnatal offspring of the expression of ENK in the hypothalamic paraventricular nucleus (PVN) and nucleus accumbens (NAc), GAL in the PVN, and OX in the perifornical lateral hypothalamus (PFLH) using real-time qPCR and in situ hybridization, and also of the cell proliferation marker, 5-bromo-2-deoxyuridine (BrdU), and its double-labeling with either neuronal nuclei (NeuN), a marker of mature neurons, or the peptides. On postnatal day 15 (P15), after two weeks without ethanol, the offspring showed increased expression of ENK in the PVN and NAc core but not shell, GAL in the PVN, and OX in the PFLH. In these same areas, prenatal ethanol compared to control increased the density at birth (P0) of neurons expressing these peptides and at P0 and P15 of neurons double-labeling BrdU and NeuN, indicating increased neurogenesis. These BrdU-positive neurons were found to express ENK, GAL and OX, indicating that prenatal ethanol promotes neurogenesis in these specific peptide systems. There were no changes in gliogenesis or apoptosis. This increase in neurogenesis and density of peptide-expressing neurons suggests the involvement of these hypothalamic and accumbal peptide systems in mediating the increased alcohol consumption observed in prenatal ethanol-exposed offspring.

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Section: Discussionsupporting

confidence: 84%

Section: Introductionmentioning

confidence: 99%

Prenatal ethanol exposure stimulates neurogenesis in hypothalamic and limbic peptide systems: Possible mechanism for offspring ethanol overconsumption

et al. 2012

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In Utero Ethanol Exposure Increases Proenkephalin, a Precursor of a Neuropeptide That Is Inhibitory to Neuronal Growth

Abstract: Although we were not able to detect a change in the concentration of the PE peptide in the nucleus accumbens or striatum, we cannot rule out the possibility that the increase in PE mRNA was reflective of a functional abnormality.

Cited by 1 publication

References 34 publications

Prenatal ethanol exposure stimulates neurogenesis in hypothalamic and limbic peptide systems: Possible mechanism for offspring ethanol overconsumption

Prenatal ethanol exposure stimulates neurogenesis in hypothalamic and limbic peptide systems: Possible mechanism for offspring ethanol overconsumption

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