Prenatal binge-like alcohol exposure alters brain and systemic responses to reach sodium and water balance. (17th December 2015)
- Record Type:
- Journal Article
- Title:
- Prenatal binge-like alcohol exposure alters brain and systemic responses to reach sodium and water balance. (17th December 2015)
- Main Title:
- Prenatal binge-like alcohol exposure alters brain and systemic responses to reach sodium and water balance
- Authors:
- Godino, A.
Abate, P.
Amigone, J.L.
Vivas, L.
Molina, J.C. - Abstract:
- Highlights: Prenatal ethanol exposures affect homeostatic responses after body sodium depletion. The 5HT – DRN system is chronically affected by prenatal ethanol exposure. The AVP hypothalamic neurons are chronically activated by prenatal ethanol exposure. Central extended Amygdala subnucleuses are chronically activated by prenatal ethanol exposure. Prenatal ethanol exposure increases the preference for alcohol during adolescence. Abstract: The aim of the present work is to analyze how prenatal binge-like ethanol exposure to a moderate dose (2.0 g/kg; group Pre-EtOH) during gestational days (GD) 17–20 affects hydroelectrolyte regulatory responses. This type of exposure has been observed to increase ethanol consumption during adolescence (postnatal day 30–32). In this study we analyzed basal brain neural activity and basal-induced sodium appetite (SA) and renal response stimulated by sodium depletion (SD) as well as voluntary ethanol consumption as a function of vehicle or ethanol during late pregnancy. In adolescent offspring, SD was induced by furosemide and a low-sodium diet treatment (FURO + LSD). Other animals were analyzed in terms of immunohistochemical detection of Fra-like (Fra-LI-ir) protein and serotonin (5HT) and/or vasopressin (AVP). The Pre-EtOH group exhibited heightened voluntary ethanol intake and a reduction in sodium and water intake induced by SD relative to controls. Basal Na and K concentrations in urine were also reduced in Pre-EtOH animals while theHighlights: Prenatal ethanol exposures affect homeostatic responses after body sodium depletion. The 5HT – DRN system is chronically affected by prenatal ethanol exposure. The AVP hypothalamic neurons are chronically activated by prenatal ethanol exposure. Central extended Amygdala subnucleuses are chronically activated by prenatal ethanol exposure. Prenatal ethanol exposure increases the preference for alcohol during adolescence. Abstract: The aim of the present work is to analyze how prenatal binge-like ethanol exposure to a moderate dose (2.0 g/kg; group Pre-EtOH) during gestational days (GD) 17–20 affects hydroelectrolyte regulatory responses. This type of exposure has been observed to increase ethanol consumption during adolescence (postnatal day 30–32). In this study we analyzed basal brain neural activity and basal-induced sodium appetite (SA) and renal response stimulated by sodium depletion (SD) as well as voluntary ethanol consumption as a function of vehicle or ethanol during late pregnancy. In adolescent offspring, SD was induced by furosemide and a low-sodium diet treatment (FURO + LSD). Other animals were analyzed in terms of immunohistochemical detection of Fra-like (Fra-LI-ir) protein and serotonin (5HT) and/or vasopressin (AVP). The Pre-EtOH group exhibited heightened voluntary ethanol intake and a reduction in sodium and water intake induced by SD relative to controls. Basal Na and K concentrations in urine were also reduced in Pre-EtOH animals while the induced renal response after FURO treatment was similar across prenatal treatments. However, the correlation between urine volume and water intake induced by FURO significantly varied across these treatments. At the brain level of analysis, the number of basal Fra-LI-ir was significantly increased in AVP magnocellular neurons of the paraventricular nucleus (PVN) and in 5HT neurons in the dorsal raphe nucleus (DRN) in Pre-EtOH pups. In the experimental group, we also observed a significant increase in Fra-LI along the nucleus of the solitary tract (NTS) and in the central extended amygdala nuclei. In summary, moderate Pre-EtOH exposure produces long-lasting changes in brain organization, affecting basal activity of central extended amygdala nuclei, AVP neurons and the inhibitory areas of SA such as the NTS and the 5HT-DRN. These changes possibly modulate the above described variations in basal-induced drinking behaviors and renal regulatory responses. … (more)
- Is Part Of:
- Neuroscience. Volume 311(2015)
- Journal:
- Neuroscience
- Issue:
- Volume 311(2015)
- Issue Display:
- Volume 311, Issue 2015 (2015)
- Year:
- 2015
- Volume:
- 311
- Issue:
- 2015
- Issue Sort Value:
- 2015-0311-2015-0000
- Page Start:
- 92
- Page End:
- 104
- Publication Date:
- 2015-12-17
- Subjects:
- 5HT serotonergic system -- 5-HT-ir 5-HT immunoreactivity -- AP area postrema -- AVP vasopressinergic system -- BNSTL lateral division of the bed nucleus of the stria terminalis -- CD sham-depleted rats -- CeA central amygdaloid nucleus -- CVOs circumventricular organs -- DAB diaminobenzidine hydrochloride -- DRN dorsal raphe nucleus -- DRV ventral subdivisions of DRN -- Fra-LI Fra like immunoreactivity -- FURO Furosemide -- FURO + LSD Furosemide and low-sodium diet -- GD gestational day -- LPBN the lateral parabrachial nucleus -- MnPO median preoptic nucleus -- Na sodium -- NHS normal horse serum -- NTS nucleus of the solitary tract -- OT immunoreactivity -- OVLT organum vasculosum of the lamina terminalis -- PaLM lateral magnocellular group -- PaMM medial magnocellular group -- PB phosphate buffer -- PDN postnatal day -- Pre-EtOH prenatally exposed animals -- Pre-Water prenatally control animals -- PVN paraventricular nucleus -- SA sodium appetite -- SD sodium depletion -- SFO subfornical organ -- SON supraoptic nucleus -- Veh vehicle
prenatal ethanol exposure -- sodium balance -- serotonergic neurons -- vasopressinergic neurons
Neurochemistry -- Periodicals
Neurophysiology -- Periodicals
Neurology -- Periodicals
Neurochimie -- Périodiques
Neurophysiologie -- Périodiques
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612.8 - Journal URLs:
- http://www.sciencedirect.com/science/journal/03064522 ↗
http://www.clinicalkey.com/dura/browse/journalIssue/03064522 ↗
http://www.clinicalkey.com.au/dura/browse/journalIssue/03064522 ↗
http://www.elsevier.com/journals ↗ - DOI:
- 10.1016/j.neuroscience.2015.10.004 ↗
- Languages:
- English
- ISSNs:
- 0306-4522
- Deposit Type:
- Legaldeposit
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