Prenatal exposure to ethanol increases ethanol consumption: a conditioned response?

Chotro, M. Gabriela; Arias, Carlos F.

doi:10.1016/s0741-8329(03)00037-5

Cited by 98 publications

(149 citation statements)

References 42 publications

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“…1 A), the dynamic range of the prenatal effect is between 3% and 6% ethanol. Notably, these same concentrations of ethanol represent a stimulus range of enhanced voluntary ethanol intake demonstrated by others (20,21) in adolescent rats. Fig.…”

mentioning

confidence: 65%

Fetal ethanol exposure increases ethanol intake by making it smell and taste better

Youngentob

Glendinning

2009

Proc. Natl. Acad. Sci. U.S.A.

130

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Human epidemiologic studies reveal that fetal ethanol exposure is highly predictive of adolescent ethanol avidity and abuse. Little is known about how fetal exposure produces these effects. It is hypothesized that fetal ethanol exposure results in stimulusinduced chemosensory plasticity. Here, we asked whether gestational ethanol exposure increases postnatal ethanol avidity in rats by altering its taste and odor. Experimental rats were exposed to ethanol in utero via the dam's diet, whereas control rats were either pair-fed an iso-caloric diet or given food ad libitum. We found that fetal ethanol exposure increased the taste-mediated acceptability of both ethanol and quinine hydrochloride (bitter), but not sucrose (sweet). Importantly, a significant proportion of the increased ethanol acceptability could be attributed directly to the attenuated aversion to ethanol's quinine-like taste quality. Fetal ethanol exposure also enhanced ethanol intake and the behavioral response to ethanol odor. Notably, the elevated intake of ethanol was also causally linked to the enhanced odor response. Our results demonstrate that fetal exposure specifically increases ethanol avidity by, in part, making it taste and smell better. More generally, they establish an epigenetic chemosensory mechanism by which maternal patterns of drug use can be transferred to offspring. Given that many licit (e.g., tobacco products) and illicit (e.g., marijuana) drugs have noteworthy chemosensory components, our findings have broad implications for the relationship between maternal patterns of drug use, child development, and postnatal vulnerability. chemosensory plasticity ͉ ethanol acceptability ͉ olfaction ͉ bitter ͉ gustation F etal ethanol exposure can have significant negative consequences for the developing human fetus. Fetal alcohol spectrum disorder describes a continuum of sequelae that can range from craniofacial malformations and mental retardation to behavioral changes such as hyperactivity and learning and memory deficits (1). There are also subtler, but nevertheless significant, clinical effects of fetal ethanol exposure. For instance, human epidemiologic studies (2, 3) report that (i) fetal ethanol exposure increases the risk of adolescent ethanol abuse, (ii) gestational exposure is the best predictor of adolescent abuse, and (iii) the earlier the age of secondary postnatal ethanol exposure, the greater the chance of long-term alcoholism. Little is known about how fetal exposure produces these changes in ethanol avidity.Numerous studies have examined how ethanol consumption during pregnancy alters the perception, preference, and consumption of ethanol by the mother's offspring. Animal studies (4, 5) have established that (i) ingested alcohol diffuses into amniotic fluid, (ii) fetuses ingest amniotic fluid and sense intrauterine ethanol, and (iii) the fetus can acquire information about ethanol-related sensory cues and display a memory of this prenatal experience. Likewise, human studies indicate that the fetus can detect and remember p...

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mentioning

confidence: 65%

Fetal ethanol exposure increases ethanol intake by making it smell and taste better

Youngentob

Glendinning

2009

Proc. Natl. Acad. Sci. U.S.A.

130

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“…Consumption of sucrose, quinine, or water was not affected by prenatal treatment, yet prenatal ethanol exposure resulted in heightened consumption of the ethanol solution and its sensory equivalent (sucrose-quinine) (102). Recent studies have confirmed these results, and the use of taste reactivity tests indicate that the palatability of ethanol is enhanced as a function of prenatal ethanol experience and that exposure to ethanol during late gestation subsequently increases ethanol consumption during adolescence (104,105). This latter effect was markedly attenuated when naloxone, a nonselective opioid antagonist, was administered to the pregnant female in conjunction with ethanol or when postnatal re-exposure to ethanol was also accompanied by naloxone administration (106).…”

Section: Fetal Learning About Ethanol Derived From Maternal Intoxicatmentioning

confidence: 90%

“…There is considerable agreement that ethanol exposure during pregnancy results in either a predisposition to consume (102,104,105) or changes upon the pattern of reactivity to ethanol (6,10,(93)(94)(95)(100)(101)(102)159,161) later in life. Recent epidemiologic studies have systematically indicated that even when controlling for variables known to affect ethanol use and abuse (e.g., genetic predisposition as assessed through family history of alcoholism, gender, co-use of other psychotropic agents throughout gestation, and different environmental factors), prenatal ethanol exposure strongly predicts later ethanol drinking patterns and ethanol-related problems (173)(174)(175)(176)(177).…”

Section: Final Considerations: Relationships Between Preclinical and mentioning

confidence: 99%

Fetal Learning About Ethanol and Later Ethanol Responsiveness: Evidence Against “Safe” Amounts of Prenatal Exposure

Abate

Pueta

Spear

et al. 2008

Exp Biol Med (Maywood)

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Near-term fetuses of different mammalian species, including humans, exhibit functional sensory and learning capabilities. The neurobiological literature indicates that the unborn organism processes sensory stimuli present in the amniotic fluid, retains this information for considerable amounts of time, and is also capable of associating such stimuli with biologically relevant events. This research has stimulated studies aimed at the analysis of fetal and neonatal learning about ethanol, a topic that constitutes the core of the present review. Ethanol has characteristic sensory (olfactory, taste, and trigeminal) attributes and can exert pharmacologic reinforcing effects. The studies under examination support the hypothesis that low to moderate levels of maternal ethanol intoxication during late pregnancy set the opportunity for fetal learning about ethanol. These levels of prenatal ethanol exposure do not generate evident morphologic or neurobehavioral alterations in the offspring, but they exert a significant impact upon later ethanol-seeking and intake behaviors. Supported by preclinical and clinical findings, this review contributes to strengthening the case for the ability of prenatal ethanol exposure to have effects on the postnatal organism. Keywords ethanol; fetal learning; associative conditioningThis review analyzes the impact of low to moderate prenatal levels of exposure to ethanol on later responding to ethanol and stimuli associated with ethanol. These levels of ethanol exposure might be viewed as "safe" but nevertheless have negative effects that might not be noticed for many years.We previously reviewed the literature, examining possible associations between early ontogenetic experiences with alcohol and subsequent affinity for ethanol ingestion and sensitivity to its reinforcing effects (postabsorptive consequences that increase behaviors aimed at obtaining ethanol or that generate preferences to stimuli signaling such consequences) (1). This review took into account fetal and infantile experiences involving acute or chronic exposure to ethanol and how they exerted significant effects upon subsequent ethanol 1To whom correspondence should be addressed at Instituto Ferreyra,

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“…Neonates exposed to the drug exhibited behavioral signs indicative of alcohol odor recognition and were observed to react to the smell of alcohol in the way alcohol-naïve pups react to the smell of their own amniotic fluid (Chotro & Spear, 1997;Domínguez, Lopez, Chotro, & Molina, 1996;Molina et al, 1999). Later in life, pups subjected to intrauterine alcohol experiences showed heightened ingestion of alcohol and of a sucrose-quinine compound, which represents a psychophysical equivalent of alcohol in the rat (Domínguez et al, 1998; also see Chotro & Arias, 2003). Taste reactivity tests indicated that palatability of ethanol is enhanced in these pups (Arias & Chotro, 2005).…”

Section: Alcohol Responsiveness As a Function Of Fetal Experiences Wimentioning

confidence: 95%

The International Society for Developmental Psychobiology 39th Annual Meeting Symposium: Alcohol and Development: Beyond fetal alcohol syndrome

Molina

Spear

et al. 2007

Developmental Psychobiology

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As has been repeatedly demonstrated, alcohol can exert deleterious morphological and physiological effects during early stages in development. The present review examines nonteratological links existing between alcohol and ontogeny. Human and animal studies are taken into consideration for the analysis of fetal, neonatal, infantile, adolescent, and adult responsiveness to the drug. Sensitivity to alcohol's chemosensory and postabsorptive properties, as well as learning and memory processes mediated by such properties, are examined from this developmental perspective. The studies under discussion indicate that, within each stage in development, we can trace alcohol-related experiences capable of determining or modulating alcohol seeking and intake patterns.

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Prenatal exposure to ethanol increases ethanol consumption: a conditioned response?

Cited by 98 publications

References 42 publications

Fetal ethanol exposure increases ethanol intake by making it smell and taste better

Fetal ethanol exposure increases ethanol intake by making it smell and taste better

Fetal Learning About Ethanol and Later Ethanol Responsiveness: Evidence Against “Safe” Amounts of Prenatal Exposure

The International Society for Developmental Psychobiology 39th Annual Meeting Symposium: Alcohol and Development: Beyond fetal alcohol syndrome

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