The effect of gestational ethanol exposure on voluntary ethanol intake in early postnatal and adult rats.

Abstract

Clinical and epidemiological studies provide strong data for a relationship between prenatal ethanol exposure and the risk for abuse in adolescent and young adult humans. However, drugacceptance results in response to fetal exposure have differed by study, age at evaluation, and experimental animal. In the present study, the authors tested whether voluntary ethanol intake was enhanced in both the infantile and adult rat (15 and 90 days of age, respectively), as a consequence of chronic fetal drug experience. Experimental rats were exposed in utero by administering ethanol to a pregnant dam in a liquid diet during gestational Days 6-20. Compared with those for isocaloric pair-fed and ad lib chow control animals, the results for experimental animals demonstrated that fetal exposure significantly increased infantile affinity for ethanol ingestion without affecting intake patterns of an alternative fluid (water). Heightened affinity for ethanol was absent in adulthood. Moreover, the results argue against malnutrition as a principal factor underlying the infantile phenomenon. These data add to a growing literature indicative of heightened early postnatal acceptance patterns resulting from maternal use or abuse of ethanol during pregnancy. Keywordsfetal ethanol exposure; postnatal ethanol affinity; ethanol abuse; ethanol drinking behavior; fetal learning It has been well established that prenatal exposure to ethanol can exert profound detrimental effects in the developing fetus. The effects can be widespread, severe, and generally permanent. Depending on timing of exposure, and its duration and dose, these include stereotypical craniofacial malformations, poor suckling reflexes, decreased birth weight NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript (Abel & Hannigan, 1995;Astley, Clarren, Little, Sampson, & Daling, 1992;Clareen & Smith, 1978;Jones, Smith, Ulleland, & Streissguth, 1973; Lemoine, Harousseau, Borteyru, & Meneut, 1968;Martin, Martin, Streissguth, & Lund, 1977;Osborn, Harris, & Weinberg, 1993;Oulette, Rosett, Rosman, & Weiner, 1977;Streissguth, Landesman-Dwyer, Martin, & Smith, 1980;Ulleland, Wennburg, Igo, & Smith, 1970;Van Dyke, MacKay, & Ziaylek, 1982), and other profound neurodevelopmental effects in the nervous system Miller, 1992b). Prenatal exposure to ethanol can cause behavioral changes, such as hyperactivity, and learning and memory deficits: Indeed, gestational exposure is a leading known cause of mental retardation (Abel & Hannigan, 1995;Abel & Sokol, 1992;Sampson et al., 1997;Stratton, Howe, & Battaglia, 1996).The above notwithstanding, there are subtler yet potentially just as detrimental long-term consequences. Recent clinical and epidemiological studies indicate that prenatal exposure to ethanol is strongly associated with the risk for ethanol abuse in adolescent and young adult humans (Alati et al., 2006;Baer, Bar, Bookstein, Sampson, & Streissguth, 1998;Streissguth, 1998;Yates, Cadoret, Troughton, Steward, & Giunta, 1998). In effect, gestational exposure...

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

“…1 also demonstrated that the increased acceptability of ethanol and QHCl to P30 animals was absent in P90 adult animals. This finding agrees with previous observations that the olfactory and ethanol intake effects of fetal exposure, while present in infant (16,17) and adolescent rats (4,5,18,19), ameliorate by adulthood (16,17). Even so, the conjunction of these data with the clinical literature (2, 3) point to the importance of adolescence as a critical transition period for perpetuating mechanisms that contribute to the development of alcoholism.…”

“…We previously found that (i) infant rats exposed to ethanol throughout gestation displayed a tuned neural and behavioral olfactory response that was specific to ethanol odor (16) and (ii) that this observation was paralleled by enhanced ethanol intake (17). These observations raised the clinically relevant possibility that the effects of fetal ethanol exposure on olfactory function may be an important contributor to an enhanced postnatal avidity for the drug.…”

“…On gestational day (G) 5, LongEvans female rats (Harlan-Sprague-Dawley) were divided into blocks of 3 weight-matched dams and randomly assigned to either the ethanol, pair-fed, or chow group. Ethanol dams were fed an ad libitum liquid diet (L10251; Research Diets) that provided 35% of daily calories from ethanol during G11-G20, after weaning onto the diet from G6 to G10 (16,17). Peak blood ethanol concentration was Ϸ150 mg/dl (16).…”

“…We again used offspring of ethanol-, pair-, and chow-fed dams. We selected P15 rats because previous observations have revealed a parallel relationship between gestational exposure, olfactory function, and ethanol avidity at this age (16,17).…”

“…Previously, it has been reported that fetal exposure to ethanol ''tuned'' both the peripheral neural and unconditioned behavioral olfactory response to ethanol odor in infant rats [postnatal day (P) 15] (16). A parallel study showed that fetal ethanol exposure also enhanced ethanol intake (17). This constellation of prenatal exposure effects persisted into the ''at-risk'' age of adolescence (i.e., P30-P42) (4,5,18,19).…”