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INTRODUCTION: Studies show alcohol-preferring mice reduce their alcohol intake during pregnancy; this study questions if the same is true for humans. The current investigation compares women's pre-pregnancy and first trimester alcohol consumption, examines if women with problem drinking diminish their alcohol intake during pregnancy, and determines if prenatal alcohol reduction is associated with characteristics of pregnancy, patients or smoking. METHODS: 126 participants in weeks 1-12 of pregnancy, recruited from Obstetric and Family Practices, completed a survey during their initial prenatal visit including two gender-specific AUDITs (Alcohol Use Disorders Identification Tests) querying current and pre-pregnancy alcohol use. AUDIT-C (AUDIT items 1-3) scores measuring pre-pregnancy and first trimester alcohol consumption were compared, analyzed and tested using general linear model repeated. A p ≤ 0.05 was accepted as significant. RESULTS: Most participants were multiparous, Caucasian high school graduates experiencing nausea and vomiting. Pre-pregnancy alcohol use was significantly (p = 0.019, Fisher's exact) higher among women seeing obstetricians. Pre-pregnancy AUDIT-C scores (m (mean) = 2.22, sd (standard deviation) = 2.19) were significantly higher (p < 0.001) than first trimester scores (m = 0.143, sd = 0.532). Among 49 with pre-pregnancy AUDIT-C scores ≥ 3, 45/49 (92%) reduced their alcohol use to zero during the first trimester. Age, race, education, marital status, parity, nausea and vomiting, gestational age and smoking were non-factors in score reduction. CONCLUSIONS: Women reported reducing their alcohol consumption during pregnancy, including those screening positive for pre-pregnancy problem drinking. First trimester alcohol reduction cannot be accounted for by smoking, patient or pregnancy characteristics; public health initiatives, psychological factors and hormonal mechanisms may be implicated.
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The terminal arbors of dopaminergic projections in the nucleus accumbens (Acb) core degenerate more rapidly, completely and permanently in a variety of neurotoxic circumstances than do those in the medial shell. It is unknown if this always reflects purely losses of the distal parts of axons from the core (as proposed in methamphetamine intoxication), or whether, in some circumstances, the disproportionate loss of core axons may also stem from an intrinsic vulnerability to degeneration of core-projecting neuronal perikarya. Experiments described here addressed this issue in the following manner. Three days after Fluoro-Gold (FG), a retrogradely transported tracer, had been iontophoresed selectively into the core or medial shell of male Sprague-Dawley rats, each received an infusion of saline vehicle containing or lacking 6-hydroxydopamine (6-OHDA) in the ipsilateral medial forebrain bundle (MFB). Twenty-one days later the brains were processed to exhibit ventral mesencephalic neurons containing FG. Application of an unbiased sampling method revealed substantially greater losses of FG labeled neurons relative to controls in rats that had received 6-OHDA lesions and deposition of FG in the Acb core as compared to the medial shell. Of the few core-projecting neurons that remained in the ventral mesencephalon after these lesions, 54% did not co-localize tyrosine hydroxylase immunoreactivity (TH-ir) and, thus, were not expected to degenerate. The capacity to selectively remove core-projecting dopaminergic neurons may be useful in the determination of molecular correlates of vulnerability and resistance to neurotoxicity and to possibly test the role of the core in reinforcement paradigms.
