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1.
This study examined the associations between prenatal cocaine exposure and quality of mother-infant play interactions at 13 months of infant ages. We investigated whether maternal psychological distress and infant reactivity mediated or moderated this association. Participants consisted of 220 (119 cocaine exposed and 101 non-cocaine exposed) mother-infant dyads participating in an ongoing longitudinal study of prenatal cocaine exposure. Results indicated that mothers who used cocaine during pregnancy displayed higher negative affect and lower sensitivity toward their infant during play interactions at 13 months, and that their infants were less responsive toward them. Contrary to hypothesis, this association was not mediated by maternal psychological distress or by infant reactivity. However, results for both the cocaine and non-cocaine exposed infants were supportive of a transactional model where lower maternal sensitivity at 1 month was predictive of higher infant reactivity at 7 months, which in turn was predictive of lower maternal warmth/sensitivity at 13 months, controlling for potential stability in maternal behavior. Results also indicated that as hypothesized, infant reactivity moderated the association between maternal cocaine use during pregnancy and maternal warmth/sensitivity at 13 months of age. Cocaine-using mothers who experienced their infants as being more reactive in early infancy were less warm/sensitive toward them in later infancy. Results have implications for parenting interventions that may be targeted toward improving maternal sensitivity among cocaine-using mothers with more reactive infants.  相似文献   

2.
BACKGROUND: In experimental models, prenatal cocaine exposure has been found to perturb monoaminergic development. In humans, numerous studies have sought clinical correlates, but few have focused on dose-related effects, especially as regards neurologic function beyond the neonatal period. OBJECTIVE: To assess whether prenatal cocaine exposure has adverse effects on infant neurologic, developmental and behavioral outcomes and whether any effects are dose-dependent. DESIGN/METHODS: Infants (398) were enrolled at birth from an urban hospital. Drug exposure was ascertained with biomarkers in hair (n=395), urine (n=170) and meconium (n=109). Children were followed prospectively and 286 (72%) were evaluated blind to drug exposure at 6 months of age with the Bayley scales, Fagan Scale of Infant Intelligence and a standardized neurological examination. RESULTS: Certain neurological findings increased significantly by the amount of cocaine detected in maternal hair, e.g. abnormality of tone, as indicated by extensor posture was detected among 28% of cocaine-unexposed infants, 43% of infants exposed to lower and 48% exposed to higher cocaine levels in maternal hair (p<0.009). Persistent fisting increased in a similar dose-dependent manner. These associations persisted in adjusted analyses. Prenatal cocaine exposure was not associated with developmental scores (mental, motor or novelty preference) but was associated with lower orientation scores in adjusted analyses. CONCLUSIONS: At 6 months of age, prenatal cocaine exposure was associated with abnormalities of tone and posture and with lower orientation scores. Perturbations in monoaminergic systems by cocaine exposure during fetal development may explain the observed neurological and behavioral symptoms. Whether such findings in infancy increase the risk of later neurobehavioral problems requires further study.  相似文献   

3.
This study examined the direct and indirect associations between maternal cocaine use during pregnancy and mother-toddler aggression in an interactive context at 2 years of child age. We hypothesized that in addition to direct effects of cocaine exposure on maternal and child aggression, the association between maternal cocaine use and mother-toddler aggression may be indirect via higher maternal psychiatric symptoms, negative affect, or poor infant autonomic regulation at 13 months. Participants consisted of 220 (119 cocaine exposed, 101 non-cocaine exposed) mother-toddler dyads participating in an ongoing longitudinal study of prenatal cocaine exposure. Results indicated that mothers who used cocaine during pregnancy displayed higher levels of aggression toward their toddlers compared to mothers in the control group. Results from model testing indicated significant indirect associations between maternal cocaine use and maternal aggression via higher maternal negative affect as well as lower infant autonomic regulation at 13 months. Although there were no direct associations between cocaine exposure and toddler aggression, there was a significant indirect effect via lower infant autonomic regulation at 13 months. Results highlight the importance of including maternal aggression in predictive models of prenatal cocaine exposure examining child aggression. Results also emphasize the important role of infant regulation as a mechanism partially explaining associations between cocaine exposure and mother-toddler aggression.  相似文献   

4.
The literature on prenatal cocaine exposure is unclear whether immediate postpartum effects on the infant are transient, related to either acute toxicity of cocaine, or to a withdrawal effect as cocaine is metabolized, or whether they might persist. This prospective, longitudinal study was designed to test the hypotheses that newborns urine-positive for cocaine metabolites, compared to those exposed but urine-negative, and to nonexposed controls would (1) have poorer neurobehavioral scores (toxicity effect) and (2) worsen or demonstrate less improvement over the first week (withdrawal effect). We approached over 2500 pregnant women designated to deliver at our referral hospital from public health clinics; 85% consented to participate in a longitudinal study. We excluded women <18 years old with major chronic illness and prenatal drug use except cocaine, marijuana, alcohol and tobacco. From positive urine toxicologies or admissions in private, thorough interviews, 154 were identified as prenatal cocaine users; 154 were selected from noncocaine users matched on socioeconomic status (SES), race, parity and location of prenatal care (that related to perinatal risk), for a total sample size of 308. Included in this article are the 155 surviving infants who were full-term, delivered vaginally and were well and available for testing over the first week postpartum. Infant urine specimens were collected, and neurobehavorial testing was performed by certified, blinded examiners using the Neonatal Behavioral Assessment Scale on days 1, 2-4 and 5-7 postpartum. In toxicity analyses, controlling for amount of prenatal drug exposures, only autonomic regulation demonstrated significant overall and cocaine drug group effects. Urine-positive newborns had the poorest scores (i.e., more startles, tremors). However, given that planned comparisons were not significant, these data provided little support for acute toxicity effects. In withdrawal analyses, only one significant change over time varied among exposure groups. Those infants exposed and positive for cocaine metabolites increased their scores on regulation of state on days 2-4 and decreased them on days 5-7 (when withdrawal might be evident). However, their scores on days 5-7 were not significantly lower than their initial scores, nor different from the days 5-7 scores of the exposed negatives or control infants, lending little support for withdrawal effects. Our data support those of other controlled studies in failing to demonstrate devastating early effects of prenatal cocaine exposure. They add to our understanding that effects observed do not appear to be related to acute toxicity nor to cocaine withdrawal. The uncertainty of persistent effects of cocaine exposure warrants long-term follow-up.  相似文献   

5.
The primary purpose of this study was to examine pathways from prenatal cigarette exposure to physiological regulation at 2 months of age. Specifically, we explored the possibility that any association between prenatal cigarette exposure and infant physiological regulation was moderated by fetal growth, prenatal or postnatal environmental tobacco smoke (ETS) exposure or maternal depressive symptomatology during pregnancy. We evaluated whether exposed infants who were also exposed to ETS after birth, were small for gestational age (SGA) or had mothers with higher depressive symptoms during pregnancy had the highest levels of physiological dysregulation. Respiratory sinus arrhythmia (RSA) was obtained from 234 (166 exposed and 68 nonexposed) infants during sleep. As expected, cigarette-exposed infants had significantly lower RSA than nonexposed infants. This association was not moderated by prenatal or postnatal ETS exposure, or maternal depressive symptomatology during pregnancy. However, small for gestational age status did moderate this association such that nonexposed infants who were not small for gestational age had a significantly higher RSA than nonexposed small for gestational age infants and exposed infants. These findings provide additional evidence that prenatal cigarette exposure is directly associated with dysregulation during infancy.  相似文献   

6.
Prenatal exposure to cocaine, alcohol, and cigarettes has been linked to decreased birth weight and length. Unclear, however, is whether growth deficits persist into childhood. Women who were pregnant, African-American, not HIV-positive, and who delivered singleton infants were extensively screened throughout pregnancy for cocaine, alcohol, cigarette, and other illicit drug use. Of the approximately 1100 eligible subjects, 665 families were located at a 7-year postbirth follow-up and 540 participated. After appropriate control for potential confounders and prenatal exposures, prenatal exposure to cocaine, alcohol, and cigarettes each independently predicted birth weight and length. At age 7, prenatal cocaine exposure was significantly related to height deficits after accounting for other prenatal exposures and significant confounders. Children at age 7 exposed to cocaine in utero were up to 1 in. shorter and twice as likely to fall below the 10th percentile in height as the control children after accounting for other significant confounders including other prenatal exposures. Maternal age moderated the relation between prenatal exposures and child growth. Children born to women over 30 and exposed to cocaine were up to 2 in. shorter and four times more likely to have clinically significant height deficits at age 7. Children of older women and exposed to moderate-to-high levels of alcohol prenatally were up to 14 lb lighter and five times more likely to fall below the 10th percentile in weight. Similar growth restriction was not associated with prenatal exposures for children born to younger mothers. These outcomes add to the growing body of literature detailing long-term effects of prenatal drug exposure, suggesting differential effects for cocaine and alcohol, and indicating that maternal age may moderate these effects. Mechanisms for growth restriction and failure of catch-up under conditions of prenatal exposures are presented, suggesting further study of these developmental outcomes.  相似文献   

7.

Objective

To evaluate the impact of prenatal cocaine exposure and small-for-gestational-age (SGA) status on childhood growth.

Study design

Cocaine exposure was defined by history or meconium metabolites. Hierarchical linear modeling was used to examine cocaine exposure and SGA status on growth, while controlling for exposure to other drugs and alcohol use.

Results

At birth cocaine-exposed infants (n = 364) had significantly lower growth parameters compared to non-exposed children (n = 771). At 6 years, weight was similar between exposed and unexposed children. SGA infants continued to be growth impaired. There was a significant interaction between prenatal cocaine exposure and SGA status at 6 years. The negative effects of cocaine on weight and height were greater among non-SGA than SGA children (432 vs. 280 gm, and 0.7 and 0.5 cm, respectively) while negative effects of SGA status on weight and height were larger in non-cocaine exposed compared to the exposed children (2.3 kg vs.1.6 kg and 2.2 and 1.0 cm).

Conclusions

Children exposed to prenatal cocaine were similar in weight to non-exposed children at 6 years of age. Cocaine had an unexplained greater detrimental effect on non-SGA than SGA children. SGA status at birth has an independent detrimental effect on childhood growth.  相似文献   

8.
This study investigated infant neurobehavioral functioning during the newborn period in 334 full-term, African American neonates (187 cocaine exposed, 147 non-cocaine exposed) enrolled prospectively at birth, with documentation of drug exposure status through maternal interview and urine and meconium toxicology assays. Infants were assessed using the Brazelton Neonatal Behavioral Assessment Scale (BNBAS) during the newborn period (0–6 postnatal days). Findings from multivariate profile analyses support a consistent, modest effect of prenatal cocaine exposure on neurobehavioral functioning in full-term neonates. All of the BNBAS cluster scores, with the exception of abnormal reflexes, were similarly affected, sharing a common slope (D=−0.14; 95% CI=−0.27, −0.003; P=.046) representing a −0.14 point difference between cocaine-exposed and non-cocaine-exposed infants after controlling for prenatal exposure to alcohol, tobacco, and marijuana (ATM); maternal age, education, employment, primigravida status, and prenatal care visits; and infant sex and postnatal age in days. Fetal growth was also related to neurobehavioral functioning and, in part, mediated the relationship between cocaine exposure and the BNBAS cluster scores. Cocaine exposure during each trimester similarly influenced infant neurobehavioral profiles, with cocaine-associated deficits most pronounced in infants with exposure in all three trimesters. Results from qualitative and quantitative urine and meconium bioassay indicators further substantiated these results. Findings, while significant, represent modest effect sizes in full-term infants.  相似文献   

9.
Studies of both preclinical and human models of prenatal cocaine exposure suggest that one mechanism for the impact of cocaine on developing neural systems may be through functional alterations in monoaminergically regulated arousal systems. Conceptually, arousal regulation refers to a set of multimodal central nervous system mechanisms underlying cortical activation in response to internal and/or external stimulation. The emerging capacity for moment-to-moment regulation of states of arousal influences attentional states (e.g., posterior cortex) and executive functions (prefontal cortex) and thus information processing and learning as well as socialization. Furthermore, as a gating mechanism for response to novel and/or stressful conditions, arousal regulation is also a central construct for understanding stress reactivity and response to acute chronic trauma. In this paper, we review the findings of prenatal cocaine exposure in both preclinical and human studies with a particular focus on studies of neurobehavioral, neurocognitive functioning. A theoretical model of interactive arousal systems is presented as one possibility for integrating the profile of apparent cocaine-related neurobehavioral impairments in infants and young children prenatally exposed to cocaine.  相似文献   

10.
The objective of this longitudinal prospective cohort study was to determine whether level of prenatal cocaine exposure, or the interaction between level of prenatal cocaine exposure and contextual risk variables, was associated with a higher rate of infant-caregiver insecure attachment and disorganized attachment, or with alterations in infant crying or avoidant behavior, after controlling for prenatal exposure to alcohol, tobacco, and marijuana, the quality of the proximal caregiving environment, and other covariates. Subjects were 154 full-term 12-month-old infants (64 unexposed, 61 with lighter cocaine exposure, 29 with heavier cocaine exposure) and their primary caregivers from low-income, urban backgrounds. Exposure status was determined in the maternity ward by biologic assay (infant meconium and/or maternal or infant urine) and maternal self-report. At the 12-month follow-up visit, infants were videotaped with their primary caregiver in Ainsworth's Strange Situation. Reliable coders masked to exposure status scored videotapes for attachment variables, amount of crying, and level of avoidance. Contrary to popular perceptions, level of prenatal cocaine exposure was not significantly related to secure/insecure attachment status, disorganized attachment status, or rated level of felt security. Foster care status also was not associated with attachment status. However, heavier prenatal cocaine exposure, in interaction with maternal contextual variables (public assistance or multiparity) was associated with alterations in infant socio-affective behavior, including a higher level of behavioral disorganization, more avoidance of the caregiver, and less crying.  相似文献   

11.
OBJECTIVE: The present study examined the impact of both perinatal maternal depression and cocaine use on infant neurobehavior at 1 month of age in a large, multi-site study. METHODS: Infant neurobehavior was examined in 1053 infants at 1 month of age using the NICU Network Neurobehavioral Scale (NNNS). Mothers were interviewed using The Addiction Severity Index to determine present and past psychiatric history. Four groups were derived from the total sample: 385 prenatally cocaine-exposed infants, 76 whose mothers reported current postpartum depression (DEP/COC) and 309 without current postpartum depression (nonDEP/COC); 668 infants were not exposed to cocaine, 104 whose mothers reported current postpartum depression (DEP/nonCOC), 564 without current postpartum depression (nonDEP/nonCOC). A 2x2 Analysis of Covariance was used with covariates (birthweight, maternal age, SES, nicotine, alcohol, and research site) to examine infant neurobehavior in these four conditions. Secondary analyses were conducted to examine the effects of amount and timing of prenatal cocaine exposure. RESULTS: DEP group by COC exposure status interactions were significant; there was only a DEP effect in the nonCOC infants. Infants in the nonCOC/DEP group had poorer self-regulation and more stress signs, excitability, and arousal than infants in the other groups. CONCLUSIONS: Postpartum maternal depression has negative effects on infant neurobehavior at 1 month of age. Prenatal cocaine exposure may serve to suppress or buffer the effects of postpartum depression on infant neurobehavior. Maternal mood could explain some of the inconsistencies found in the prenatal cocaine exposure literature.  相似文献   

12.
We prospectively ascertained gestational cocaine use by neonatal urine and hair tests in 600 mother infant pairs in 3 nurseries in Toronto. The 37 (6.25%) babies who tested positive for cocaine and their mothers were compared to the 563 nonexposed with regard to pregnancy outcome and neonatal complications. Mothers using cocaine were not different in their ages, racial distribution, and obstetric history from those nonexposed. Cocaine-using women had significantly higher risk for vaginal bleeding (16% vs 6%, P < 0.05), hepatitis B carrier state (8% vs 0.8%, P < 0.005), and perhaps more urinary tract infections (8% vs 2.5%, P = 0.08). cocaine-using mothers were significantly more likely to smoke cigarettes (29% vs 10%, P < 0.001). Infants exposed to cocaine in utero were of lower birth weight (3162 ± 645 [SD] g vs 3391 ± 573, P < 0.05) and birth length (49.9 ± 2.9 cm vs 51.1 ± 3.1 cm, P < 0.05). Further stratification of babies exposed to cocaine by maternal cigarette smoking suggests that cigarette smoking accounted for most of this variability [birth weight of babies exposed to cocaine and cigarettes 2899 ± 7.50 g (and 50% of them weighed less than 2500 g), vs 3423 ± 612 (and only 8% less than 2500 g) in those exposed to cocaine only (P < 0.05). Babies exposed to cocaine in utero were significantly more likely to need initial medical support or resuscitation (52% vs 30%, P < 0.05). We conclude that gestational exposure to cocaine, ascertained by a sensitive biologic marker, is associated with substantial perinatal risks. It is probable that some of these risks are caused by clustering of other risk factors such as maternal smoking and hepatitis carrier state. Because routine clinical markers and urine testing often fail to distinguish fetal exposure to cocaine, more common use of the hair test should be considered, especially for babies with complicated perinatal courses.  相似文献   

13.
Maternal cocaine use and infant behavior   总被引:1,自引:0,他引:1  
We hypothesized that prenatal cocaine exposure results in less optimal infant behavior and more impaired maternal-infant interaction in healthy term infants. Infants were evaluated with the Neonatal Behavioral Assessment Scale (NBAS) at days 1-3 and 11-30 of age, and mother-infant pairs with the Nursing Child Assessment of Feeding Scale (NCAFS) at 7-16 weeks of age. Drug use was determined from confidential interviews, urine assays and medical records. Cocaine-exposed infants (N = 51) were no different than unexposed comparison infants (N = 60) on the first NBAS exam. On the second NBAS exam, 20 cocaine-exposed infants had slightly lower motor cluster scores compared with those of 32 unexposed infants (p = 0.01), but this difference was reduced after control for several confounding variables. The NCAFS detected no differences between groups in maternal or infant behavior. Infants in this population showed no clinically meaningful effects of cocaine exposure on behavior or maternal-infant interaction.  相似文献   

14.
The current study estimates the longitudinal effects of severity of prenatal cocaine exposure on language functioning in an urban sample of full-term African-American children (200 cocaine-exposed, 176 noncocaine-exposed) through age 7 years. The Miami Prenatal Cocaine Study sample was enrolled prospectively at birth, with documentation of prenatal drug exposure status through maternal interview and toxicology assays of maternal and infant urine and infant meconium. Language functioning was measured at ages 3 and 5 years using the Clinical Evaluation of Language Fundamentals--Preschool (CELF-P) and at age 7 years using the Core Language Domain of the NEPSY: A Developmental Neuropsychological Assessment. Longitudinal latent growth curve analyses were used to examine two components of language functioning, a more stable aptitude for language performance and a time-varying trajectory of language development, across the three time points and their relationship to varying levels of prenatal cocaine exposure. Severity of prenatal cocaine exposure was characterized using a latent construct combining maternal self-report of cocaine use during pregnancy by trimesters and maternal and infant bioassays, allowing all available information to be taken into account. The association between severity of exposure and language functioning was examined within a model including factors for fetal growth, gestational age, and IQ as intercorrelated response variables and child's age, gender, and prenatal alcohol, tobacco, and marijuana exposure as covariates. Results indicated that greater severity of prenatal cocaine exposure was associated with greater deficits within the more stable aptitude for language performance (D = -0.071, 95% CI = -0.133, -0.009; p = 0.026). There was no relationship between severity of prenatal cocaine exposure and the time-varying trajectory of language development. The observed cocaine-associated deficit was independent of multiple alternative suspected sources of variation in language performance, including other potential responses to prenatal cocaine exposure, such as child's intellectual functioning, and other birth and postnatal influences, including language stimulation in the home environment.  相似文献   

15.
Prenatal cocaine exposure has been associated with behavior problems at school age. However, the correspondence between use of cocaine and alcohol during pregnancy is often high, making appropriate allocation of variance and control for other exposures and their interactions difficult. Additionally, gender-specific effects are not typically reported. The purpose of the current study was to determine the degree to which gender-specific effects of prenatal cocaine exposure on teacher-reported child externalizing behavior problems were evident when evaluated in relation to prenatal alcohol exposure. Subjects were singleton infants of mothers who were prospectively evaluated during pregnancy. At age seven, 499 children (214 exposed prenatally to cocaine) were evaluated in our laboratory and teacher reports were solicited. Analyses stratified by gender and prenatal alcohol exposure status, and controlled for significant pre- and postnatal confounders, revealed that among boys with prenatal alcohol exposure, those with persistent cocaine exposure throughout pregnancy had significantly higher levels of Delinquent Behavior compared to boys with no cocaine exposure. Boys with any prenatal cocaine exposure were twice as likely as unexposed boys to have clinically significant Externalizing Behavior scores. However, no association was found between prenatal cocaine exposure and scores on Externalizing Behavior and specific syndromes for boys with no prenatal alcohol exposure. Among girls with no prenatal alcohol exposure, those with persistent cocaine exposure had significantly higher levels of Externalizing Behaviors and Aggressive Behaviors compared to girls with no prenatal cocaine exposure after control for confounding, and were almost five times as likely to have clinically significant Externalizing Behavior scores. However, for girls with prenatal alcohol exposure, no association between prenatal cocaine exposure and scores on Externalizing Behavior and specific syndromes was found after control for confounding. The current findings support gender- and alcohol-moderated effects of prenatal cocaine exposure on school-age teacher-reported child behavior problems. These findings are similar to what we have reported for independent parent-reported behavioral evaluation.  相似文献   

16.
Children exposed prenatally to cocaine show deficits in emotion regulation and inhibitory control. While controlling for the measures of medical complication in the perinatal period, environmental risk, and prenatal polydrug exposure (alcohol, tobacco, and marijuana), we examined the effects of prenatal cocaine exposure and gender on attention and inhibitory control in 203 children at ages 6, 9, and 11. Cocaine exposure affected the performance of males, but not females. Heavily exposed males showed deficits in the attention and the inhibition tasks. In addition, a significantly greater proportion of heavily exposed males (21%) than unexposed males (7%) or heavily exposed females (7%) failed to complete the task (p < 0.01). Even without those poorest performing subjects, the overall accuracy for heavily exposed males (81%) was significantly reduced (p < 0.05) compared to lightly exposed males (87%) and unexposed males (89%). The findings highlight the importance of considering gender specificity in cocaine exposure effects. Processes by which cocaine effects may be specific to males are discussed.  相似文献   

17.
BACKGROUND: A very large number of women in the reproductive age group consume cocaine, leading to grave concerns regarding the long term health of millions of children after in utero exposure. The results of controlled studies have been contradictory, leading to confusion, and, possible, misinformation and misperception of teratogenic risk. OBJECTIVE: To systematically review available data on pregnancy outcome when the mother consumed cocaine. METHODS: A meta-analysis of all epidemiologic studies based on a priori criteria was conducted. Comparisons of adverse events in subgroups of exposed vs. unexposed children were performed. Analyses were based on several exposure groups: mainly cocaine, cocaine plus polydrug, polydrug but no cocaine, and drug free. RESULTS: Thirty three studies met our inclusion criteria. For all end points of interest (rates of major malformations, low birth weight, prematurity, placental abruption, premature rupture of membrane [PROM], and mean birth weight, length and head circumference), cocaine-exposed infants had higher risks than children of women not exposed to any drug. However, most of these adverse effects were nullified when cocaine exposed children were compared to children exposed to polydrug but no cocaine. Only the risk of placental abruption and premature rupture of membranes were statistically associated with cocaine use itself. CONCLUSIONS: Many of the perinatal adverse effects commonly attributed to cocaine may be caused by the multiple confounders that can occur in a cocaine using mother. Only the risk for placental abruption and PROM could be statistically related to cocaine. For other adverse effects, additional studies will be needed to ensure adequate statistical power.  相似文献   

18.
Dysmorphologic and anthropometric assessments were performed on 154 6-year-old children prenatally exposed to cocaine (PCE) and 131 high-risk controls (NCE) of similar race and social class. Adjusted mean height z scores demonstrated a dose-response with metahydroxybenzoylecgonine above a threshold of 100 ng/g of meconium and greater cocaine exposure predicted lower weight for height z score. Higher average alcohol exposure throughout pregnancy and 3rd trimester predicted lower head circumference and weight z scores, respectively. Severity of marijuana use also predicted lower height for age but greater weight for height. There was not an increased rate of minor anomalies among the PCE cohort, nor was a consistent phenotype identified. After controlling for covariates, higher average prenatal cigarette exposure predicted higher incidence of cranial facial abnormalities. First trimester alcohol exposure predicted greater rates of ear abnormalities and third trimester marijuana exposure predicted greater rates of chest and head shape abnormalities. These finding indicate that prenatal cocaine exposure has a negative effect on specific growth outcomes including standardized height and weight for height, but not a systematic pattern of structural abnormalities.  相似文献   

19.
RATIONALE: At least 40,000 infants born each year in the U.S. are estimated to have been exposed to crack cocaine and, therefore, may be at risk for increased vulnerability to cocaine addiction. OBJECTIVES: The present study tested the hypothesis that prenatal exposure to cocaine significantly increased subsequent cocaine-taking behavior in mice. METHODS: Swiss Webster male mice that had been exposed to cocaine in utero were tested at 5 months of age in the cocaine self-administration paradigm. They were the offspring of dams that received one of the following treatments during gestation days 8-17: cocaine (40 mg/kg or 20 mg/kg per day; COC40 and COC20 mice, respectively), saline with access to food ad libitum (SAL mice), or saline with access to food restricted to that of the COC40 dams (i.e., pair-fed; SPF40 mice). Mice were initially trained to lever press for a condensed-milk solution, were implanted with an indwelling intravenous (i.v.) catheter and, subsequently, allowed to self-administer cocaine (0.25, 0.5, 1.0, or 2.0 mg/kg per injection) under a fixed ratio (FR) 1 schedule of reinforcement. RESULTS: Latency for acquisition of food-reinforced responding appeared to be independent of prenatal treatment, as was acquisition of cocaine self-administration, which was found to be dose dependent. Both COC40 and SAL mice reached cocaine self-administration criteria at 1.0 mg/kg or 2.0 mg/kg per injection doses, while neither group did so at lower doses. It was also observed that, at each of the doses tested, a higher number of COC40 mice reached criteria for acquisition. A logistic regression analysis confirmed that the likelihood for acquiring cocaine self-administration was positively correlated to prenatal exposure to cocaine and the dose of cocaine tested. CONCLUSIONS: These data provide evidence, for the first time, that prenatal exposure to higher doses of cocaine increase the probability of acquiring cocaine self-administration at moderate doses during adulthood and modulate vulnerability to cocaine-taking behavior in mice.  相似文献   

20.
This investigation employed a longitudinal analysis of rat operant behavior under two different schedules of reinforcement following prenatal exposure to cocaine. Offspring were derived from four maternal exposure groups: 50 mg/kg cocaine, their pair-fed controls, 25 mg/kg cocaine, and freely fed controls. Cocaine was administered via gavage from gestation day 6-20. A maternal fostering procedure was used. Pairs of male and female littermates were assigned to a 7-, 14-, or 21-month cohort and at the appropriate age were trained to respond on one lever in a two-lever operant chamber. Reinforcement was delivered with a series of random ratio (RR) schedules where the RR value was increased across sessions. After RR training, animals were examined with a delayed spatial alternation (DSA) procedure in the same chambers. Male offspring responded at higher rates than females during high-probability RR schedules, whereas advancing age was associated with lower response rates during low-probability RR schedules in both males and females. Prenatal cocaine exposure exerted only limited effects on RR responding during transition and did not affect DSA behavior. The results of this longitudinal analysis suggest that prenatal cocaine does not exert global or far-reaching learning deficits in prenatally exposed rats.  相似文献   

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