Hello Tipsters- This is an important issue (effects of prenatal cocaine exposure in humans) that I have used for demonstrating to students the importance of critical thinking. . . as well as the importance of looking to the animal literature when considering neuroscientific factors. I have pasted some recent abstracts from this literature below.
Ethics, of course, limit our ability to test hypotheses in humans experimentally. However, a quick review of the recent literature on this issue in humans indicates that the jury may still be out on this one. Perhaps the biggest lesson for our students is to question what they read in any journalistic report. . . That no important decisions should be made based on such material, but on a review of the scientific evidence. I have used this direct comparison of journalistic reports and primary research papers as a teaching tool. Marc Breedlove's web site (or his newsletter) provides an excellent tool for this purpose for biologically-oriented courses. http://www.biopsychology.com/ Best, Sandra ************************************************** J Pediatr Psychol. 2004 Oct;29(7):543-54. Related Articles, Links Expressive and receptive language functioning in preschool children with prenatal cocaine exposure. Morrow CE, Vogel AL, Anthony JC, Ofir AY, Dausa AT, Bandstra ES. Department of Pediatrics, University of Miami School of Medicine, Miami, Florida 33101, USA. [EMAIL PROTECTED] OBJECTIVE: To estimate the relationship between severity of prenatal cocaine exposure and expressive and receptive language skills in full-term, African American children at age 3 years. METHODS: Language was assessed at age 3 using the Clinical Evaluation of Language Fundamentals-Preschool (CELF-P). The sample included 424 children (226 cocaine exposed, 198 non-cocaine exposed) who received preschool language assessments at age 3, drawn from a cohort of 476 children enrolled prospectively at birth. RESULTS: Structural equation modeling was used to regress expressive and receptive language as intercorrelated response variables on level of prenatal cocaine exposure, measured by a latent construct including maternal self-report of cocaine use and maternal/infant urine toxicology assays and infant meconium. Results indicated a.168 SD decrease in expressive language functioning for every unit increase in exposure level (95% CI = -.320, -.015; p =.031) after consideration for fetal growth and gestational age as correlated response variables. Receptive language was more modestly related to prenatal cocaine exposure and was not statistically significant. Results for expressive language remained stable with inclusion of the McCarthy general cognitive index as a response variable (expressive language beta = -.173, 95% CI = -.330, -.016; p =.031), and with adjustment for maternal age and prenatal exposures to alcohol, tobacco, and marijuana (expressive language beta = -.175, 95% CI = -.347, -.003; p =.046). Additional child and caregiver environmental variables assessed at age 3 were also evaluated in varying statistical models with similar results. CONCLUSION: The evidence from this study supports a gradient relationship between increased level of prenatal cocaine exposure and decreased expressive language functioning in preschool-aged cocaine-exposed children. PMID: 15347702 [PubMed - in process] Neurotoxicol Teratol. 2004 Sep-Oct;26(5):617-27. Related Articles, Links Four-year language outcomes of children exposed to cocaine in utero. Lewis BA, Singer LT, Short EJ, Minnes S, Arendt R, Weishampel P, Klein N, Min MO. Department of Pediatrics, Case Western Reserve University School of Medicine, 10900 Euclid Avenue, Cleveland, OH 44106, USA. [EMAIL PROTECTED] A large cohort of children exposed to cocaine in utero (n=189) were followed prospectively from birth to 4 years of age and compared to nonexposed children (n=185) on the Clinical Evaluation of Language Fundamentals-Preschool (CELF-P), a measure of receptive and expressive language abilities. Children exposed to cocaine in utero performed more poorly on the expressive and total language measures than nonexposed children after controlling for confounding variables, including prenatal exposure to alcohol, marijuana, and tobacco, as well as medical and sociodemographic variables. Children exposed to cocaine had more mild receptive language delays than nonexposed children and were less likely to have higher expressive abilities. Also, maternal factors such as language ability, performance IQ, race, and education correlated with child language abilities. Prenatal cigarette and marijuana exposure were related to deficits in specific language skills. Children placed in adoptive or foster care who were cocaine exposed demonstrated superior language skills compared to children exposed to cocaine who remained in biological relative or mother's care. These findings support a cocaine-specific effect on language skills in early childhood that may be modified with an enriched environment. PMID: 15315811 [PubMed - in process] J Dev Behav Pediatr. 2004 Aug;25(4):254-63. Related Articles, Links Prenatal cocaine: quantity of exposure and gender moderation. Delaney-Black V, Covington C, Nordstrom B, Ager J, Janisse J, Hannigan JH, Chiodo L, Sokol RJ. Department of Pediatrics, School of Medicine, Wayne State University, Detroit, Michigan, USA. [EMAIL PROTECTED] Animal but few human studies have demonstrated gender-influenced differences in outcome related to prenatal cocaine exposure. Pregnant participants in a prospective pregnancy study were interviewed for drug use. Exposure was considered positive if history or laboratory tests were positive. An ordinal measure of exposure was also constructed. Six years later, the child and primary caretaker were tested to assess drug use in the home since birth and teacher-assessed child behavior. Data were complete for 473 children (204 cocaine exposed). Twenty-four of the exposed children (12%) were considered to have persistent pregnancy exposure based on positive urine screen at delivery. Boys with any prenatal cocaine exposure scored significantly higher (more problem behaviors) than nonexposed boys on the hyperactivity item. In contrast, no similar cocaine effect was observed for girls. When cocaine exposure was expressed as the three-level ordinal variable, boys, but not girls, with persistent exposure had more behavior problems (0.5 to 1.0 SD higher). Even after control for important covariates, boys with persistent exposure had more problems in central processing, motor skills, handling abstract concepts, and passivity to the environment. The magnitude of the relations reported in this research were moderate to large. In summary, both gender and the level of exposure had a significant behavioral effect on school-age behavior. In these analyses, the behavior of boys, but not girls, prenatally exposed to cocaine was significantly and negatively affected, and these findings remained after control for covariates, including prenatal alcohol or other illicit drug exposures and postnatal drug use in the home. Copyright 2004 Lippincott Williams and Wilkins, Inc. Neurotoxicol Teratol. 2004 Nov-Dec;26(6):783-97. Related Articles, Links Beneficial effects of the sigma1 receptor agonists igmesine and dehydroepiandrosterone against learning impairments in rats prenatally exposed to cocaine. Meunier J, Maurice T. Laboratoire de Plasticite Cerebrale, CNRS FRE 2693, Universite de Montpellier II, Place Eugene Bataillon, Montpellier cedex 534095, France. In utero cocaine (IUC) exposure results in offspring rats in complex neurochemical and behavioral alterations, particularly affecting learning and memory processes. We examined here the impact of IUC exposure on memory functions in male and female offspring rats and report that selective sigma(1) (sigma(1)) receptor agonists are effective in reversing the deficits. Dams received a daily cocaine, 20 mg/kg ip, injection between gestational days E17 to E20. Learning was examined in offspring between day P30 and P41 using delayed alternation in the T-maze, water-maze learning and passive avoidance. Both male and female rats prenatally exposed to cocaine showed delayed alternation deficits and impairments of acquisition of a fixed platform position in the water maze, as shown by higher acquisition latencies and diminutions of time spent in the training quadrant during the probe test. The acquisition of a daily changing platform position also demonstrated impaired working memory. Finally, passive avoidance deficits were observed. Pretreatment with the synthetic sigma(1) agonist igmesine (0.1-1 mg/kg ip) or the neuroactive steroid dehydroepiandrosterone (DHEA 10-40 mg/kg ip) reversed the prenatal cocaine-induced learning deficits in offspring rats for each test. The sigma(1) antagonist BD1063 (1 mg/kg ip) failed to affect performances alone but blocked the igmesine and DHEA effects, confirming the involvement of the sigma(1) receptor. IUC exposure thus results in marked memory deficits, affecting spatial and nonspatial short- and long-term memories in juvenile male and female offspring rats. The activation of the sigma(1) neuromodulatory receptor allows a complete behavioral recovery of the memory functions in prenatally cocaine-exposed rats. PMID: 15451042 [PubMed - in process] Int J Dev Neurosci. 2004 Aug-Oct;22(5-6):309-20. Related Articles, Links Neuropathological consequences of prenatal cocaine exposure in the mouse. Ren JQ, Malanga CJ, Tabit E, Kosofsky BE. Laboratory of Molecular and Developmental Neuroscience, Department of Neurology, Massachusetts General Hospital, Room 2508, 149 13th Street, Charlestown, MA 02129, USA. We have developed an animal model in Swiss Webster mice to identify mechanisms by which prenatal exposure to cocaine results in persistent alterations in brain structure and function. Clinical data suggests that children who demonstrate the largest impairments in prenatal brain growth, which are positively correlated with the highest level of prenatal cocaine exposure, are more likely to demonstrate selective impairment in postnatal brain growth, as well as postnatal impairments in motor function, attention and language skills. We conducted neuroanatomic studies to identify the postnatal evolution of structural changes in the primary somatosensory (SI) cortex of the developing mouse brain following prenatal exposure to cocaine. Our previous work, and that of others, provides evidence that many of the processes underlying corticogenesis are disrupted by gestational exposure of the developing mouse brain to cocaine, and that from the earliest phases of corticogenesis that there is an imprecision in the development of cortical lamination. We performed morphometric comparisons between the brains of animals prenatally exposed to varying amounts of cocaine with vehicle and malnutrition controls on postnatal (P) days P9 and P50. We found that on P50, but not P9, the relative number of cortical neurons in S1 is significantly less in cocaine exposed animals as compared with controls. The significant decrease in the number of cells in cocaine exposed animals on P50 is evident as a decreased density of cells restricted to the infragranular compartment (layers V and VI). Those changes are not seen in malnourished animals. Taken together our findings support the conclusion that cocaine-induced alterations in SI cortical cytoarchitectonics are in part a consequence of altered postnatal survival of infragranular cortical neurons, which are lost during the interval between P9 and P50. Determining whether a similar process is evident in a subset of humans following in utero cocaine exposure is a high priority for future clinical brain imaging studies, because analogous structural changes could impact the brain function and behavioral repertoire of infants and children following significant prenatal exposures. PMID: 15380830 [PubMed - in process] Int J Dev Neurosci. 2004 Aug-Oct;22(5-6):285-96. Related Articles, Links Prenatal intravenous cocaine and the heart rate-orienting response: a dose-response study. Foltz TL, Snow DM, Strupp BJ, Booze RM, Mactutus CF. Department of Biology, University of Kentucky, Lexington, KY, USA. Attentional dysfunction is a persistent behavioral abnormality that is emerging as one of the cardinal features in the investigations of the teratogenic effects of cocaine in humans and rodents. The present study sought to extend this work by using a dose-response design with an alternate strain of rat. Virgin Long-Evans female rats, implanted with an IV access port prior to breeding were administered saline, 0.5, 1.0, or 3.0 mg/kg of cocaine HCl from gestational day (GD) GD8-21 (1x per day-GD8-14, 2x per day-GD15-21). Cocaine had no significant effect on maternal or litter parameters. At 14-15 days of age, 1 male and 1 female from each litter were tested to evaluate the heart rate orienting response (HR-OR). Following 20 min for acclimation, pups were presented an olfactory stimulus for 20s per trial, across four trials, and with an intertrial interval of 2 min. The initial baseline HR was not significantly different across the treatment groups, although cocaine did alter the stability of the QRS complex duration. The magnitude of the HR-OR averaged across trials increased as a linear function of dosage of cocaine. A more complex (quadratic) interaction between cocaine dose and sex of the offspring was also noted. When examined across trials, the controls failed to display any significant within-session variation in the HR-OR; in contrast all of the prenatal cocaine treated groups displayed either sensitization (low and high dose) or habituation of the response (middle dose). Analysis of the peak HR-OR confirmed that the controls were indeed displaying the response on at least one trial of the session, albeit not consistently on any specific trial. The more vigorous HR-OR of the prenatal cocaine groups, relative to vehicle controls, most likely reflects an alteration in development of the neural basis of response; as previously shown, the most vigorous response to the olfactory stimulus is seen early (12 days of age) and progressively decreases across the preweaning period. In sum, prenatal exposure to cocaine, at least when administered by the IV route, provides reproducible alterations in attentional processes, as indexed by the noradrenergically-mediated HR-OR. The documentation of a linear dose-response function suggests that there is likely no threshold for the drug-induced alteration. Moreover, the sex of the animal also appears to play some role in the nature of the expression of the altered HR-OR. PMID: 15380828 [PubMed - in process] Synapse. 2004 Aug;53(2):74-89. Related Articles, Links Prenatal cocaine exposure decreases nigrostriatal dopamine release in vitro: effects of age and sex. Glatt SJ, Trksak GH, Cohen OS, Simeone BP, Jackson D. Department of Psychology, Northeastern University, Boston, Massachusetts, USA. [EMAIL PROTECTED] The present study examined the effects of prenatal cocaine (PCOC) exposure, age, sex, and estrous phase on the functional development of nigrostriatal dopamine (DA) neurons. Striatal tissue was obtained from prepubescent and adult rats of both sexes after bidaily exposure to saline (1 ml/kg) or cocaine (20 mg/kg/ml saline) from embryonic days 15-21. Tissue levels, basal release, and electrically evoked (1 or 8 Hz) overflow of endogenous DA and its metabolite, 3,4-dihydroxyphenylacetic acid (DOPAC), as well as their efflux in response to superfusion with the DA transport blocker, nomifensine (10 microM), were measured from superfused striatal slices. Generally, these measures were highest in tissue from males and adults. Tissue DA and DOPAC levels and the rate of DA turnover were unaffected by PCOC exposure. Slices from PCOC-exposed juvenile and adult male rats exhibited significantly reduced basal and electrically evoked DA release at both stimulation intensities, in conjunction with higher levels of presynaptic DA reuptake. Female rats were largely spared from the effects of PCOC exposure, and measures did not vary with estrous phase. These findings demonstrate that the effects of PCOC exposure on various parameters of nigrostriatal DA neuronal function are not uniform across age, sex, or phases of the estrous cycle. These novel alterations in nigrostriatal DA transmission are in need of independent replication, but they may have profound implications for behavioral activities regulated by these neurons and, thus, may provide a basis for sex-selective effects of PCOC in exposed humans. Possible mechanisms of deleterious effects of PCOC exposure in select groups are discussed. Copyright 2004 Wiley-Liss, Inc. PMID: 15170820 [PubMed - indexed for MEDLINE] In a message dated 11/1/2004 12:50:50 PM Eastern Standard Time, "Paul Okami" <[EMAIL PROTECTED]> writes: >Thanks, Dennis. �Year after year after year--since 1994--I have been trying >to expose this myth to students. �Even though JAMA, Journal of Teratology >and Neurotoxicology, and other medical journals have published solid >research demonstrating that cocaine is not a human teratogen, the Oprah >Winfries of the world continue to perpetuate this myth, greedy clinicians >continue to run clinics and receive research grants, and so forth. �It's >disgusting. > >Paul Okami > > > > >----- Original Message ----- >From: "Dennis Goff" <[EMAIL PROTECTED]> >To: "Teaching in the Psychological Sciences" <[EMAIL PROTECTED]> >Sent: Monday, November 01, 2004 11:48 AM >Subject: crack babies the myth > > >Some of you might find use for a story that was published in the >Columbia Journalism Review about the media myth of crack babies. (I saw >it on Arts and Letters Daily.) The story shows how the media's myth has >adversely affected some individuals. This short article could be read by >students and used to start a number of critical thinking exercises. >http://www.cjr.org/issues/2004/5/voices-blake.asp > >Dennis > >Dennis M. Goff >Professor of Psychology >Randolph-Macon Woman's College >[EMAIL PROTECTED] > > >--- >You are currently subscribed to tips as: [EMAIL PROTECTED] >To unsubscribe send a blank email to [EMAIL PROTECTED] > > > >--- >You are currently subscribed to tips as: [EMAIL PROTECTED] >To unsubscribe send a blank email to [EMAIL PROTECTED] > -- �****************************************************** � � � � Sandra M. Nagel, Ph.D. � � � � Associate Professor, Psychology � � � � Saginaw Valley State University � � � � 166 Brown Hall � � � � 7400 Bay Road � � � � University Center, MI 48710 � � � � http://www.svsu.edu/~smnagel/research/ � � � � Office: (989) 964-4635 � � � � Fax: (989) 790-7656 � � � � E-Mail: [EMAIL PROTECTED] � � � �***************************************************
