Fetal Alcohol and Drug Effects

Chiriboga, Claudia A.

doi:10.1097/01.nrl.0000094941.96358.d1

Cited by 96 publications

(60 citation statements)

References 122 publications

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“…Human studies of the effects of in utero methadone exposure are often confounded by maternal alcohol, tobacco, and/or supplemental opioid use [1,3,4,34]. The present study compares the effects of in utero methadone to in utero morphine (the predominant active metabolite of heroin) exposure in an animal model free of the confounding factors related to maternal polypharmacy, nutritional deficiencies, or disease states.…”

Section: Discussionmentioning

confidence: 99%

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Respiratory effects of chronic in utero methadone or morphine exposure in the neonatal guinea pig

Nettleton¹,

Wallisch²,

Olsen³

2008

Neurotoxicology and Teratology

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This study uses a neonatal guinea pig model to compare the effects of in utero methadone or morphine exposure upon breathing control. We hypothesize that in utero methadone exposure will result in similar respiratory disturbances to those seen in morphine exposed neonates, but that the onset will be slower and the duration longer, due to methadone's longer elimination half-life. Pregnant DunkinHartley guinea pigs received once-daily injections of methadone, morphine, or vehicle (saline) during the last half of gestation and pups were studied 3, 7, or 14 days after birth. In utero methadone or morphine exposure resulted in decreased birth weight compared to vehicle, and pups experienced a withdrawal syndrome which included increased locomotor activity and respiratory disturbances but no change in rectal temperature. Both opioid exposures increased inspiratory minute ventilation during CO 2 challenge at 3 days after birth, but only in morphine exposed pups was this withdrawal effect still present on day 7. Surprisingly, only morphine exposure increased inspiratory minute ventilation during room air breathing. We conclude that in utero methadone exposure is not equivalent to in utero morphine exposure. With respect to neonatal respiratory control, methadoneinduced changes in respiration are only apparent during hypercapnia.

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Section: Discussionmentioning

confidence: 99%

“…However, these studies are often confounded by the use of alcohol, tobacco, cocaine, and/or illicit supplemental opioids; any one or combination of which can affect perinatal development [1,3,4,34]. In addition, poor maternal nutrition and disease state impact fetal development, and could account for low birth weight [11].…”

Section: Introductionmentioning

confidence: 99%

Respiratory effects of chronic in utero methadone or morphine exposure in the neonatal guinea pig

Nettleton¹,

Wallisch²,

Olsen³

2008

Neurotoxicology and Teratology

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“…Prolonged exposure to alcohol during gestation and lactation correlates with a pattern of abnormal development in newborns (Chiriboga, 2003;Lemoine et al, 2003;Sokol et al, 2003;Goodlett et al, 2005). Jones and Smith (1973) called this developmental disturbance "fetal alcohol syndrome" (FAS).…”

Section: Introductionmentioning

confidence: 99%

Reversal of Neuronal Migration in a Mouse Model of Fetal Alcohol Syndrome by Controlling Second-Messenger Signalings

Kumada¹,

Lakshmana²,

Komuro³

2006

J. Neurosci.

131

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The brains of fetal alcohol syndrome patients exhibit impaired neuronal migration, but little is known about the mechanisms underlying this abnormality. Here we show that Ca 2ϩ signaling and cyclic nucleotide signaling are the central targets of alcohol action in neuronal cell migration. Acute administration of ethanol reduced the frequency of transient Ca 2ϩ elevations in migrating neurons and cGMP levels and increased cAMP levels. Experimental manipulations of these second-messenger pathways, through stimulating Ca 2ϩ and cGMP signaling or inhibiting cAMP signaling, completely reversed the action of ethanol on neuronal migration in vitro as well as in vivo. Each second messenger has multiple but distinct downstream targets, including Ca 2ϩ /calmodulin-dependent protein kinase II, calcineurin, protein phosphatase 1, Rho GTPase, mitogen-activated protein kinase, and phosphoinositide 3-kinase. These results demonstrate that the aberrant migration of immature neurons in the fetal brain caused by maternal alcohol consumption may be corrected by controlling the activity of these second-messenger pathways.

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“…With respect to motor function, cannabis can cause hypermotility (increased motor activity, movement) followed by lethargy, lack of coordination or ataxia, muscle twitches, tremors and weakness, and problems speaking (dysarthia). Pregnant women should avoid cannabinoids, as this been linked to the impairment of fetal development (Hurd et al, 2005;Huizink et al, 2006), even though the evidence for this is inconsistent (Chiriboga, 2003).…”

Section: Adverse Eventsmentioning

confidence: 99%