Structural Effects and Neurofunctional Sequelae of Developmental Exposure to Psychotherapeutic Drugs: Experimental and Clinical Aspects

Costa, Lucio G.; Steardo, Luca; Cuomo, V.

doi:10.1124/pr.56.1.5

Cited by 67 publications

(43 citation statements)

References 589 publications

(626 reference statements)

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“…Thus, whether the altered emotionality found in THC-exposed rats could be due to a direct effect of the drug on brain areas involved in emotional behavior and/or to an indirect effect of the drug on maternal behavior is an interesting issue which deserves more investigation. Interestingly, our previous findings (Antonelli et al 2005) showed a reduction of USVs in rat pups prenatally exposed to the synthetic cannabinoid agonist WIN55,212-2, thus highlighting how different time windows of exposure to a psychotropic agent can induce even opposite neurofunctional effects (Costa et al 2004). However, differences in cannabinoid agonist used, tested dose (cannabinoids can induce either anxiolytic-or anxiogenic-like behaviors depending on the dose, Millan 2003), and treatment schedule (acute vs. chronic treatment) could also account for the apparent discrepancies between the present study and previous reports (Antonelli et al 2005;McGregor et al 1996).…”

Section: Discussionmentioning

confidence: 94%

Effects of perinatal exposure to delta-9-tetrahydrocannabinol on the emotional reactivity of the offspring: a longitudinal behavioral study in Wistar rats

et al. 2008

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Section: Discussionmentioning

confidence: 94%

Effects of perinatal exposure to delta-9-tetrahydrocannabinol on the emotional reactivity of the offspring: a longitudinal behavioral study in Wistar rats

et al. 2008

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“…Gestational or neonatal exposure to benzodiazepines can affect brain chemistry and behavior causing hyperactivity or learning deficits [3,4]. Despite the common use of carbamazepine in humans, very few neurobehavioral studies in animals have been conducted with this AED.…”

Section: Animal Studies On Behavioral Effects Of In Utero Aed Exposurementioning

confidence: 99%

Cognitive/behavioral teratogenetic effects of antiepileptic drugs

Meador

Baker

Cohen

et al. 2007

Epilepsy & Behavior

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The majority of children of mothers with epilepsy are normal, but they are at increased risk for developmental delay. Antiepileptic drugs (AEDs) appear to play a role. Our current knowledge is reviewed, including research design issues and recommendations for future research. In animals, exposure of the immature brain to some AEDs can produce widespread neuronal apoptosis and behavioral deficits. The risks of AEDs in humans are less clear, but recent studies raise concerns, especially for valproate. There is a critical need for well-designed systematic research to improve our understanding of AED effects on the fetal brain. KeywordsAntiepileptic drugs; Anticonvulsant drugs; Pregnancy; Teratogenesis; Development; Cognition; Behavior Animal studies on behavioral effects of in utero AED exposureAnimal studies have demonstrated that in utero antiepileptic drug (AED) exposure can produce behavioral as well as anatomical defects, which can occur at dosages lower than those required to produce somatic malformations [1,2]. Gestational or neonatal exposure to benzodiazepines can affect brain chemistry and behavior causing hyperactivity or learning deficits [3,4]. Despite the common use of carbamazepine in humans, very few neurobehavioral studies in animals have been conducted with this AED. In utero carbamazepine exposure did not produce hyperexcitability in primates [5]. Perinatal phenobarbital exposure in rats reduces brain weight [6]. Mice exposed prenatally to phenobarbital have neuronal deficits, reduced brain weight, and impaired development of reflexes, open-field activity, schedule-controlled behavior, spatial learning, and cate-cholamine brain levels [7][8][9][10][11][12]. Gestational or neonatal exposure to phenytoin reduces brain weight [13,14], alters neuronal membranes in the hippocampus [15], delays neurodevelopment [16], and impairs spatial learning and motor coordination [17][18][19][20][21][22][23][24][25]. Hyperactivity has been observed in rats and primates following prenatal exposure to phenytoin [5,23,25]. Gestational primidone in rats produces learning deficits and reduces open-field activity [26]. In utero valproate exposure can alter neuronal membranes [27], decrease brain weight in mice [28], and result in adverse neurobehavioral effects [29,30].

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“…3 In addition to anatomic defects, in utero AED exposure has been associated with behavioral/cognitive defects. [4][5][6] The risk of AED teratogenesis must be balanced against potentially grave risks posed by seizures to both the mother and the child. Maternal deaths during pregnancy in women with epilepsy are 10 times more common than in women without epilepsy; this increase appears to be due to seizures, which are often related to discontinuing AED therapy or poor compliance.…”

mentioning

confidence: 99%