The serotonin-1A agonist ipsapirone prevents ethanol-associated death of total rhombencephalic neurons and prevents the reduction of fetal serotonin neurons

Druse, Mary J.; Tajuddin, Nuzhath F.; Gillespie, Roberta A.; Dickson, Elizabeth; Atieh, Mohammed; Pietrzak, Constance A; Le, Phong T.

doi:10.1016/j.devbrainres.2004.02.009

Cited by 29 publications

(54 citation statements)

References 62 publications

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“…This finding confirms earlier studies from this laboratory (Druse et al, 2004;2007) and reports that detected ethanol-associated apoptosis in neurons from other brain regions. For example, previous studies found that ethanol increases apoptosis in the developing neural crest (Dunty et al, 2001) and cerebellar granule cells (Ramachandran et al, 2001) as well as in cells from cortex (Cheema et al, 2000) and forebrain (Ikonomidou et al, 2000).…”

Section: Discussionsupporting

confidence: 82%

“…Importantly, the neuroprotective effects of the 5-HT 1A agonist ipsapirone (Druse et al, 2004 and of the astroglial protein S100B were accompanied by maintenance of normal to elevated activity of PI-3K-> pAkt (Druse et al, 2005;2007). The latter effects were associated with increased expression of the genes encoding the anti-apoptotic proteins XIAP (ipsapirone or S100B treatments), Bcl-XL (ipsapirone) and/or Bcl-2 (S100B) 2007) in ethanol-treated neurons.…”

Section: Discussionmentioning

confidence: 80%

“…Neurons were maintained in culture for a total of 5 days (DIV1 to DIV6). Previous studies in this laboratory showed that by DIV6, 5-HT neurons comprised ∼20% to 30% of fetal rhombencephalic neurons and glial fibrillary acidic protein (GFAP) positive astrocytes accounted for < 5% of the cells (Druse et al, 2004).…”

Section: Experimental Procedures Neuronal Culturesmentioning

confidence: 99%

“…Dissection and culturing of fetal rhombencephalic neurons have been described by this laboratory (Druse et al, 2004. Rhombencephalic tissue was dissected from gestation day 14 (G14) embryos taken from timed-pregnancy Sprague-Dawley rats, where G=0 corresponds to the day of insemination (Honegger and Monnet-Tschudi, 1997;Eriksen and Druse, 2001).…”

Section: Experimental Procedures Neuronal Culturesmentioning

confidence: 99%

“…In fact, this laboratory finds that the loss of the developing serotonin (5-HT) neurons of the dorsal and median raphe region (Tajuddin and Druse, 1999; is caused by ethanol-associated apoptosis (Druse et al, 2004;2007). Moreover, these effects are accompanied by a decrease in the activity of the phosphatidylinositol 3'kinase (PI-3K) → pAkt pro-survival pathway and the downstream reduction in the expression of NF-kB dependent genes that encode pro-survival/anti-apoptotic proteins (Druse et al, 2005, e.g.…”

Section: Introductionmentioning

confidence: 99%

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Antioxidants prevent ethanol-associated apoptosis in fetal rhombencephalic neurons

Antonio

Druse

2008

Brain Research

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It is well known that ethanol damages the developing nervous system by augmenting apoptosis. Previously, this laboratory reported that ethanol augments apoptosis in fetal rhombencephalic neurons, and that the increased apoptosis is associated with reduced activity of the phosphatidylinositol 3'kinase pathway and downstream expression of pro-survival genes. Other laboratories have shown that another mechanism by which ethanol induces apoptosis in developing neurons is through the generation of reactive oxygen species (ROS) and the associated oxidative stress.The present study used an in vitro model to investigate the potential neuroprotective effects of several antioxidants against ethanol-associated apoptosis in fetal rhombencephalic neurons. The investigated antioxidants included three phenolics: (-)-epigallocatechin-3-gallate (EGCG), a flavanoid polyphenol found in green tea; curcumin, found in tumeric; and resveratrol (3,5,4'-trihydroxystilbene), a component of red wine. Additional antioxidants, including melatonin, a naturally occurring indole, and α-lipoic acid, a naturally occurring dithiol, were also investigated.These studies demonstrated that a 24-hour treatment of fetal rhombencephalic neurons with 75 mM ethanol caused a 3-fold increase in the percentage of apoptotic neurons. However, co-treatment of these cultures with any of the five different antioxidants prevented ethanol-associated apoptosis. Antioxidant treatment did not alter the extent of apoptosis in control neurons, i.e., those cultured in the absence of ethanol. These studies showed that several classes of antioxidants can exert neuroprotection against ethanol-associated apoptosis in fetal rhombencephalic neurons.

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Section: Discussionsupporting

confidence: 82%

Section: Discussionmentioning

confidence: 80%

Section: Experimental Procedures Neuronal Culturesmentioning

confidence: 99%

Section: Experimental Procedures Neuronal Culturesmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Antioxidants prevent ethanol-associated apoptosis in fetal rhombencephalic neurons

Antonio

Druse

2008

Brain Research

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From Research to Practice: An Integrative Framework for the Development of Interventions for Children with Fetal Alcohol Spectrum Disorders

Kodituwakku

2011

Neuropsychol Rev

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Since fetal alcohol syndrome was first described over 35 years ago, considerable progress has been made in the delineation of the neurocognitive profile in children with prenatal alcohol exposure. Preclinical investigators have made impressive strides in elucidating the mechanisms of alcohol teratogenesis and in testing the effectiveness of pharmacological agents and dietary supplementation in the amelioration of alcohol-induced deficits. Despite these advances, only limited progress has been made in the development of evidence-based comprehensive interventions for functional impairment in alcohol-exposed children. Having performed a search in PubMed and PsycINFO using key words, interventions, treatment, fetal alcohol syndrome, prenatal alcohol exposure, and fetal alcohol spectrum disorders, we found only 12 papers on empirically-based interventions. Only two of these interventions had been replicated and none met the criteria of "well-established," as defined by Chambless and Hollon (Journal of Consulting and Clinical Psychology 66(1):7-18, 1998). There has been only limited cross-fertilization of ideas between preclinical and clinical research with regard to the development of interventions. Therefore, we propose a framework that allows integrating data from preclinical and clinical investigations to develop comprehensive intervention programs for children with fetal alcohol spectrum disorders. This framework underscores the importance of multi-level evaluations and interventions.

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A neurodevelopmental framework for the development of interventions for children with fetal alcohol spectrum disorders

Kodituwakku

2010

Alcohol

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Despite considerable data published on cognitive and behavioral disabilities in children with FASD, relatively little information is available on behavioral or pharmacological interventions for alcohol affected children. The main goals of this paper, therefore, are to summarize published intervention studies of FASD and to present a neurodevelopmental framework, based on recent findings from a number of disciplines, for designing new therapies for alcohol affected children. This framework assumes a neuroconstructionist view, which posits that reciprocal interactions between neural activity and the brain's hardware lead to the progressive formation of intra and inter-regional neural connections. In this view, behavioral interventions can be conceptualized as a series of guided experiences that are designed to produce neural activation. Based on evidence from cognitive neuroscience, it is hypothesized that specific interventions targeting executive attention and self-regulation may produce greater generalizable results than those aimed at domain specific skills in children with FASD. In view of reciprocal interactions between environmental effects and neural structures, the proposed framework suggests that the maximum effects of interventions can eventually be achieved by optimally combining behavioral methods and cognition enhancing drugs.

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The serotonin-1A agonist ipsapirone prevents ethanol-associated death of total rhombencephalic neurons and prevents the reduction of fetal serotonin neurons

Cited by 29 publications

References 62 publications

Antioxidants prevent ethanol-associated apoptosis in fetal rhombencephalic neurons

Antioxidants prevent ethanol-associated apoptosis in fetal rhombencephalic neurons

From Research to Practice: An Integrative Framework for the Development of Interventions for Children with Fetal Alcohol Spectrum Disorders

A neurodevelopmental framework for the development of interventions for children with fetal alcohol spectrum disorders

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