Hippocampal increased cell death and decreased cell density elicited by nicotine and/or ethanol during adolescence are reversed during drug withdrawal

Oliveira-da-Silva, Andreia; Manhães, Alex C.; Cristina-Rodrigues, Fabiana; Filgueiras, Cláudio C.; Abreu‐Villaça, Yael

doi:10.1016/j.neuroscience.2010.01.060

Cited by 23 publications

(13 citation statements)

References 75 publications

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“…Observed increases in cPLA 2 activity correspond with previous literature demonstrating increased cellular death [4] and decreased neurogenesis [5] following adolescent exposure to ethanol. Chronic ethanol is known to induce a multitude of pro-inflammatory markers and contribute to CNS degradation, particularly during critical periods of development such as adolescence [38].…”

Section: Discussionsupporting

confidence: 87%

“…Interestingly, adolescents display differential behavioral responses following ethanol consumption compared to adults, such as reduced sensitivity to ethanol's sedative/hypnotic effects [3]. This is problematic, as decreased soporific sensitivity to ethanol likely lengthens consumption periods and further amplifies detrimental CNS effects, such as decreased neurogenesis and increased levels of cellular death [4, 5]. Thus, it is imperative to understand the molecular underpinnings underlying reduced ethanol-sensitivity during adolescence as they likely contribute to alcohol use disorders later in life.…”

Section: Introductionmentioning

confidence: 99%

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Cytoplasmic Phospholipase A2 Modulation of Adolescent Rat Ethanol-Induced Protein Kinase C Translocation and Behavior

et al. 2015

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Ethanol consumption typically begins during adolescence, a developmental period which exhibits many age-dependent differences in ethanol behavioral sensitivity. Protein kinase C (PKC) activity is largely implicated in ethanol-behaviors, and our previous work indicates that regulation of novel PKC isoforms likely contributes to decreased high-dose ethanol sensitivity during adolescence. The cytoplasmic Phospholipase A2 (cPLA2) signaling cascade selectivity modulates novel and atypical PKC isoform activity, as well as adolescent ethanol hypnotic sensitivity. Therefore, the current study was designed to ascertain adolescent cPLA2 activity both basally and in response to ethanol, as well as it's involvement in ethanol-induced PKC isoform translocation patterns. cPLA2 expression was elevated during adolescence, and activity was increased only in adolescents following high-dose ethanol administration. Novel, but not atypical PKC isoforms translocate to cytosolic regions following high-dose ethanol administration. Inhibiting cPLA2 with AACOCF3 blocked ethanol-induced PKC cytosolic translocation. Finally, inhibition of novel, but not atypical, PKC isoforms when cPLA2 activity was elevated, modulated adolescent high-dose ethanol-sensitivity. These data suggest that the cPLA2/PKC pathway contributes to the acute behavioral effects of ethanol during adolescence.

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Section: Discussionsupporting

confidence: 87%

Section: Introductionmentioning

confidence: 99%

Cytoplasmic Phospholipase A2 Modulation of Adolescent Rat Ethanol-Induced Protein Kinase C Translocation and Behavior

et al. 2015

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“…However, a recent in vivo study in adolescent mice showed that whereas exposure to either ethanol or nicotine resulted in reductions in hippocampal neuronal and glial cell densities concomitant administration of these two drugs reduced the adverse effects compared to each drug alone (Oliveira-da-Silva et al 2009). Moreover, the detrimental effects of all such treatments were abolished by prolonged withdrawal (Oliveira-da-Silva et al 2010). Thus, the in vivo dynamics of nicotinic receptor subtypes and their modulation by a number of endogenous factors including acetylcholine as well as the complexity of alcohol interactions with numerous receptors may yield a different outcome in whole animal compared to the in vitro setting.…”

Section: Discussionmentioning

confidence: 99%

Toxic Effects of Low Alcohol and Nicotine Combinations in SH-SY5Y Cells are Apoptotically Mediated

2011

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It is well established that combination of heavy drinking and smoking has severe health consequences. However, at relatively low concentrations, both alcohol and nicotine may have beneficial effects including neuroprotection. Thus, protective effects of low alcohol concentration against beta-amyloid-induced toxicity in organotypic hippocampal slices and protective effects of nicotine against salsolinol-induced toxicity in human-derived neuroblastoma cells (SH-SY5Y) have been reported. In this study, we sought to determine whether alcohol might also be protective against salsolinol-induced toxicity in SH-SY5Y cells and whether the combination of low doses of alcohol and nicotine might have an additive or synergistic effect. Pre-exposure of SH-SY5Y cells to either ethanol (1 or 10 mM) or nicotine (20 or 50 μM) significantly attenuated salsolinolinduced toxicity. However, contrary to the expectation the combination of low doses of alcohol and nicotine not only did not provide any synergistic or additive protective effect, but exacerbated salsolinol-induced toxicity. Indeed, simple combination of low alcohol and nicotine resulted in significant toxicity in SH-SY5Y cells. This toxicity, reflected in a reduction in cell viability was associated with an increase in apoptosis as determined by caspase-3 measurement. These in vitro results suggest that combination of even low concentrations of alcohol and nicotine may activate apoptotic mechanisms that can lead to cell toxicity and detrimental consequences.

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“…An important issue that remains to be fully addressed is the duration of these effects of nicotine on brain structure and whether or not they are fully reversed following withdrawal. A recent study in adolescent mice (P30-45) that were chronically exposed to nicotine in their drinking water suggests most observed effects were reversed by the time animals reached young adulthood (Oliveira-da-Silva et al, 2010). …”

Section: Psychostimulants and Adolescencementioning

confidence: 99%

The effects of abused drugs on adolescent development of corticolimbic circuitry and behavior

Gulley

Juraska

2013

Neuroscience

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Adolescence is a period of significant neurobiological change that occurs as individuals transition from childhood to adulthood. Because the nervous system is in a relatively labile state during this stage of development, it may be especially sensitive to experience-induced plasticity. One such experience that is relatively common to adolescents is the exposure to drugs of abuse, particularly alcohol and psychostimulants. In this review, we highlight recent findings on the long-lasting effects of exposure to these drugs during adolescence in humans as well as in animal models. Whenever possible, our focus is on studies that use comparison groups of adolescent- and adult-exposed subjects as this is a more direct test of the hypothesis that adolescence represents a period of enhanced vulnerability to the effects of drug-induced plasticity. Lastly, we suggest areas of future investigation that are needed and methodological concerns that should be addressed.

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Hippocampal increased cell death and decreased cell density elicited by nicotine and/or ethanol during adolescence are reversed during drug withdrawal

Cited by 23 publications

References 75 publications

Cytoplasmic Phospholipase A2 Modulation of Adolescent Rat Ethanol-Induced Protein Kinase C Translocation and Behavior

Cytoplasmic Phospholipase A2 Modulation of Adolescent Rat Ethanol-Induced Protein Kinase C Translocation and Behavior

Toxic Effects of Low Alcohol and Nicotine Combinations in SH-SY5Y Cells are Apoptotically Mediated

The effects of abused drugs on adolescent development of corticolimbic circuitry and behavior

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