Adolescent Rats Exposed to Repeated Ethanol Treatment Show Lingering Behavioral Impairments

Sircar, Ratna; Sircar, Debashish

doi:10.1097/01.alc.0000175012.77756.d9

Cited by 101 publications

(92 citation statements)

References 48 publications

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“…The acquisition of (spatial) memory is associated with a temporary increase in glutamate dehydrogenase mRNA throughout the hippocampus (Cavallaro et al, 1997). Hence the lasting reduction we observed in glutamate dehydrogenase 1 may represent an underlying cause for the greater sensitivity that adolescents display to alcohol-induced memory disturbance (Sircar and Sircar, 2005).…”

Section: Adolescent Protein Changes Due To Alcohol Treatmentmentioning

confidence: 72%

“…Similarly, those aged 21 to 24 performed worse on semantic and figural memory tasks than those aged 25 to 29 when given alcohol . Likewise, adolescent rats display greater impairment than adult rats in spatial memory acquisition under the influence of alcohol (Markwiese et al, 1998;White et al, 2000) and display memory performance deficits for much longer than adults (Sircar and Sircar, 2005).…”

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confidence: 98%

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Proteomic Analysis Demonstrates Adolescent Vulnerability to Lasting Hippocampal Changes Following Chronic Alcohol Consumption

Hargreaves

Quinn

Kashem

et al. 2008

Alcoholism Clin & Exp Res

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Background: Excessive teenage alcohol consumption is of great concern because alcohol may adversely alter the developmental trajectory of the brain. The aim of the present study was to assess whether chronic intermittent alcohol intake during the adolescent period alters hippocampal protein expression to a greater extent than during adulthood.Methods: Adolescent [postnatal day (PND) 27] and adult (PND 55) male Wistar rats were given 8 hours daily access to beer (4.44% ethanol v ⁄ v) in addition to ad libitum food and water for 4 weeks. From a large subject pool, subgroups of adolescent and adult rats were selected that displayed equivalent alcohol intake (average of 6.1 g ⁄ kg ⁄ day ethanol). The 4 weeks of alcohol access were followed by a 2-week alcohol-free washout period after which the hippocampus was analyzed using 2-DE proteomics.Results: Beer consumption by the adult group resulted in modest hippocampal changes relative to alcohol naı¨ve adult controls. The only changes observed were an up-regulation of citrate synthase (a precursor to the Krebs cycle) and fatty acid binding protein (which facilitates fatty acid metabolism). In contrast, adolescent rats consuming alcohol showed more widespread hippocampal changes relative to adolescent controls. These included an increase in cytoskeletal protein T-complex protein 1 subunit epsilon (TCP-1) and a decrease in the expression of 10 other proteins, including glyceraldehyde-3-phosphate dehydrogenase (GAPDH), triose phosphate isomerise, alpha-enolase, and phosphoglycerate kinase 1 (all involved in glycolysis); glutamate dehydrogenase 1 (an important regulator of glutamate); methylmalonate-semialdehyde dehydrogenase (involved in aldehyde detoxification); ubiquitin carboxyl-terminal hydrolase isozyme L1 (a regulator of protein degradation); and synapsin 2 (involved in synaptogenesis and neurotransmitter release).Conclusions: These results suggest the adolescent hippocampus is more vulnerable to lasting proteomic changes following repeated alcohol exposure. The proteins most affected include those related to glycolysis, glutamate metabolism, neurodegeneration, synaptic function, and cytoskeletal structure.

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Section: Adolescent Protein Changes Due To Alcohol Treatmentmentioning

confidence: 72%

mentioning

confidence: 98%

Proteomic Analysis Demonstrates Adolescent Vulnerability to Lasting Hippocampal Changes Following Chronic Alcohol Consumption

Hargreaves

Quinn

Kashem

et al. 2008

Alcoholism Clin & Exp Res

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“…114 Chronic ethanol exposure has also been shown consistently to result in long-term cognitive impairments; again, adolescent rats seem to be especially sensitive to these effects. 115 Studies with rats also suggested that repeated periods of heavy drinking followed by withdrawal may be particularly neurotoxic, especially in adolescence. 116 For example, chronic intermittent ethanol exposure is the rat analog of human binge drinking.…”

Section: Alcohol and The Developing Adolescent Brainmentioning

confidence: 99%

A Developmental Perspective on Alcohol and Youths 16 to 20 Years of Age

Brown¹,

McGue²,

et al. 2008

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Late adolescence (ie, 16 -20 years of age) is a period characterized by escalation of drinking and alcohol use problems for many and by the onset of an alcohol use disorder for some. This heightened period of vulnerability is a joint consequence of the continuity of risk from earlier developmental stages and the unique neurologic, cognitive, and social changes that occur in late adolescence. We review the normative neurologic, cognitive, and social changes that typically occur in late adolescence, and we discuss the evidence for the impact of these transitions on individual drinking trajectories. We also describe evidence linking alcohol abuse in late adolescence with neurologic damage and social impairments, and we discuss whether these are the bases for the association of adolescent drinking with increased risks of mental health, substance abuse, and social problems in adulthood. Finally, we discuss both the challenges and successes in the treatment and prevention of adolescent drinking problems. I N THE UNITED States, alcohol involvement sometimes starts but more often escalates between 16 and 20 years of age, when youths are also experiencing dramatic physical, emotional, and social changes. Specifically, a variety of forms of hazardous drinking emerge during middle to late adolescence and, for many youths, these problematic patterns of drinking continue to escalate through 18 to 20 years of age, the period of greatest risk for the onset of an alcohol use disorder (AUD).In seeking to understand youth development and alcohol involvement, it is important to consider all dimensions of functioning, because the interrelated cognitive, biological, social, and affective changes that occur during adolescence not only affect each another but also influence an individual's risk of problem drinking. In particular, the timing, sequence, and synchrony of developmentally specific transitions can affect how well youths master new roles, as well as continuities and discontinuities in their behavior. Therefore, developmental models representing a range of theoretical orientations, including systems theory, behavioral genetics, and developmental psychopathology, hold great promise for advancing our understanding of the processes that underlie adolescent changes, including the emergence of alcohol use and abuse.The need for developmental approaches is underscored by the existence of a consistent body of research showing that the escalation in drinking and the emergence of AUDs in middle and late adolescence have behavioral, social, and biological roots from earlier developmental stages. Moreover, it is becoming increasingly clear that alcohol involvement in adolescence has both short-and long-term effects on health and well-being at later developmental stages. Importantly, the consequences of adolescent drinking seem to differ from those associated with adult drinking, because there is increasing evidence that adolescents are especially vulnerable to the adverse effects of heavy alcohol use on both biological and socia...

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“…Así, se ha observado que las ratas adolescentes expuestas a un patrón BD presentan mayor afectación estructural, especialmente en regiones como el CPF o el hipocampo, que ratas adultas expuestas a niveles equivalentes de alcohol (Crews, Braun, Hoplight, Switzer y Knapp, 2000;Pascual, Pla, Miñarro y Guerri, 2014;White y Swartzwelder, 2004). Del mismo modo, las ratas adolescentes con un patrón BD presentan peor rendimiento que las adultas en tareas que implican aprendizaje y memoria (Markwiese, Acheson, Levin, Wilson y Swartzwelder, 1998;Risher et al, 2013;Sircar y Sircar, 2005), lo cual parece ser indicativo de una mayor afectación neurocognitiva en las ratas más jóvenes.…”

Section: Vulnerabilidad Del Cerebro Adolescente a Los Efectos Del Alcunclassified

Anomalías neurocognitivas asociadas al consumo intensivo de alcohol (binge drinking) en jóvenes y adolescentes: Una revisión

et al. 2014

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Adolescent Rats Exposed to Repeated Ethanol Treatment Show Lingering Behavioral Impairments

Cited by 101 publications

References 48 publications

Proteomic Analysis Demonstrates Adolescent Vulnerability to Lasting Hippocampal Changes Following Chronic Alcohol Consumption

Proteomic Analysis Demonstrates Adolescent Vulnerability to Lasting Hippocampal Changes Following Chronic Alcohol Consumption

A Developmental Perspective on Alcohol and Youths 16 to 20 Years of Age

Anomalías neurocognitivas asociadas al consumo intensivo de alcohol (binge drinking) en jóvenes y adolescentes: Una revisión

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