A Mouse Model for Adolescent Alcohol Abuse: Stunted Growth and Effects in Brain

Huang, Chi-Ming; Titus, Jennifer A.; Bell, Richard L.; Kapros, Tamás; Chen, Jie; Huang, Rosa H.

doi:10.1111/j.1530-0277.2012.01759.x

Cited by 12 publications

(9 citation statements)

References 83 publications

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“…Over the course of the entire experiment, adolescent body weight increased steadily from an average of 14 g on PND 28 to an average of 21 g on PND 42. The rate of body weight gain did not change following tianeptine pretreatment and is consistent with the published literature for mouse body weight at these ages (Huang et al., ).…”

Section: Resultssupporting

confidence: 91%

CaMKIIα–GluA1 Activity Underlies Vulnerability to Adolescent Binge Alcohol Drinking

Agoglia

Holstein

Reid

2015

Alcoholism Clin & Exp Res

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Background Binge drinking during adolescence is associated with increased risk for developing alcohol use disorders (AUDs); however, the neural mechanisms underlying this liability are unclear. In this study, we sought to determine if binge-drinking alters expression or phosphorylation of two molecular mechanisms of neuroplasticity, calcium/calmodulin dependent kinase II alpha (CaMKIIα) and the GluA1 subunit of AMPA receptors (AMPAR) in addiction-associated brain regions. We also asked if activation of CaMKIIα-dependent AMPAR activity escalates binge-like drinking. Methods To address these questions, CaMKIIαT286 and GluA1S831 protein phosphorylation and expression were assessed in the amygdala and striatum of adolescent and adult male C57BL/6J mice immediately after voluntary binge-like alcohol drinking (blood alcohol > 80mg/dL). In separate mice, effects of the CaMKIIα-dependent pGluA1S831-enhancing drug tianeptine were tested on binge-like alcohol consumption in both age groups. Results Binge-like drinking decreased CaMKIIαT286 phosphorylation (pCaMKIIαT286) selectively in adolescent amygdala with no effect in adults. Alcohol also produced a trend for reduced pGluA1S831 expression in adolescent amygdala but differentially increased pGluA1S831 in adult amygdala. No effects were observed in the nucleus accumbens or dorsal striatum. Tianeptine increased binge-like alcohol consumption in adolescents but decreased alcohol consumption in adults. Sucrose consumption was similarly decreased by tianeptine pretreatment in both ages. Conclusions These data show that the adolescent and adult amygdalae are differentially sensitive to effects of binge-like alcohol drinking on plasticity-linked glutamate signaling molecules. Tianeptine-induced increases in binge-like drinking only in adolescents suggest that differential CaMKIIα-dependent AMPAR activation may underlie age-related escalation of binge drinking.

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Section: Resultssupporting

confidence: 91%

CaMKIIα–GluA1 Activity Underlies Vulnerability to Adolescent Binge Alcohol Drinking

Agoglia

Holstein

Reid

2015

Alcoholism Clin & Exp Res

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“…65 It is widely acknowledged that the human adolescent brain is not fully mature, 66,67 and there is evidence from animal studies that exposure to alcohol during adolescence can affect subsequent brain/behavior development. 68,69 Voluntary consumption of ethanol (at a concentration of 8.5 g/L that led to a dose of 1.0-1.5 g/kg), caffeine (at a concentration of 170 mg/L that led to a dose of 20-30 mg/kg), or an ethanol-caffeine combination during late adolescence in male and female rats had effects on the subsequent adult behavior that were dependent on the sex of the rats. 70 Males showed more ambulation after exposure to the alcohol-caffeine mixture, while females exposed to the mixture showed the opposite effects, that is, suppressed ambulation.…”

Section: Caffeine-ethanol Interactions: Effects On Locomotionmentioning

confidence: 99%

The Impact of Caffeine on the Behavioral Effects of Ethanol Related to Abuse and Addiction: A Review of Animal Studies

López-Cruz

Salamone

Correa

2013

Journal of Caffeine Research

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The impact of caffeine on the behavioral effects of ethanol, including ethanol consumption and abuse, has become a topic of great interest due to the rise in popularity of the so-called energy drinks. Energy drinks high in caffeine are frequently taken in combination with ethanol under the popular belief that caffeine can offset some of the intoxicating effects of ethanol. However, scientific research has not universally supported the idea that caffeine can reduce the effects of ethanol in humans or in rodents, and the mechanisms mediating the caffeine-ethanol interactions are not well understood. Caffeine and ethanol have a common biological substrate; both act on neurochemical processes related to the neuromodulator adenosine. Caffeine acts as a nonselective adenosine A 1 and A 2A receptor antagonist, while ethanol has been demonstrated to increase the basal adenosinergic tone via multiple mechanisms. Since adenosine transmission modulates multiple behavioral processes, the interaction of both drugs can regulate a wide range of effects related to alcohol consumption and the development of ethanol addiction. In the present review, we discuss the relatively small number of animal studies that have assessed the interactions between caffeine and ethanol, as well as the interactions between ethanol and subtype-selective adenosine receptor antagonists, to understand the basic findings and determine the possible mechanisms of action underlying the caffeine-ethanol interactions.Caffeine as a Modulator of Ethanol Abuse C affeine and ethanol are widely consumed recreational drugs.

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“…Female binge drinkers (BD) had thicker left frontal cortices whereas male binge drinkers (BD) had thinner left frontal cortices compared to gender matched controls [107,102]. The existing literature also indicates that females often consume more ethanol and/or respond differently to ethanol than their male counterparts [103], although only small differences in mass measurements of the brain, the cerebellum, and the corpus callosum were seen either as a result of age (from P70 to 225), gender, or ethanol treatment.…”

Section: The Physiological Effects Of Alcohol Abusementioning

confidence: 93%

“…Results from a recent longitudinal brain imaging study of male P rats (from P88 to 578) have revealed that free-choice ethanol consumption attenuated the growth and expansion of brain structures, including the corpus callosum and hippocampus [103]. In the case of the hippocampus, these changes may relate to the inhibition of neurogenesis established to take place in this structure [102].…”

Section: The Physiological Effects Of Alcohol Abusementioning

confidence: 99%