The effect of chronic intermittent ethanol exposure on spatial memory in adolescent rats: The dissociation of metabolic and cognitive tolerances

Skike, Candice E. Van; Novier, Adelle; Diaz-Granados, Jaime L.; Matthews, Douglas B.

doi:10.1016/j.brainres.2012.03.006

Cited by 19 publications

(16 citation statements)

References 27 publications

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“…Similar to the findings presented here, we previously found that intermittent ethanol exposure during early and mid adolescence, as well as adulthood, did not affect spatial memory assessed by performance on a spontaneous alternation task (Fernandez et al, 2017). Additionally, AIE does not yield acquisition impairments on the Morris water maze, radial arm maze or the Barnes maze (Van Skike et al, 2012; Risher et al, 2013; Swartzwelder et al, 2014). In the current study, we also found spatial learning to be unaffected by AIE when assessed using a Barnes maze.…”

Section: Discussionmentioning

confidence: 96%

Adolescent binge ethanol exposure alters specific forebrain cholinergic cell populations and leads to selective functional deficits in the prefrontal cortex

Fernandez

Savage

2017

Neuroscience

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Adolescence has been identified as a vulnerable developmental time period during which exposure to drugs can have long-lasting, detrimental effects. Although adolescent binge-like ethanol (EtOH) exposure leads to a significant reduction of forebrain cholinergic neurons, EtOH’s functional effect on acetylcholine (ACh) release during behavior has yet to be examined. Using an adolescent intermittent ethanol exposure model (AIE), rats were exposed to binge-like levels of EtOH from postnatal day (PD) 25–55. Three weeks following the final EtOH exposure, cholinergic functioning was assessed during a spontaneous alternation protocol. During maze testing, ACh levels increased in both the hippocampus and prefrontal cortex. However, selectively in the prefrontal cortex, AIE rats displayed reduced levels of behaviorally-relevant ACh efflux. We found no treatment differences in spatial exploration, spatial learning, spatial reversal, or novel object recognition. In contrast, AIE rats were impaired during the first attentional set shift on an operant set-shifting task, indicative of an EtOH-mediated deficit in cognitive flexibility. A unique pattern of cholinergic cell loss was observed in the basal forebrain following AIE: Within the medial septum/diagonal band there was a selective loss (30%) of choline acetyltransferase (ChAT) positive neurons that were nestin negative (ChAT+/ nestin−); whereas in the Nucleus basalis of Meynert (NbM) there was a selective reduction (50%) in ChAT+/ nestin+. These results indicate that early adolescent binge EtOH exposure leads to a long-lasting frontocortical functional cholinergic deficit, driven by a loss of ChAT+/ nestin+ neurons in the NbM, which was associated with impaired cognitive flexibility during adulthood.

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Section: Discussionmentioning

confidence: 96%

Adolescent binge ethanol exposure alters specific forebrain cholinergic cell populations and leads to selective functional deficits in the prefrontal cortex

Fernandez

Savage

2017

Neuroscience

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“…Van Skike and colleagues (2012) found that CIE-treated adolescents showed reduced BEC levels in response to acute EtOH but showed similar EtOH-induced spatial impairments. The authors speculate that metabolic tolerance, but the lack of overt cognitive tolerance, may have been partially explained by EtOH-induced hippocampal allopregnanolone levels (Van Skike et al, 2012).…”

Section: Discussionmentioning

confidence: 99%

Differences in Behavioral Responding in Adult and Aged Rats Following Chronic Ethanol Exposure

Novier

Ornelas

Diaz-Granados

et al. 2016

Alcohol Clin Exp Res

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The elderly may be vulnerable to EtOH withdrawal as modified-CIE aged rats displayed anxiety-like behavior compared to controls during withdrawal despite achieving lower blood EtOH concentrations during treatment than younger adults. Our data also indicate that modified-CIE and EtOH withdrawal cause persistent cognitive impairments in both age groups. The results from this study provide further evidence indicating the elderly may be sensitive to the effects of alcohol.

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“…This indicates that adolescent animals develop significant cognitive tolerance to ethanol after an extended, but intermittent exposure paradigm. Interestingly, this same group showed that a different chronic intermittent exposure paradigm, using exposure to ethanol vapor over a shorter (4-day) period during adolescence, did not result in cognitive tolerance (Van Skike et al, 2012). This raises the question of whether longer exposure periods might be necessary to induce cognitive tolerance in adolescent animals, or if the pharmacokinetic differences between vapor exposure and parenteral administration might account for the differences in observed tolerance.…”

Section: Introductionmentioning

confidence: 99%

Effect of sub-chronic intermittent ethanol exposure on spatial learning and ethanol sensitivity in adolescent and adult rats

Swartzwelder

Hogan

M-Louise

et al. 2014

Alcohol

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It has become clear that adolescence is a period of distinct responsiveness to the acute effects of ethanol on learning and other cognitive functions. However, the effects of repeated intermittent ethanol exposure during adolescence on learning and cognition are less well studied, and other effects of repeated ethanol exposure such as withdrawal and chronic tolerance complicate such experiments. Moreover, few studies have compared the effects of repeated ethanol exposure during adolescence and adulthood, and they have yielded mixed outcomes that may be related to methodological differences and/or secondary effects of ethanol on behavioral performance. One emerging question is whether relatively brief intermittent ethanol exposure (i.e., sub-chronic exposure) during adolescence or adulthood might alter learning at a time after exposure when chronic tolerance would be expected, and whether tolerance to the cognitive effects of ethanol might influence the effect of ethanol on learning at that time. To address this, male adolescent and adult rats were pre-treated with sub-chronic daily ethanol (five doses [4.0 g/kg, i.p.] or saline at 24-h intervals, across 5 days). Two days after the last pre-exposure, spatial learning was assessed on 4 consecutive days using the Morris water maze. Half of the animals from each treatment cell received ethanol (2.0 g/kg, i.p.) 30 min prior to each testing session and half of the animals received saline. Ethanol pre-exposure altered water maze performance in adolescent animals but not in adults, and acute ethanol exposure impaired learning in animals of both ages independent of pre-exposure condition. There was no evidence of cognitive tolerance in animals of either age group. These results indicate that a relatively short period of intermittent ethanol exposure during adolescence, but not adulthood, alters baseline water maze performance shortly after pre-exposure and does not induce cognitive tolerance to the effects of ethanol in either age group.

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The effect of chronic intermittent ethanol exposure on spatial memory in adolescent rats: The dissociation of metabolic and cognitive tolerances

Cited by 19 publications

References 27 publications

Adolescent binge ethanol exposure alters specific forebrain cholinergic cell populations and leads to selective functional deficits in the prefrontal cortex

Adolescent binge ethanol exposure alters specific forebrain cholinergic cell populations and leads to selective functional deficits in the prefrontal cortex

Differences in Behavioral Responding in Adult and Aged Rats Following Chronic Ethanol Exposure

Effect of sub-chronic intermittent ethanol exposure on spatial learning and ethanol sensitivity in adolescent and adult rats

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