Opposite effects of acute ethanol exposure on GAP-43 and BDNF expression in the hippocampus versus the cerebellum of juvenile rats

Kulkarny, Vibhati; Wiest, Nathaniel E.; Marquez, C.P.; Nixon, S.C.; Valenzuela, C. Fernando; Perrone‐Bizzozero, Nora I.

doi:10.1016/j.alcohol.2010.12.004

Cited by 17 publications

(9 citation statements)

References 72 publications

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“…Recently, pathophysiology and etiology of acute alcohol intoxication through experimental practice on rodent models have gotten much attention, among which rat models have been universally adopted to discover the influence of acute alcohol intoxication on the central nervous system (CNS) [8,9]. Abundant rat models of acute alcohol intoxication have shown that acute alcohol intoxication may stimulate genetic expression of neural cells of the cerebellum, which may take significant part in the prognosis and treatment of CNS lesions [10,11].…”

Section: Introductionmentioning

confidence: 99%

RETRACTED ARTICLE: Identification of gene expression profile in the rat brain resulting from acute alcohol intoxication

Kong

Yang

et al. 2014

Mol Biol Rep

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This study aimed to identify gene expression profile in the rat brain resulting from acute alcohol intoxication (AAI). Eighteen SD rats were divided into the alcohol-treated group (n = 9) and saline control group (n = 9). Periorbital blood samples were taken to determine their blood alcohol content by gas chromatography. Tissue sections were analyzed by H and E staining and biochemical assays. Real-time reverse transcription PCR was used to validate microarray data. Statistical analysis was carried out using SPSS18.0 software (Version 18.0, SPSS Inc., Chicago, IL, USA). H and E staining demonstrated that alcohol-treated rats showed no obvious pathological changes in nerve cells compared with those in the control group. Biochemical tests revealed that alcohol-treated rats had lower superoxide dismutase activity than those in the control group (167.3 ± 10.3 U/mg vs. 189.2 ± 5.9 U/mg, P < 0.05). Furthermore, the malondialdehyde levels in alcohol-treated rats were higher than those in the control group (3.48 ± 0.24 mmol/mg vs. 2.51 ± 0.23 mmol/mg, P < 0.05). Microarray data presented 366 up-regulated genes and 300 down-regulated genes in the AAI rat brain. Gene ontology analysis identified 31 genes up-regulated and 39 down-regulated among all differentially expressed genes. Twenty-four pathways showed significant differences, including 12 pathways involved with up-regulated genes and 12 pathways involved with down-regulated genes. Selected genes showed significantly different expression in both alcohol-treated and control groups (P < 0.05). Gene expression analysis enabled clustering of alcohol intoxication-related genes by function. These genes expression may be potential targets for treatment or drug screening for acute alcohol intoxication.

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Section: Introductionmentioning

confidence: 99%

RETRACTED ARTICLE: Identification of gene expression profile in the rat brain resulting from acute alcohol intoxication

Kong

Yang

et al. 2014

Mol Biol Rep

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“…Another possibility would be to consider that LTP has been reduced previously to LTD and that the neuronal network compensated for this reduction after 48 hours. Indeed, one study reported an elevation of BDNF mRNA in the hippocampus ( Kulkarny et al, 2011 ) with a BEC of 174mg/dL 2 hours after 2-hour ethanol vapours. Therefore, a role for BDNF may be envisaged in our experiments.…”

Section: Discussionmentioning

confidence: 99%

Two Binges of Ethanol a Day Keep the Memory Away in Adolescent Rats: Key Role for GLUN2B Subunit

Ferron

Bennouar

Kervern

et al. 2015

IJNPPY

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Background:Binge drinking is common in adolescents, but the impact of only a few binges on learning and memory appears underestimated. Many studies have tested the effects of long and intermittent ethanol exposure on long-term synaptic potentiation, and whether long-term synaptic depression is affected remains unknown.Methods:We studied the effects of one (3g/kg, i.p.; blood ethanol content of 197.5±19mg/dL) or 2 alcohol intoxications (given 9 hours apart) on adolescent rat’s memory and synaptic plasticity in hippocampus slice after different delay.Results:Animals treated with 2 ethanol intoxications 48 hours before training phase in the novel object recognition task failed during test phase. As learning is related to NMDA-dependent mechanisms, we tested ketamine and found the same effect as ethanol, whereas D-serine prevented learning deficit. In hippocampus slice, NMDA-dependent long-term synaptic depression was abolished 48 hours after ethanol or ketamine but prevented after D-serine or in a low-Mg2+ recording medium. Long-term synaptic depression abolition was not observed 8 days after treatment. An i.p. treatment with MK-801, tetrahydroisoxazolopyridine, or muscimol was ineffective, and long-term synaptic potentiation, intrinsic excitability, and glutamate release remained unaffected. The input/ouput curve for NMDA-fEPSPs was shifted to the left 48 hours after the binges with a stronger contribution of GluN2B subunit, leading to a leftward shift of the Bienenstock-Cooper-Munro relationship. Interestingly, there were no cellular effects after only one ethanol injection.Conclusion:Two ethanol “binges” in adolescent rats are sufficient to reversibly abolish long-term synaptic depression and to evoke cognitive deficits via a short-lasting, repeated blockade of NMDA receptors only, inducing a change in the receptor subunit composition. Furthermore, ethanol effects developed over a 48-hour period of abstinence, indicating an important role of intermittence during a repeated long-duration binge behavior.

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“…Serum levels of BDNF are also elevated in naïve individuals following exposure to Δ 9 -tetrahydrocannabinol (THC), the main psychoactive component in marijuana, a commonly abused drug (D’Souza et al, 2009). Studies in rodents have also shown that there is an increase in hippocampal BDNF protein and mRNA expression following ethanol exposure (McGough et al, 2004; Kulkarny et al, 2011), but BDNF mRNA expression has also been found to decrease following ethanol exposure (Tapia-Arancibia et al, 2001; Raivio et al, 2012). Although data directly linking BDNF levels in MFs to addiction is not available, it seems reasonable to suggest that increased BDNF-dependent MF plasticity could contribute to a hippocampal-dependent memory of pleasurable experience that is part of addiction.…”

Section: Discussionmentioning

confidence: 99%

Brain-derived neurotrophic factor–estrogen interactions in the hippocampal mossy fiber pathway: Implications for normal brain function and disease

2013

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The neurotrophin BDNF and the steroid hormone estrogen exhibit potent effects on hippocampal neurons during development and in adulthood. BDNF and estrogen have also been implicated in the etiology of diverse types of neurological disorders or psychiatric illnesses, or have been discussed as potentially important in treatment. Although both are typically studied independently, it has been suggested that BDNF mediates several of the effects of estrogen in hippocampus, and that these interactions play a role in the normal brain as well as disease. Here we focus on the mossy fiber (MF) pathway of the hippocampus, a critical pathway in normal hippocampal function, and a prime example of a location where numerous studies support an interaction between BDNF and estrogen in the rodent brain. We first review the temporal and spatially-regulated expression of BDNF and estrogen in the MFs, as well as their receptors. Then we consider the results of studies that suggest that 17β-estradiol alters hippocampal function by its influence on BDNF expression in the MF pathway. We also address the hypothesis that estrogen influences hippocampus by mechanisms related not only to the mature form of BDNF, acting at trkB receptors, but also by regulating the precursor, proBDNF, acting at p75NTR. We suggest that the interactions between BDNF and 17β-estradiol in the MFs are potentially important in the normal function of the hippocampus, and have implications for sex differences in functions that depend on the MFs and in diseases where MF plasticity has been suggested to play an important role, Alzheimer’s disease, epilepsy and addiction.

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Opposite effects of acute ethanol exposure on GAP-43 and BDNF expression in the hippocampus versus the cerebellum of juvenile rats

Cited by 17 publications

References 72 publications

RETRACTED ARTICLE: Identification of gene expression profile in the rat brain resulting from acute alcohol intoxication

RETRACTED ARTICLE: Identification of gene expression profile in the rat brain resulting from acute alcohol intoxication

Two Binges of Ethanol a Day Keep the Memory Away in Adolescent Rats: Key Role for GLUN2B Subunit

Brain-derived neurotrophic factor–estrogen interactions in the hippocampal mossy fiber pathway: Implications for normal brain function and disease

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