The consequences of beer consumption in rats: acute anxiolytic and ataxic effects and withdrawal-induced anxiety

Gallate, Jason; Morley, Kirsten C.; Ambermoon, Polly; McGregor, Iain S.

doi:10.1007/s00213-002-1291-z

Cited by 41 publications

(35 citation statements)

References 46 publications

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“…The failure in the proper foot placement in AgNPs exposed rats implied that AgNPs might have potential to induce cerebellar ataxia-like disease. This is in correspondence with the ataxic effect in rats produced by beer consumption (Gallate et al, 2003). A decrease in activity or time spent in the center of the open field indicated the increase in animal anxiety or reduction in their exploration potential (Dulawa et al, 1999).…”

Section: Discussionsupporting

confidence: 71%

Silver nanoparticle exposure induces rat motor dysfunction through decrease in expression of calcium channel protein in cerebellum

et al. 2015

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Silver nanoparticles cause cerebellar ataxia-like symptom in rats. Silver nanoparticles induce rat motor dysfunction. Silver nanoparticles decrease calcium channel protein expression in rat cerebellum. Silver nanoparticles (AgNPs) are currently used widely, however, their impact on central nervous system still remains ambiguous and needs to be elucidated. This study is performed to investigate the neurotoxicity of AgNPs and illustrate the potential molecular mechanism. Neonatal Sprague-Dawley (SD) rats are exposed to AgNPs by intranasal instillation for 14 weeks. It is demonstrated that AgNPs exposure causes cerebellar ataxia like symptom in rats, evidenced by dysfunction of motor coordination and impairment of locomotor activity. Observation of cerebellum section reveals that AgNPs can provoke destruction of cerebellum granular layer with concomitant activation of glial cells. AgNPs treatment decreases calcium channel protein (CACNA1A) levels in cerebellum without changing potassium channel protein (KCNA1) levels. The levels of silver in rat cerebellum tissue are correlated with exposure doses. In vitro experiments reveal that AgNPs treatment significantly reduces the protein and mRNA levels of CACNA1A in primary cultured cerebellum granule cells (CGCs). These findings suggest that AgNPs-induced rat motor dysfunction is associated with CACNA1A expression decrease, which reveals the underlying molecular mechanism for the neurotoxicity of AgNPs. Possible counteractions may accordingly be suggested to attenuate the unexpected harmful effects in biological applications of AgNPs.

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Section: Discussionsupporting

confidence: 71%

Silver nanoparticle exposure induces rat motor dysfunction through decrease in expression of calcium channel protein in cerebellum

et al. 2015

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“…The anxiolytic effects of ethanol have been extensively described (Bilkei-Gorzo et al, 1998;Colombo et al, 1995;Ferreira et al, 2000;Gallate et al, 2003;Hall et al, 1998;Martijena et al, 2001;Martin-Garcia and Pallares, 2005;Varlinskaya and Spear, 2002). In fact, although a previous study indicated that adolescent rats may be less sensitive than adults to the anxiolytic effects of ethanol (Varlinskaya and Spear, 2002), a recent study (Hefner and Holmes, 2007) showed that adolescent C57BL/6J mice exhibit increased sensitivity to anxiolytic-like effects of ethanol when compared to adults.…”

Section: Anxiolytic Effects During Adolescent Exposurementioning

confidence: 99%

“…Excessive alcohol consumption by anxious patients, presumably due to the anxiolytic properties of alcohol, has led to the hypothesis that anxiety could be a critical factor in the etiology of alcohol drinking (Colombo et al, 1995). The anxiolytic-like effects of ethanol associated with forced and acute administration (Bilkei-Gorzo et al, 1998;Ferreira et al, 2000;Hall et al, 1998;Martijena et al, 2001;Varlinskaya and Spear, 2002) or voluntary ethanol consumption (Colombo et al, 1995;Gallate et al, 2003) have been extensively described in different rodent tests. In addition, in contrast to the effect described during exposure, the occurrence of an anxiogenic-like effect during ethanol withdrawal has been reported (Kliethermes, 2005).…”

Section: Introductionmentioning

confidence: 99%

Combined Exposure to Nicotine and Ethanol in Adolescent Mice Differentially Affects Anxiety Levels during Exposure, Short-Term, and Long-Term Withdrawal

Abreu‐Villaça

Nunes

Queiroz-Gomes

et al. 2007

Neuropsychopharmacol

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Smoking and consumption of alcoholic beverages are frequently associated during adolescence. This association could be explained by the cumulative behavioral effects of nicotine and ethanol, particularly those related to anxiety levels. However, despite epidemiological findings, there have been few animal studies of the basic neurobiology of the combined exposure in the adolescent brain. In the present work we assessed, through the use of the elevated plus maze, the short-and long-term anxiety effects of nicotine (NIC) and/or ethanol (ETOH) exposure during adolescence (from the 30th to the 45th postnatal day) in four groups of male and female C57BL/6 mice: (1) Concomitant NIC (nicotine free-base solution (50 mg/ml) in 2% saccharin to drink) and ETOH (ethanol solution (25%, 2 g/kg) i.p. injected every other day) exposure; (2) NIC exposure; (3) ETOH exposure; (4) Vehicle. C57BL/6 mice were selected, in spite of the fact that they present slower ethanol metabolism, because they readily consume nicotine in the concentration used in the present study. During exposure (45th postnatal day: PN45), our results indicated that ethanol was anxiolytic in adolescent mice and that nicotine reverted this effect. Short-term drug withdrawal (PN50) elicited sex-dependent effects: exposure to nicotine and/or ethanol was anxiogenic only for females. Although neither nicotine nor ethanol effects persisted up to 1 month postexposure (PN75), the coadministration elicited an anxiogenic response. In spite of the fact that generalizations based on the results from a single strain of mice are prone to shortcomings, our results suggest that the deficient response to the anxiolytic effects of ethanol in adolescents co-exposed to nicotine may drive higher ethanol consumption. Additionally, increased anxiety during long-term smoking and drinking withdrawal may facilitate relapse to drug use.

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“…Acutely, ethanol alters memory (eg Givens, 1995), motor coordination (eg Gallate et al, 2003; but see Metz et al, 2003), and anxiety-related behaviors (eg Gallate et al, 2003;Langen et al, 2002;Ryabinin, 1998). Beside hyperlocomotion and hyperthermia, MDMA alters motor coordination (Marston et al, 1999), anxiety (Bhattacharya et al, 1998;Morley and McGregor, 2000;Sumnall et al, 2004), and cognitive functions (Braida et al, 2002;Ho et al, 2004;Marston et al, 1999; but see Ricaurte et al, 1993).…”

Section: Long-term Effects Of Etoh And/or Mdma On Behaviormentioning

confidence: 99%

Ethanol, 3,4-Methylenedioxymethamphetamine (Ecstasy) and Their Combination: Long-Term Behavioral, Neurochemical and Neuropharmacological Effects in the Rat

Cassel

Riegert

Rutz³

et al. 2005

Neuropsychopharmacol

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This study investigated long-term behavioral, neurochemical, and neuropharmacological effects of ethanol-(7)-3,4-methylenedioxymethamphetamine (MDMA, ecstasy) combinations. Over 4 consecutive days, male Long-Evans rats received 1.5 g/kg ethanol and/or 10 mg/kg MDMA, or saline. Rectal temperatures were taken in some rats. Starting 4 days after the last injection, we tested working memory, sensory-motor coordination, and anxiety. Subsequently, we measured cortical, striatal, septal, and hippocampal monoamines (last MDMA injection-euthanasia delay: 20 days), or electrically evoked release of serotonin (5-HT) in cortical and hippocampal slices, and its modulation in the presence of CP 93,129 (3-(1,2,5,6-tetrahydropyrid-4-yl)pyrrollo[3,2-b]pyrid-5-one) or methiotepin (last MDMA injection-euthanasia delays: 3-6 weeks). Ethanol attenuated the MDMA-induced hyperthermia, but only on the first day. In the longterm, MDMA reduced 5-HT and 5-hydroxyindoleacetic acid (5-HIAA) content in most brain regions. The behavioral and neurochemical effects of the ethanol-MDMA combination were comparable to those of MDMA alone; sensory-motor coordination was altered after ethanol and/or MDMA. In hippocampal slices from rats given ethanol and MDMA, the CP 93,129-induced inhibition and methiotepininduced facilitation of 5-HT release were stronger and weaker, respectively, than in the other groups. This is the first study addressing long-term effects of repeated MDMA and EtOH combined treatments in experimental animals. Whereas the drug combination produced the same behavioral and neurochemical effects as MDMA alone, our neuropharmacological results suggest that MDMA-EtOH interactions may have specific long-term consequences on presynaptic modulation of hippocampal 5-HT release, but not necessarily related to MDMA-induced depletion of 5-HT. Thus, it is likely that the psycho(patho)logical problems reported by ecstasy users drinking alcohol are not solely due to the consumption of MDMA.

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The consequences of beer consumption in rats: acute anxiolytic and ataxic effects and withdrawal-induced anxiety

Abstract: These results are the first to our knowledge to show that rats will consume beer at levels that produce clear effects on anxiety and on motor co-ordination, and that will eventually produce behavioural signs of withdrawal.

Cited by 41 publications

References 46 publications

Silver nanoparticle exposure induces rat motor dysfunction through decrease in expression of calcium channel protein in cerebellum

Silver nanoparticle exposure induces rat motor dysfunction through decrease in expression of calcium channel protein in cerebellum

Combined Exposure to Nicotine and Ethanol in Adolescent Mice Differentially Affects Anxiety Levels during Exposure, Short-Term, and Long-Term Withdrawal

Ethanol, 3,4-Methylenedioxymethamphetamine (Ecstasy) and Their Combination: Long-Term Behavioral, Neurochemical and Neuropharmacological Effects in the Rat

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