Dexamethasone Reverses the Ethanol-Induced Anxiolytic Effect in Rats

Ferreira, Vânia Maria Moraes; Takahashi, Reinaldo Ν.; Morato, Gina Struffaldi

doi:10.1016/s0091-3057(00)00255-0

Cited by 20 publications

(10 citation statements)

References 34 publications

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“…4). Drug concentrations were similar to those used elsewhere (Abrahám et al 1996;Ferreira et al 2000;Di et al 2003) and pretraining infusions were also ineffective (data not shown). Thus, intrahippocampal dexamethasone infusion failed to mimic the facilitating influence of a pretraining stress session or systemic dexamethasone on fear memory consolidation following the weak training protocol.…”

Section: Experiments 4 and 5: Effect Of Intrahippocampal Dexamethasonsupporting

confidence: 77%

Stress response recruits the hippocampal endocannabinoid system for the modulation of fear memory

Alvares¹,

Engelke²,

Diehl³

et al. 2010

Learn. Mem.

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The modulation of memory processes is one of the several functions of the endocannabinoid system (ECS) in the brain, with CB1 receptors highly expressed in areas such as the dorsal hippocampus. Experimental evidence suggested an important role of the ECS in aversively motivated memories. Similarly, glucocorticoids released in response to stress exposure also modulates memory formation, and both stress and dexamethasone activate the ECS. Here, we investigate the interaction between the ECS and glucocorticoids in the hippocampus in the modulation of fear memory consolidation. Two protocols with different shock intensities were used in order to control the level of aversiveness. Local infusion of AM251 into the hippocampus immediately after training was amnestic in the strong, but not in the weak protocol. Moreover, AM251 was amnestic in animals stressed 0, but not 30-min prior to the weak protocol, reverting the stress-induced facilitatory effect. Finally, intrahippocampal AM251 infusion reduced memory in animals that received dexamethasone immediately, but not 30 min before training. These results are (1) consistent with the view that the dorsal hippocampus ECS is activated on demand, in a rapid and short-lived fashion in order to modulate the consolidation of an aversive memory, and (2) show that this recruitment seems to be mediated by glucocorticoids, either in the hippocampus or in other brain regions functionally associated with the hippocampus.

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Section: Experiments 4 and 5: Effect Of Intrahippocampal Dexamethasonsupporting

confidence: 77%

Stress response recruits the hippocampal endocannabinoid system for the modulation of fear memory

Alvares¹,

Engelke²,

Diehl³

et al. 2010

Learn. Mem.

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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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“…Conversely, acute administration of Eth has been shown to stimulate dopamine release preferentially in the nucleus accumbens (Imperato & Di Chiara, 1986) and induce anxiolytic-like behaviour in rodents in different anxiety paradigms, such as the traditional elevated plus maze (Correa et al 2008 ;Ferreira et al 2000 ;Prediger et al 2004 ;Wilson et al 2004), the plus-maze discriminative avoidance task (PM-DAT) model (Gulick & Gould, 2009a, b, 2011Kameda et al 2007), the light/dark box (Correa et al 2008) and the defensive prod-burying test (Wilson et al 2004). Interestingly, acute Eth administration (0.25-2.5 g/kg) reduced the avoidance response to lemon odour acquired by the association of odour intra-oral infusion of sucrose or citric acid in infant and pre-weanling rats, and this result has been suggested to be likely mediated by the anxiolytic properties of Eth (Pautassi et al 2005(Pautassi et al , 2006.…”

Section: Discussionmentioning

confidence: 99%

“…Eth was the best candidate because it is a drug of abuse known to produce anxiolytic behaviours in both rodents and humans (Correa et al 2008 ;Ferreira et al 2000 ;Prediger et al 2004 ;Sripada et al 2010 ;Wilson et al 2004). Thus, the purpose of the present paper was to compare the locomotor-stimulating effect of acute administration of Eth and the locomotor sensitization induced by repeated administration of Eth in Swiss mice tested in a completely novel environment (Nov) and in Swiss mice previously habituated to this same environment (Hab).…”

Section: Introductionmentioning

confidence: 99%

Acute and chronic ethanol differentially modify the emotional significance of a novel environment: implications for addiction

Fukushiro

Josino

Saito

et al. 2011

Int. J. Neuropsychopharm.

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Using open-field behaviour as an experimental paradigm, we demonstrated a complex interaction between the rewarding/stimulating effects and the anxiogenic/stressful effects of both novelty and acute or chronic amphetamine in mice. As a consequence of this interaction, acute amphetamine-induced hyperlocomotion was inhibited, whereas the expression of its sensitization was facilitated in a novel environment. In the present study, we aimed to investigate the interactions between exposure to a novel environment and the acute and chronic effects of ethanol (Eth), a drug of abuse known to produce anxiolytic-like behaviour in mice. Previously habituated and non-habituated male Swiss mice (3 months old) were tested in an open field after receiving an acute injection of Eth or following repeated treatment with Eth. Acute Eth administration increased locomotion with a greater magnitude in mice exposed to the apparatus for the first time, and this was thought to be related to the attenuation of the stressful effects of novelty produced by the anxiolytic-like effect of acute Eth, leading to a subsequent prevalence of its stimulant effects. However, locomotor sensitization produced by repeated Eth administration was expressed only in the previously explored environment. This result might be related to the well-known tolerance of Eth-induced anxiolytic-like behaviour following repeated treatment, which would restore the anxiogenic effect of novelty. Our data suggest that a complex and plastic interaction between the emotional and motivational properties of novelty and drugs of abuse can critically modify the behavioural expression of addiction-related mechanisms.

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Dexamethasone Reverses the Ethanol-Induced Anxiolytic Effect in Rats

Cited by 20 publications

References 34 publications

Stress response recruits the hippocampal endocannabinoid system for the modulation of fear memory

Stress response recruits the hippocampal endocannabinoid system for the modulation of fear memory

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

Acute and chronic ethanol differentially modify the emotional significance of a novel environment: implications for addiction

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