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André L Takatsu-Coleman,
Camilla L Patti,
Karina A Zanin,
Adriano Zager, Rita C Carvalho,
Aline R Borçoi,
Liliane M B Ceccon,
Laís F Berro,
Sergio Tufik,
Monica L Andersen,
Roberto Frussa-Filho
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ABSTRACT: Background: Although mood-congruent memory (MCM), or the tendency to recall information consistent with one's mood, is a robust phenomenon in human depression, to our knowledge, it has never been demonstrated in animals. Methods: Mice were subjected to social isolation (SI) or crowding for 12 hours and had their depressive-like behaviour (evaluated by the forced swim, tail suspension, sucrose preference and splash tests) or their serum corticosterone concentrations evaluated. In addition, we determined the temporal forgetting curve of the plus-maze discriminative avoidance task (PM-DAT) and examined the effects of SI or crowding on memory retrieval in the PM-DAT. Finally, we verified the effects of metyrapone pretreatment on reinstatement of memory retrieval or on the increase of corticosterone levels induced by SI. Results: Twelve hours of SI produced depressive-like behaviour, enhanced corticosterone concentration and reinstated retrieval of a forgotten discriminative aversive (i.e., negatively valenced) task. Depressive-like behaviour was critical for this facilitative effect of SI because 12 hours of crowding neither induced depressive-like behaviour nor enhanced retrieval, although it increased corticosterone levels at the same magnitude as SI. However, corticosterone increase was a necessary condition for MCM in mice, in that the corticosterone synthesis inhibitor metyrapone abolished SI-induced retrieval reinstatement. Limitations: Our study did not investigate the effects of the social manipulations proposed here in a positively valenced task. Conclusion: To our knowledge, the present paper provides the first evidence of MCM in animal models.
Journal of psychiatry & neuroscience: JPN 11/2012; 37(6):120050. · 5.34 Impact Factor
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ABSTRACT: Previous studies have demonstrated that stress or glucocorticoids impair the retrieval of spatial memory in rodents and declarative memory in humans. However, the effects on memory retrieval of stress introduced a long time after learning have not been well studied. We investigated whether a mild, extrinsic stressor (1-s 0.1 or 0.3 mA foot shock) would reactivate low baseline retrieval of an aversive memory (the plus-maze discriminative avoidance task, PM-DAT) and if it would be modulated by glucocorticoids. In experiment 1, male Swiss mice received pre-test foot shock (n=10 mice/group) 7 days after training and just before testing. A time-retrieval curve for low baseline retrieval for the subsequent experiments was also determined (experiment 2, n=10 mice/group). We investigated if pre-test foot shock could modify corticosterone release (experiment 3, n=8-9 mice/group) and reinstate retrieval in the PM-DAT (experiment 4, n=15 mice/group). The effects of metyrapone (100 mg/kg) on retrieval reinstatement (experiment 5, n=15 mice/group) and serum corticosterone enhancement (experiments 6, n=7-9 mice/group) induced by foot shock were analyzed. Finally, the effects of foot shock itself on PM-DAT exploration were verified (experiment 7, n=10 mice/group). We demonstrated here that foot shock reinstated the retrieval of a low baseline, discriminative avoidance task 30 (but not 7) days after training. This facilitative effect was not dependent on corticosterone secretion because metyrapone abolished the enhancement of corticosterone concentration but did not reverse the stress-induced reinstatement of retrieval.
Stress (Amsterdam, Netherlands) 10/2012; · 3.21 Impact Factor
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ABSTRACT: Modafinil (MOD), a psychostimulant used to treat narcolepsy, excessive daytime sleepiness, and sleepiness due to obstructive sleep apnea, appears to promote a possible facilitatory effect on cognitive function. In the present study, we investigated the effects of the acute administration of MOD on the different steps of emotional memory formation and usage (acquisition, consolidation and retrieval) as well as the possible participation of the state-dependency phenomenon on the cognitive effects of this compound. Mice were acutely treated with 32, 64 or 128 mg/kg MOD before training or testing or immediately after training and were subjected to the plus-maze discriminative avoidance task. The results showed that although pre-training MOD administration did not exert any effects on learning, the doses of 32 or 64 mg/kg induced emotional memory deficits during testing. Still, the post-training acute administration of the higher doses of MOD (64 and 128 mg/kg) impaired associative memory consolidation. When the drug was administered pre-test, only the 32 mg/kg dose impaired the task retrieval. Importantly, the cognitive impairing effects induced by 32 mg/kg MOD were not related to the phenomenon of state-dependency. In all, our findings provide pre-clinical evidence of potential emotional memory amnesia induced by MOD. This article is part of a Special Issue entitled 'Cognitive Enhancers'.
Neuropharmacology 07/2012; 64(1):365-70. · 4.81 Impact Factor
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ABSTRACT: The high prevalence of psychostimulant abuse observed in schizophrenic patients may be related to the development of mesolimbic dopaminergic supersensitivity (MDS) or nigrostriatal dopaminergic supersensitivity (NDS) in response to the chronic blockade of dopamine receptors produced by typical neuroleptic treatment. We compared the effects of withdrawal from long-term administration of the typical neuroleptic haloperidol (Hal) and/or the atypical agent risperidone (Ris) on MDS and NDS, behaviorally evaluated by amphetamine-induced locomotor stimulation (AILS) and apomorphine-induced stereotypy (AIS) in mice, respectively. We further evaluated the duration of MDS and investigated the specific role of dopamine D2 receptors in this phenomenon by administering the D2 agonist quinpirole (Quin) to mice withdrawn from long-term treatment with these neuroleptics. Withdrawal (48 hours) from long-term (20 days) Hal (0.5 mg/kg i.p.) (but not 0.5 mg/kg Ris i.p.) treatment potentiated both AILS and AIS. Ris co-administration abolished the potentiation of AILS and AIS observed in Hal-withdrawn mice. Ten days after withdrawal from long-term treatment with Hal (but not with Ris or Ris + Hal), a potentiation in AILS was still observed. Only Hal-withdrawn mice presented an attenuation of locomotor inhibition produced by Quin. Our data suggest that the atypical neuroleptic Ris has a pharmacological property that counteracts the compensatory MDS and NDS developed in response to the chronic blockade of dopamine receptors imposed by Ris itself or by typical neuroleptics such as Hal. They also indicate that MDS may be long lasting and suggest that an upregulation of dopamine D2 receptors in response to long-term treatment with the typical neuroleptic is involved in this phenomenon.
Addiction Biology 04/2009; 14(3):283-93. · 4.83 Impact Factor
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ABSTRACT: Numerous studies have described memory deficits following sleep deprivation. There is also evidence that the absence of sleep increases brain oxidative stress. The present study investigates the effects of a pro-oxidant agent--3-nitropropionic acid (3-NP)--on hippocampal oxidative stress and passive avoidance performance of sleep-deprived mice. Mice were repeatedly treated i.p. with saline or 5 or 15 mg/kg 3-NP and sleep-deprived for 24 h by the multiple platform method--groups of 4-5 animals placed in water tanks, containing 12 platforms (3 cm in diameter) surrounded by water up to 1 cm beneath the surface or kept in their home cage (control groups). The results showed that: (1) neither a 24 h sleep deprivation period nor 3-NP repeated treatment alone were able to induce memory deficits and increased hippocampal lipid peroxidation; (2) this same protocol of sleep deprivation, combined with 15 mg/kg 3-NP repeated treatment, induced memory deficits and an increase in hippocampal lipid peroxidation. The results support the involvement of hippocampal oxidative stress in the memory deficits induced by sleep deprivation and the hypothesis that normal sleep would prevent oxidative stress.
Progress in Neuro-Psychopharmacology and Biological Psychiatry 02/2007; 31(1):65-70. · 3.25 Impact Factor
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ABSTRACT: We investigated the effects of reserpine (0.1-0.5 mg/kg) on the performance of mice in the plus-maze discriminative avoidance task (DAVT), which simultaneously evaluates memory and motor activity. All doses induced memory impairment (increased aversive arm time) but only 0.5 mg/kg reserpine decreased locomotion (entries in enclosed arms). The results suggest that the DAVT evaluation in reserpine-treated mice can be a useful model for studying cognitive deficits accompanied by motor impairments.
Brain Research 12/2006; 1122(1):179-83. · 2.73 Impact Factor
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ABSTRACT: The present study aimed to investigate the effects of sleep deprivation (SD) on the dose-dependent stimulant effect of ethanol (ETOH) on the open-field behavior of female and male mice. Sleep-deprived (48 h, multiple platforms method) or home-cage control female mice were treated with saline (SAL) or 1.4, 1.8 or 2.2g/kg ETOH 5 min before behavioral testing. ETOH produced a dose-dependent increase in open-field locomotor behavior. This locomotor stimulant effect did not reflect a general stimulation in motor activity, since it was accompanied by a simultaneous decrease in rearing frequency as well as by no modification in immobility duration. The effects of ETOH on these three behavioral parameters were specifically modified by SD: the locomotor stimulant effect was abolished, the rearing inhibitory effect was potentiated and the lack of effect on immobility was changed to increase in immobility. Similar results were obtained for male mice although the effects of SD had a lower magnitude. The present findings demonstrate that the acute effect of ETOH on mice's motor activity are behaviorally complex and can be specifically modulated by SD.
Brain Research Bulletin 05/2006; 69(3):332-7. · 2.82 Impact Factor
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ABSTRACT: The differential outcomes of social isolation and crowding environment on the effects of single or repeated administration of ethanol on open-field behavior were examined in female mice. Whereas housing conditions did not alter the increase in locomotor activity induced by ethanol single administration, behavioral sensitization (a progressive increase of a drug effect following repeated drug administration) to the locomotor activating effect of ethanol was significantly greater in crowded mice as compared to isolated and control groups. Single administration of ethanol significantly decreased rearing frequency and increased immobility duration, there being tolerance to these ethanol behavior effects after repeated treatment. Social isolation attenuated the increase in immobility behavior induced by single administration of ethanol and potentiated the tolerance of ethanol-induced rearing decrease, verified after repeated treatment. These results point out that both sensitization and tolerance to the behavioral effects of ethanol can be critically influenced by housing conditions.
Pharmacology Biochemistry and Behavior 10/2005; 82(1):40-5. · 2.53 Impact Factor
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ABSTRACT: A biphasic effect of morphine on locomotion has been extensively described. Nevertheless, the effects of this opioid on other behavioral parameters have been overlooked. The aim of the present study was to verify the effects of different doses of morphine on motor behaviors observed in an open-field. Adult female mice were injected with saline or morphine (10, 15 and 20 mg/kg, i.p.) and observed in an open-field for quantification of locomotor and rearing frequencies as well as duration of immobility and grooming. The lowest dose of morphine decreased locomotion (and increased immobility duration) while the highest dose increased it. All doses tested decreased rearing and grooming. Thus, the effects of morphine on locomotion do not parallel to its effects on rearing and grooming. Our results indicate that locomotion not always reflects the effect of drugs on motor activity, which can be better investigated when other behavioral parameters are concomitantly taken into account.
Pharmacology Biochemistry and Behavior 09/2005; 81(4):923-7. · 2.53 Impact Factor
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Nilza P Araujo,
Vanessa C Abílio,
Regina H Silva,
Renata C Pereira, Rita C Carvalho,
Carla Gonzalez,
Rogério G Bellot,
Juliana P M V Castro,
Daniela F Fukushiro,
Marcelo S D Rodrigues,
Cibele C Chinen,
Roberto Frussa-Filho
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ABSTRACT: Recently, we have described the antidyskinetic property of the GABA mimetic drug valproic acid on reserpine-induced oral dyskinesia, an animal model that has been related to tardive as well as acute dyskinesias, which are associated with important neuropathologies. The present study investigates the effects of different doses of the GABA mimetic anticonvulsant topiramate on the manifestation of reserpine-induced orofacial dyskinesia. Female EPM-M1 mice received two injections of control solution or of 0.5 mg/kg reserpine separated by 48 h. Twenty-four hours after the second reserpine or control solution injection, animals were acutely treated with control solution or topiramate (1, 3, 10 or 30 mg/kg) and were observed for quantification of oral dyskinesia or general activity in an open-field. In order to verify the effects of topiramate per se on oral dyskinesia or general activity, female EPM-M1 mice were acutely treated with control solution or 1, 3, 10 or 30 mg/kg topiramate and observed for quantification of oral dyskinesia and general activity. The highest dose of topiramate completely abolished the manifestation of reserpine-induced oral dyskinesia whereas the doses of 3 and 10 mg/kg significantly attenuated it. None of the doses of the anticonvulsant modified spontaneous locomotion frequency or oral movements, whereas spontaneous rearing frequency was decreased by 3, 10 and 30 mg/kg topiramate. The highest dose of topiramate did not modify general activity in reserpine-treated mice. These results support the potential therapeutic use of topiramate in the treatment of oral dyskinesias.
Brain Research Bulletin 01/2005; 64(4):331-7. · 2.82 Impact Factor
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ABSTRACT: Several clinical studies demonstrate that the absence of periods of sleep is closely related to occurrence of anxiety symptoms. However, the basis of these interactions is poorly understood. Studies performed with animal models of sleep deprivation and anxiety would be helpful in the understanding of the mechanisms underlying this relationship, but some animal studies have not corroborated clinical data, reporting anxiolytic effects of sleep deprivation.
The aim of the present study was to verify the effects of different protocols of sleep deprivation in mice tested in the elevated plus-maze and to assess the effect of chlordiazepoxide and clonidine.
Three-month-old male mice were sleep-deprived for 24 or 72 h using the methods of single or multiple platforms in water tanks. Mice kept in their home cages were used as controls. Plus-maze behavior was observed immediately after the deprivation period.
Mice that were sleep-deprived for 72 h spent a lower percent time in the open arms of the apparatus than control animals. This sleep deprivation-induced anxiety-like behavior was unaffected by treatment with chlordiazepoxide (5.0 and 7.5 mg/kg IP), but reversed by an administration of 5 or 10 microg/kg IP clonidine.
The results indicate that under specific methodological conditions sleep deprivation causes an increase in anxiety-like behavior in mice exposed to the elevated plus-maze.
Psychopharmacologia 12/2004; 176(2):115-22. · 4.08 Impact Factor
