Anxiety, defence and the elevated plus-maze

Rodgers, R.J.; Dalvi, Ashutosh

doi:10.1016/s0149-7634(96)00058-9

Cited by 854 publications

(532 citation statements)

References 56 publications

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“…Relative increases of open arm as compared to closed arm parameters are typically considered to reflect anxiolytic effects, whereas relative decreases in closed arm as compared to open arm parameters are thought to reflect anxiogenic effects (Pellow, Chopin, File, Briley, 1985;Rodgers & Dalvi, 1997; for more recent studies combining the elevated plus maze with hippocampal manipulations: Kjelstrup et al, 2002;Bannerman et al, 2002;Rezayat et al, 2005;Bertoglio et al, 2006). …”

Section: Experiments 1: Effects Of Muscimol Infusion Into the Dorsal Omentioning

confidence: 99%

Temporary inhibition of dorsal or ventral hippocampus by muscimol: Distinct effects on measures of innate anxiety on the elevated plus maze, but similar disruption of contextual fear conditioning

Zhang

Bast

et al. 2014

Behavioural Brain Research

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Section: Experiments 1: Effects Of Muscimol Infusion Into the Dorsal Omentioning

confidence: 99%

Temporary inhibition of dorsal or ventral hippocampus by muscimol: Distinct effects on measures of innate anxiety on the elevated plus maze, but similar disruption of contextual fear conditioning

Zhang

Bast

et al. 2014

Behavioural Brain Research

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“…Each test lasted 10 min and all testing sessions were performed between 0300 and 0700 in a sound attenuated room. (Elliott et al, 2004;Ferandes and File, 1996;Hogg, 1996;Rodgers and Dalvi, 1997). Considering that Entries OA is related to levels of locomotor activity, and that locomotor activity may be affected by activation or suppression effects of nicotine and ethanol, the percentage of open arms entries (%Entries OA: the number of entries in open arms divided by number of entries in open + closed arms (Entries OA + CA), an index that corrects for altered locomotor activity, was also used as a measure of anxiety (Elliott et al, 2004;Ferandes and File, 1996;Hogg, 1996;Rodgers and Dalvi, 1997).…”

Section: Animal Treatment and Behavioral Testingmentioning

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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“…The elevated plus-maze (open arms: 50 Â 10 cm; closed arms: 50 Â 10 Â 40 cm; elevation: 50 cm) is a valid, reliable measure of anxiety, as well as the anxiolytic effects of drugs, including the BZs (Pellow et al, 1985;Rodgers and Dalvi, 1997). Before hippocampal slice preparation, rats were moved to a novel environment 30-60 min prior to placement in the plus-maze.…”

Section: Behavioral Testingmentioning

confidence: 99%

Transient Plasticity of Hippocampal CA1 Neuron Glutamate Receptors Contributes to Benzodiazepine Withdrawal-Anxiety

Sickle

Kong

Tietz

2004

Neuropsychopharmacol

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Withdrawal from 1-week oral administration of the benzodiazepine (BZ), flurazepam (FZP) is associated with enhanced AMPA receptor (AMPAR)-mediated and reduced NMDA receptor (NMDAR)-mediated excitation in CA1 pyramidal neurons 2-days after cessation of FZP administration. The present study examined temporal regulation of glutamate receptor-mediated whole-cell currents in CA1 neurons from hippocampal slices prepared from 0-, 1-, 2-, and 4-day FZP-withdrawn rats in relation to expression of anxiety-like behavior during BZ withdrawal. AMPAR-mediated miniature excitatory postsynaptic current (mEPSC) amplitude was significantly increased in CA1 neurons from 1-and 2-day FZP-withdrawn rats, while evoked NMDAR EPSC amplitude was reduced only in neurons from 2-day FZP-withdrawn rats. Withdrawal-anxiety, measured in the elevated plus-maze, was observed 1 day, but not 0, 2, or 4 days, after FZP treatment with 1-day withdrawn rats spending significantly reduced time in open arms compared to controls. CA1 neuron hyperexcitability was evident from the significant increase in the frequency of extracellular, 4-AP-induced spike discharges in slices from 1-day FZP-withdrawn rats. Systemic injection of the NMDAR antagonist MK-801 (0.25 mg/kg) on day 1 of withdrawal prevented reduced NMDAR-mediated currents in CA1 neurons from 2-day FZP-withdrawn rats, whereas AMPAR-mediated currents remained upregulated. Furthermore, MK-801 'unmasked' withdrawal-anxiety in the same 2-day FZP-withdrawn rats. Systemic injection of the AMPAR antagonist GYKI-52466 (0.5 mg/kg) at the onset of withdrawal blocked increased AMPAR-mediated currents and withdrawal-anxiety in 1-day FZP-withdrawn rats. These findings suggest that increased CA1 neuron AMPAR-mediated excitation may contribute to hippocampal hyperexcitability and expression of withdrawal-anxiety after prolonged BZ exposure via NMDAR-mediated neural circuits.

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Anxiety, defence and the elevated plus-maze

Cited by 854 publications

References 56 publications

Temporary inhibition of dorsal or ventral hippocampus by muscimol: Distinct effects on measures of innate anxiety on the elevated plus maze, but similar disruption of contextual fear conditioning

Temporary inhibition of dorsal or ventral hippocampus by muscimol: Distinct effects on measures of innate anxiety on the elevated plus maze, but similar disruption of contextual fear conditioning

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

Transient Plasticity of Hippocampal CA1 Neuron Glutamate Receptors Contributes to Benzodiazepine Withdrawal-Anxiety

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