Behavioural and adrenocortical responses to nicotine measured in rats with selective lesions of the 5‐hydroxytryptaminergic fibres innervating the hippocampus

Balfour, David J.K.; Benwell, M. E. M.; Graham, Catherine; Vale, A. L.

doi:10.1111/j.1476-5381.1986.tb10266.x

Cited by 21 publications

(7 citation statements)

References 27 publications

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“…Our results showing no significant anxiogenic effect below 0.5 mg/kg are in broad agreement with those of Balfour et al (1986), who found no effects with 0.4 mg/kg of the racemate [which would be equivalent to a lower dose of the (-)-enantiomer because the (+)-enantiomer has little action on rat nicotinic receptors in the brain (Brioni et al 1997)]. However, our results contrast with the anxiolytic effect reported by Brioni et al (1994) after injection of 0.3 mg/kg nicotine.…”

Section: Discussionsupporting

confidence: 95%

Modulation of behaviour on trials 1 and 2 in the elevated plus-maze test of anxiety after systemic and hippocampal administration of nicotine

Ouagazzal¹,

Kenny²,

File³

1999

Psychopharmacology

115

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The results on both trials in the plus-maze after systemic administration of nicotine add to previous reports from the social interaction test that high doses of nicotine have anxiogenic effects. However, the effects of nicotine in the dorsal hippocampus are different in all three anxiety tests (anxiogenic in social interaction, ineffective on trial 1, anxiolytic on trial 2) showing that nicotinic cholinergic control in this brain region may vary depending on the state and/or type of anxiety generated by the test. The brain region(s) underlying the anxiogenic effects of IP nicotine on both trials in the plus-maze remain to be identified.

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Section: Discussionsupporting

confidence: 95%

Modulation of behaviour on trials 1 and 2 in the elevated plus-maze test of anxiety after systemic and hippocampal administration of nicotine

Ouagazzal¹,

Kenny²,

File³

1999

Psychopharmacology

115

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“…This result is also consistent with previous findings indicating that serotonin and DA play a critical role in the control of Nic SA (Balfour et al. , 1986; Corrigall & Coen, 1989; Corrigall, 1992; Olausson et al.…”

Section: Discussionsupporting

confidence: 94%

Monoamine oxidase A rather than monoamine oxidase B inhibition increases nicotine reinforcement in rats

Guillem

Vouillac

Azar

et al. 2006

Eur J of Neuroscience

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Although nicotine is considered to be responsible for the addictive properties of tobacco, growing evidence underlines the importance of non-nicotine components in smoking reinforcement. It has been shown that tobacco smoke contains monoamine oxidase (MAO) A and B inhibitors and decreases MAO-A and MAO-B activity in smokers. Here, we investigated the effects of clorgyline hydrochloride (irreversible MAO-A inhibitor; 2 mg/kg/day), selegiline (irreversible MAO-B inhibitor; 4 mg/kg) and the beta-carboline norharmane hydrochloride (reversible MAO-B inhibitor; 5 mg/kg/day) treatments on nicotine self-administration (30 microg/kg/infusion, free base) in rats. Independent of the responsiveness to novelty and locomotor activity stimulation, only clorgyline hydrochloride treatment increased the intake of nicotine in a fixed-ratio schedule (FR5) of reinforcement. When a progressive-ratio schedule was implemented, both clorgyline hydrochloride and norharmane hydrochloride treatments potentiated the reinforcing effects of nicotine, whereas selegiline had no effect. Taken together, these results indicate that MAO-A inhibition interacts with nicotine to enhance its rewarding effects in rats and suggest that other compounds present in tobacco, such as beta-carboline, may also play an important role in sustaining smoking behavior in humans.

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“…Therefore, using the elevated plus-maze, which has the ability to detect the anxiogenic as well as anxiolytic effects of drugs (Pellow et al, 1985), the possibility that ibogainepretreated animals experience anxiety when they are subsequently exposed to nicotine was investigated. Consistent with previous reports (Balfour et al, 1986), nicotine itself did not produce effects which would be indicative of anxiolysis nor anxiogenesis in this behavioural test although nicotine did result in a very significant increase in the overall activity of both the vehicle and ibogaine-pretreated rats. Furthermore, there was no change in the overall activity of the saline-treated control rats which could be attributed to their receiving an injection of ibogaine 22h previously.…”

Section: Discussionsupporting

confidence: 92%

Neurochemical and behavioural interactions between ibogaine and nicotine in the rat

Benwell

Holtom

Moran

et al. 1996

British J Pharmacology

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1 In vivo brain microdialysis has been employed to investigate the effects of ibogaine on nicotineinduced changes in dopamine overflow in the nucleus accumbens (NAc) of freely moving rats. The effects of the compound on locomotor responses to nicotine and behaviour in the elevated plus-maze were also examined. 2 No changes were observed in the dopamine overflow or the locomotor activity of the animals following the administration of ibogaine (40 mg kg-', i.p.). However, ibogaine, administered 22 h earlier, significantly (P<0.01) attenuated the increase in dopamine overflow but not the hyperlocomotion, evoked by nicotine. 3 In the elevated plus-maze test, significant reductions in the open:total runway entries in both salinetreated controls (P<0.05) and nicotine-treated (P<0.01) rats were obtained when the animals were tested 22 h after pretreatment with ibogaine (40 mg kg-', i.p.). The total activity was significantly (P <0.01) greater in the nicotine-treated rats but this response was not affected by ibogaine pretreatment. 4 Administration of ibogaine was associated with reductions in the tissue levels of 5-hydroxyindoleacetic acid (5-HIAA) in the NAc (P<0.01) and striatum (P<0.05) and an increase in the level of this metabolite in the medial prefrontal cortex (mPFC) (P<0.01) while the levels of dopamine and 5-hydroxytryptamine (5-HT) in the mPFC were reduced (P < 0.05). The DOPAC/dopamine (P < 0.05) and 5-HIAA/5-HT (P <0.01) ratios were significantly increased in the mPFC for at least 7 days after a single treatment with ibogaine. 5 Ibogaine attenuates the nicotine-induced increases in dopamine overflow in the NAc and may, therefore, inhibit the rewarding effects of this drug. However, the long lasting anxiogenesis induced by ibogaine warrant further investigation before its use could be recommended for smokers.

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Behavioural and adrenocortical responses to nicotine measured in rats with selective lesions of the 5‐hydroxytryptaminergic fibres innervating the hippocampus

Abstract: 1 The effects of acute and subchronic (7)

Cited by 21 publications

References 27 publications

Modulation of behaviour on trials 1 and 2 in the elevated plus-maze test of anxiety after systemic and hippocampal administration of nicotine

Modulation of behaviour on trials 1 and 2 in the elevated plus-maze test of anxiety after systemic and hippocampal administration of nicotine

Monoamine oxidase A rather than monoamine oxidase B inhibition increases nicotine reinforcement in rats

Neurochemical and behavioural interactions between ibogaine and nicotine in the rat

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