Effects of nicotine and amphetamine on latent inhibition in human subjects

Thornton, Jasper C.; Dawe, Sharon; Lee, C.; Capstick, Claire; Corr, Philip J.; Cotter, Paul A.; Frangou, Sophia; Gray, Nicola S.; Russell, Michael A.; Gray, Jeffrey A.

doi:10.1007/bf02805990

Cited by 155 publications

(69 citation statements)

References 60 publications

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“…Consistent with the widely documented difficulty to ignore irrelevant stimuli in schizophrenia, LI is disrupted in some subsets of schizophrenic patients (Baruch et al 1988;Dunn and Scibilia 1996;Gray et al 1992aGray et al , 1995Vaitl and Lipp 1997; but see Swerdlow et al 1996b;Williams et al 1998), and this disruption is modeled by loss of LI in amphetamine-treated rats (Killcross et al 1994a;Solomon et al 1981;Weiner et al 1981Weiner et al , 1984Weiner et al , 1988 and in normal humans (Gray et al 1992b; Thornton et al 1996). The validity of the model is further strengthened by findings that the neural substrates of LI in the rat include the hippocampal formation and the nucleus accumbens, consistent with the temporal lobe and mesolimbic pathology implicated in the pathophysiology of schizophrenia (for review, see Weiner 1990;.…”

mentioning

confidence: 75%

The Latent Inhibition Model Dissociates between Clozapine, Haloperidol, and Ritanserin

Shadach

2000

Neuropsychopharmacology

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mentioning

confidence: 75%

The Latent Inhibition Model Dissociates between Clozapine, Haloperidol, and Ritanserin

Shadach

2000

Neuropsychopharmacology

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“…The efficacy of amphetamine to disrupt LI has been shown in rats as well as in humans (Solomon and Staton, 1982;Weiner et al, 1988;Gray et al, 1992;Thornton et al, 1996), which parallels reports of LI disruption in schizophrenia patients as well as schizoptypal individuals (Baruch et al, 1988;NS Gray et al, 1995;Escobar et al, 2002). This has led to the application of the LI paradigm to assess schizophrenia-related psychopathology in animals, including its recent application to genetically modified mice (Gainetdinov et al, 2001;Kilts, 2001;Miyakawa et al, 2003).…”

Section: Introductionmentioning

confidence: 82%

Expression of the CS- and US-Pre-Exposure Effects in the Conditioned Taste Aversion Paradigm and Their Abolition Following Systemic Amphetamine Treatment in C57BL6/J Mice

Meyer

Chang

Feldon

et al. 2004

Neuropsychopharmacol

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In classical conditioning, pre-exposures to either the to-be-conditioned stimulus (CS) or unconditioned stimulus (US) can retard subsequent conditioning between the CS and US. The present experiment evaluated the expression of these two pre-exposure effects in mice of the C57BL6/J strain, one of the most common background strains for genetically altered mice. We tested whether their expression would be disrupted by amphetamine treatment (2.5 mg/kg, i.p.) in a conditioned taste aversion paradigm with sucrose as the CS and lithium chloride-induced gastric malaise as the US. We found that one pre-exposure (PE) to either the CS or the US reduced aversion to sucrose solution in the controls following conditioning, but no such tendency was evident in the amphetamine-treated mice. The present study represents the first report of amphetamine-induced disruption of the CS-PE effect (ie latent inhibition) in mice, and the first attempt to compare it directly with the US-PE effect in any species. It extended previous reports in rats and humans, suggesting that the sensitivity of latent inhibition to amphetamine is largely comparable across species, thereby lending credence to the use of the latent inhibition effect as a behavioral assay for psychotic-like phenotype in transgenic mice. The parallel observation in the US-PE effect further indicates that its expression, at least in the present conditioned taste aversion paradigm, may also be under similar influence of the dopaminergic system.

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“…Disruption of LI reflects a selective attention deficit, whereby animals lose the capacity to ignore the irrelevant stimulus, and is also observed in amphetamine-treated humans, as well as in high-schizotypal humans (Braunstein-Bercovitz et al, 2002;Gray et al, 1992b;Salgado et al, 2000;Swerdlow et al, 2003;Thornton et al, 1996) and in acutely psychotic schizophrenia patients (Baruch et al, 1988;Gray et al, 1992aGray et al, , 1995bRascle et al, 2001; but also see Swerdlow et al, 2005). A failure to inhibit attention to irrelevant stimuli is likely to give rise to aberrantly increased salience perception and distractibility that are associated with psychotic symptoms (Kapur et al, 2005;Weiner and Arad, 2009).…”

Section: Discussionmentioning

confidence: 99%

Contrasting Effects of Increased and Decreased Dopamine Transmission on Latent Inhibition in Ovariectomized Rats and Their Modulation by 17β-Estradiol: An Animal Model of Menopausal Psychosis?

Arad

Weiner

2010

Neuropsychopharmacol

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Women with schizophrenia have later onset and better response to antipsychotic drugs (APDs) than men during reproductive years, but the menopausal period is associated with increased symptom severity and reduced treatment response. Estrogen replacement therapy has been suggested as beneficial but clinical data are inconsistent. Latent inhibition (LI), the capacity to ignore irrelevant stimuli, is a measure of selective attention that is disrupted in acute schizophrenia patients and in rats and humans treated with the psychosisinducing drug amphetamine and can be reversed by typical and atypical APDs. Here we used amphetamine (1 mg/kg)-induced disrupted LI in ovariectomized rats to model low levels of estrogen along with hyperfunction of the dopaminergic system that may be occurring in menopausal psychosis, and tested the efficacy of APDs and estrogen in reversing disrupted LI. 17b-Estradiol (50, 150 mg/kg), clozapine (atypical APD; 5, 10 mg/kg), and haloperidol (typical APD; 0.1, 0.3 mg/kg) effectively reversed amphetamine-induced LI disruption in sham rats, but were much less effective in ovariectomized rats; 17b-estradiol and clozapine were effective only at high doses (150 mg/kg and 10 mg/kg, respectively), whereas haloperidol failed at both doses. Haloperidol and clozapine regained efficacy if coadministered with 17b-estradiol (50 mg/kg, an ineffective dose). Reduced sensitivity to dopamine (DA) blockade coupled with spared/potentiated sensitivity to DA stimulation after ovariectomy may provide a novel model recapitulating the combination of increased vulnerability to psychosis with reduced response to APD treatment in female patients during menopause. In addition, our data show that 17b-estradiol exerts antipsychotic activity.

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Effects of nicotine and amphetamine on latent inhibition in human subjects

Cited by 155 publications

References 60 publications

The Latent Inhibition Model Dissociates between Clozapine, Haloperidol, and Ritanserin

The Latent Inhibition Model Dissociates between Clozapine, Haloperidol, and Ritanserin

Expression of the CS- and US-Pre-Exposure Effects in the Conditioned Taste Aversion Paradigm and Their Abolition Following Systemic Amphetamine Treatment in C57BL6/J Mice

Contrasting Effects of Increased and Decreased Dopamine Transmission on Latent Inhibition in Ovariectomized Rats and Their Modulation by 17β-Estradiol: An Animal Model of Menopausal Psychosis?

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