Tryptophan depletion impairs object-recognition memory in the rat: Reversal by risperidone

Jenkins, Trisha A.; Elliott, J.; Ardis, T.C.; Cahir, Marie; Reynolds, Gavin P.; Bell, Robert A.; Cooper, Stephen

doi:10.1016/j.bbr.2009.12.030

Cited by 38 publications

(29 citation statements)

References 57 publications

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“…Future studies adopting longer time-points are necessary to further investigate this hypothesis. Tryptophan-dietary depletion impairs object-recognition memory and is accompanied by a reduction in 5-HT in several brain areas, such as the hippocampus, frontal cortex, and striatum (Jenkins et al 2010). Also, it is reported that intra-striatal hypoxanthine administration provoke impairment of spatial learning and memory in rats without affecting striatal dopaminergic system, although serotoninergic pathways seem to have been affected (Bavaresco et al 2007).…”

Section: Discussionmentioning

confidence: 98%

Behavioral, Neurochemical and Histological Alterations Promoted by Bilateral Intranigral Rotenone Administration: A New Approach for an Old Neurotoxin

et al. 2011

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Rotenone exposure in rodents provides an interesting model for studying mechanisms of toxin-induced dopaminergic neuronal injury. However, several aspects remain unclear regarding the effects and the accuracy of rotenone as an animal model of Parkinson's disease (PD). In order to counteract these limitations, this study characterized a precise neurotoxin-delivery strategy employing the bilateral intranigral administration protocol of rotenone as a reliable model of PD. We performed bilateral intranigral injections of rotenone (12 μg) and subsequent general activity (1, 10, 20, and 30 days after rotenone) and cognitive (7, 8, 15, and 30 days after rotenone) evaluations followed by neurochemical and immunohistochemical tests. We have observed that rotenone was able to produce a remarkable reduction on the percentage of tyrosine hydroxylase immunoreactive neurons (about 60%) within the substantia nigra pars compacta. Dopamine (DA) was severely depleted at 30 days after rotenone administration, similarly to its metabolites. In addition, an increase in DA turnover was detected at the same time-point. In parallel, striatal serotonin and its metabolite were found to be increased 30 days after the neurotoxic insult, without apparent modification in the serotonin turnover. Besides, motor behavior was impaired, mainly 1 day after rotenone. Furthermore, learning and memory processes were severely disrupted in different time-points, particularly at the training and test session (30 days). We now provide further evidence of a time-dependent neurodegeneration associated to cognitive impairment after the single bilateral intranigral administration of rotenone. Thus, it is proposed that the current rotenone protocol provides an improvement regarding the existing rotenone models of PD.

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Section: Discussionmentioning

confidence: 98%

Behavioral, Neurochemical and Histological Alterations Promoted by Bilateral Intranigral Rotenone Administration: A New Approach for an Old Neurotoxin

et al. 2011

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“…Even this low dose reduces object exploration and clearly has non-specific behavioural effects, as evidenced by the data shown here, however we usually observe efficacy even under these conditions in the PCP model, so are confident of its lack of efficacy in the present study. Others have shown efficacy against MK801 (Bubenikova-Valesova et al, 2008) and tryptophan-depletion (Jenkins et al, 2010) induced deficits in animal studies. This suggests that, although risperidone may be efficacious in reversing cognitive deficits in a disease model, it is not pro-cognitive in "normal" animals when the deficit is induced by task manipulation.…”

Section: Discussionmentioning

confidence: 99%

Nicotinic α7 and α4β2 agonists enhance the formation and retrieval of recognition memory: Potential mechanisms for cognitive performance enhancement in neurological and psychiatric disorders

McLean

Grayson

Marsh

et al. 2016

Behavioural Brain Research

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In the current study we investigated the efficacy of donepezil, risperidone and selective nicotinic α7 and α4β2 receptor agonists to reverse a delay-induced deficit in recognition memory. Adult female hooded-Lister rats received drug treatments and were tested in the novel object recognition (NOR) task following a 6 hour inter-trial interval (ITI). In all treatment groups there was no preference for the left or right identical objects in the acquisition trial. In the retention trial vehicle, risperidone (0.16mg/kg), PNU-282987, an α7 agonist (5mg/kg) and RJR-2403, an α4β2 agonist (1mg/kg) treated rats were unable to discriminate between the novel and familiar objects following a 6 hour ITI. In contrast, donepezil (1.0mg/kg), PNU-282987 (10mg/kg) and RJR-2403 (0.1mg/kg) treated rats spent significantly more time exploring the novel compared to the familiar object following the 6 hour ITI, indicative of enhanced cognitive performance (P<0.05-P<0.01). Interestingly, these compounds were efficacious when administered either before the acquisition or the retention trial of the task, suggesting an important role for nicotinic receptor subtypes in the formation and retrieval of recognition memory.

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“…Emerging evidence suggests that cortical and hippocampal SERT expression is important for memory formation (Meneses et al, 2011). With regard to recognition memory, SERT knockout rats show pronounced deficits (Olivier et al, 2009), and both chronic and acute tryptophan (i.e., serotonin precursor) depletion impaired object-recognition memory in rats (Jenkins et al, 2010; Olivier et al, 2008). Recently, Tellez and colleagues (Tellez et al, 2010) demonstrated that meth-induced SERT decreases were affected by learning experience.…”

Section: Discussionmentioning

confidence: 99%

Methamphetamine-induced changes in the object recognition memory circuit

et al. 2012

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Chronic methamphetamine (meth) can lead to persisting cognitive deficits in human addicts and animal models of meth addiction. Here, we examined the impact of either contingent or noncontingent meth on memory performance using an object-in-place (OIP) task, which measures the ability to detect an object relative to its location and surrounding objects. Further, we quantified monoamine transporter levels and markers of neurotoxicity within the OIP circuitry and striatum. Male Long-Evans rats received an acute meth binge (4 × 4 mg/kg i.p., 2 hour intervals) or self-administered meth (0.02 mg/infusion, i.v.; 7 days for 1 hour/day, followed by 14 days for 6 hours/day). Rats were tested for OIP recognition memory following one week of withdrawal. Subsequently, transporters for serotonin (SERT) and norepinephrine (NET) were quantified using Western blot in tissue obtained from the hippocampus, perirhinal cortex, and prefrontal cortex. In addition, striatal dopamine transporters, tyrosine hydroxylase, and glial fibrillary acidic protein were measured to assess potential neurotoxicity. Control (saline-treated) rats spent more time interacting with the objects in the changed locations. In contrast, contingent or noncontingent meth resulted in disrupted OIP performance as seen by similar amounts of time spent with all objects, regardless of location. While only acute meth binge produced signs of neurotoxicity, both meth regimens decreased SERT in the perirhinal cortex and hippocampus. Only meth self-administration resulted in a selective decrease in NET. Meth-induced changes in SERT function in the OIP circuitry may underlie memory deficits independently of overt neurotoxic effects.

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Tryptophan depletion impairs object-recognition memory in the rat: Reversal by risperidone

Cited by 38 publications

References 57 publications

Behavioral, Neurochemical and Histological Alterations Promoted by Bilateral Intranigral Rotenone Administration: A New Approach for an Old Neurotoxin

Behavioral, Neurochemical and Histological Alterations Promoted by Bilateral Intranigral Rotenone Administration: A New Approach for an Old Neurotoxin

Nicotinic α7 and α4β2 agonists enhance the formation and retrieval of recognition memory: Potential mechanisms for cognitive performance enhancement in neurological and psychiatric disorders

Methamphetamine-induced changes in the object recognition memory circuit

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