Memory, mood, dopamine, and serotonin in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-lesioned mouse model of basal ganglia injury

Vučković, Marta; Wood, Ruth I.; Holschneider, Daniel P.; Abernathy, Avery; Togasaki, Daniel M.; Smith, Alexsandra; Petzinger, Giselle M.; Jakowec, Michael W.

doi:10.1016/j.nbd.2008.07.015

Cited by 97 publications

(70 citation statements)

References 76 publications

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“…These results were consistent with other findings that showed a cognitive impairment in delayed alternation task of spatial learning [15] , associative olfactory memory test [16] and social recognition task [17] in MPTP-treated mice. Using an identical MPTP dosing regimen and the same strain of mouse, a loss of associative olfactory memory was first detected 30 days after treatment, not at an earlier 7-day period, and in the absence of any effect on odor discrimination or motor function.…”

Section: Discussionsupporting

confidence: 93%

“…Similarly, we report an SOR memory impairment 2 weeks following MPTP treatment with no clear motor impairment as demonstrated by an increase in distanced traveled in the open field, which has been reported by others [15] . Relatedly, Dluzen and Kreutzberg [17] reported diminished social recognition at 5-10 days after a modest dose of MPTP; however, without a significant loss of DA in the striatum or other brain regions, which is in contrast to our study and the literature cited above [15,16] . Surprisingly, L -DOPA treatment, just prior to memory assessment, completely restored normal social recognition memory in the absence of a dopaminergic deficit.…”

Section: Discussioncontrasting

confidence: 85%

“…Together, these data suggest that the loss of nigrostriatal terminals was responsible for the impairment of recognition memory in MPTP-treated mice. However, given the limited scope of this paper, we cannot exclude the possibility that MPTP treatment produced neuronal loss in other brain regions, particularly mesolimbic projections, which may have contributed to this cognitive deficit [16,19,23] .…”

Section: Discussionmentioning

confidence: 98%

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Social Odor Recognition: A Novel Behavioral Model for Cognitive Dysfunction in Parkinson’s Disease

Monaghan

Leddy²,

Sung³

et al. 2010

Neurodegener Dis

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Background: Parkinson’s disease (PD) is a progressive neurodegenerative condition characterized by an increasing loss of dopaminergic neurons resulting in motor dysfunction. However, cognitive impairments in PD patients are a common clinical feature that has gained increased attention. Objective: The purpose of the current study was to evaluate the effects of an MPTP-induced dopaminergic lesion in mice on social odor recognition (SOR) memory. Methods: Mice were acutely treated with MPTP and evaluated for memory impairments in the SOR assay and characterized using biochemical and immunohistochemical methods approximately 2 weeks later. Results: Here we demonstrate that SOR memory is sensitive to MPTP treatment and that it correlates with multiple measures of nigrostriatal integrity. MPTP treatment of C57BL/6N mice produced a profound decrease in dopamine levels, dopamine transporter binding and tyrosine hydroxylase immunoreactivity in the striatum. These impairments in stratial dopaminergic function were blocked by pretreatment with the MAO-B inhibitor deprenyl. Changes in the dopaminergic system parallel those observed in SOR with MPTP treatment impairing recognition memory in the absence of a deficit in odor discrimination during learning. Deprenyl pretreatment blocked the MPTP-induced impairment of SOR memory. Conclusion: The use of the SOR memory model may provide a preclinical method for evaluating cognitive therapies for PD.

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Section: Discussionsupporting

confidence: 93%

Section: Discussioncontrasting

confidence: 85%

Section: Discussionmentioning

confidence: 98%

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Social Odor Recognition: A Novel Behavioral Model for Cognitive Dysfunction in Parkinson’s Disease

Monaghan

Leddy²,

Sung³

et al. 2010

Neurodegener Dis

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“…There are several reasons for assuming that the stimulation of an active lifestyle may be of essential benefit to the functional and neurophysiological prospects for PD patients, not only with regard to postponement of depressive symptoms (Dunn et al 2005) and dementia (Laurin et al 2001), but also deteriorations in cognitive ability and performance (van Gelder et al 2004), including associative memory and conditioned fear (Vucković et al 2008). For example, applying the physical exertions inherent to 'Nordic walking ', van Eijkeren et al (2008) showed that this relatively simple form of ambulation, requiring quadrupedal mobilization of motor centres, gave clear improvements both in quality-of-life and motility in PD patients.…”

Section: Discussionmentioning

confidence: 99%

Physical Exercise Attenuates MPTP-Induced Deficits in Mice

Archer

Fredriksson

2010

Neurotox Res

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Two experiments were performed to investigate the effects of physical exercise upon the hypokinesia induced by two different types of MPTP administration to C57/BL6 mice. In the first, mice were administered either the standard MPTP dose (2 × 20 or 2 × 40 mg/kg, 24-h interval) or vehicle (saline, 5 ml/kg); and over the following 3 weeks were given daily 30-min period of wheel running exercise over five consecutive days/week or placed in a cage in close proximity to the running wheels. Spontaneous motor activity testing in motor activity test chambers indicated that exercise attenuated the hypokinesic effects of both doses of MPTP upon spontaneous activity or subthreshold L: -Dopa-induced activity. In the second experiment, mice were either given wheel running activity on four consecutive days (30-min period) or placed in a cage nearby and on the fifth day, following motor activity testing over 60 min, injected with either MPTP (1 × 40 mg/kg) or vehicle. An identical procedure was maintained over the following 4 weeks with the exception that neither MPTP nor vehicle was injected after the fifth week. The animals were left alone (without either exercise or MPTP) and tested after 2- and 4-week intervals. Weekly exercise blocked, almost completely, the progressive development of severe hypokinesia in the MPTP mice and partially restored normal levels of activity after administration of subthreshold L: -Dopa, despite the total absence of exercise following the fifth week. In both experiments, MPTP-induced loss of dopamine was attenuated by the respective regime of physical exercise with dopamine integrity more effectively preserved in the first experiment. The present findings are discussed in the context of physical exercise influences upon general plasticity and neuroreparative propensities as well as those specific for the nigrostriatal pathway.

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“…Dopamine availability in both striatal and extrastriatal brain regions is known to be implicated in cognitive performance. Acute 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) lesioning in mice caused associative memory impairments with depletion of dopamine throughout the brain (Vucković et al 2008). Dopaminergic therapies after TBI illustrate the importance of dopamine for cognitive function/dysfunction after TBI (Bales et al 2009).…”

Section: Discussionmentioning

confidence: 99%

Hypothermia alleviates hypoxic ischemia-induced dopamine dysfunction and memory impairment in rats

Cho

Kim

et al. 2011

Animal Cells and Systems

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(2011) Hypothermia alleviates hypoxic ischemia-induced dopamine dysfunction and memory impairment in rats, Animal Cells and Systems, 15:4, 279-286, DOI: 10.1080/19768354.2011.607514 To link to this article: https://doi.org/10. 1080/19768354.2011 Hypoxic ischemia injury is a common cause of functional brain damage, resulting from a decrease in cerebral blood flow and oxygen supply to the brain. The main problems associated with hypoxic ischemia to the brain are memory impairment and dopamine dysfunction. Hypothermia has been suggested to ameliorate the neurological impairment induced by various brain insults. In this study, we investigated the effects of hypothermia on memory function and dopamine synthesis following hypoxic ischemia to the brain in rats. For this purpose, a step-down avoidance task, a radial eight-arm maze task, and immunohistochemistry for tyrosine hydroxylase (TH) and 5-bromo-2?-deoxyuridine (BrdU) were performed. The present results indicated that the hypoxic ischemia-induced disturbance of the animal's performances and spatial working memory was associated with a decrement in TH expression in the substantia nigra and striatum, and an increase in cell proliferation in the hippocampal dentate gyrus. Hypothermia treatment improved the animals' performance and spatial working memory by suppressing the decrement in TH expression in the substantia nigra and striatum and the increase in cell proliferation in the dentate gyrus. We suggest that hypothermia can be an efficient therapeutic modality to facilitate recovery following hypoxic ischemia injury to the brain, presumably by modulating the dopaminergic cell loss.

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Memory, mood, dopamine, and serotonin in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-lesioned mouse model of basal ganglia injury

Cited by 97 publications

References 76 publications

Social Odor Recognition: A Novel Behavioral Model for Cognitive Dysfunction in Parkinson’s Disease

Social Odor Recognition: A Novel Behavioral Model for Cognitive Dysfunction in Parkinson’s Disease

Physical Exercise Attenuates MPTP-Induced Deficits in Mice

Hypothermia alleviates hypoxic ischemia-induced dopamine dysfunction and memory impairment in rats

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