Emotional, cognitive and neurochemical alterations in a premotor stage model of Parkinson's disease

Tadaiesky, M.T.; Dombrowski, Patrícia A.; Figueiredo, Cláudia P.; Cargnin-Ferreira, Eduardo; Cunha, Cláudio Da; Takahashi, Reinaldo Ν.

doi:10.1016/j.neuroscience.2008.08.035

Cited by 274 publications

(184 citation statements)

References 42 publications

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“…This latter route of administration offers three advantages: First, the progressive and less extensive lesion is more relevant to PD. Second, this regimen has been shown to produce nonmotor symptoms of PD, including cognitive, psychiatric, and gastrointestinal dysfunction (Branchi et al 2008;Tadaiesky et al 2008;Cannon and Greenamyre 2010). Third, the ease of stereotactically injecting a large structure such as the striatum enhances the likelihood of success in mice.…”

Section: K Tieumentioning

confidence: 99%

A Guide to Neurotoxic Animal Models of Parkinson's Disease

Tieu¹

2011

Cold Spring Harbor Perspectives in Medicine

408

299

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Parkinson's disease (PD) is a neurological movement disorder primarily resulting from damage to the nigrostriatal dopaminergic pathway. To elucidate the pathogenesis, mechanisms of cell death, and to evaluate therapeutic strategies for PD, numerous animal models have been developed. Understanding the strengths and limitations of these models can significantly impact the choice of model, experimental design, and data interpretation. The primary objectives of this article are twofold: First, to assist new investigators who are contemplating embarking on PD research to navigate through the available animal models. Emphasis will be placed on common neurotoxic murine models in which toxic molecules are used to lesion the nigrostriatal dopaminergic system. And second, to provide an overview of basic technical requirements for assessing the pathology, structure, and function of the nigrostriatal pathway.

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Section: K Tieumentioning

confidence: 99%

A Guide to Neurotoxic Animal Models of Parkinson's Disease

Tieu¹

2011

Cold Spring Harbor Perspectives in Medicine

408

299

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“…In addition to basal ganglia dysfunction, several studies showed that mesofrontal dopamine is also affected in PD (Tadaiesky et al, 2008;Prediger et al, 2006;Ashby, Alfonso-Reese, Turken, & Waldron, 1998). Furthermore, some argue that dopaminergic medications (including both the dopamine precursor L-dopa and dopaminergic agonists) increase dopamine levels in prefrontal cortex (PFC; see Silberstein et al, 2005;Kaasinen et al, 2001;Carey, Pinheiro-Carrera, Dai, Tomaz, & Huston, 1995).…”

Section: Introductionmentioning

confidence: 99%

A Neurocomputational Model of Dopamine and Prefrontal–Striatal Interactions during Multicue Category Learning by Parkinson Patients

Moustafa¹,

Gluck²

2011

Journal of Cognitive Neuroscience

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Abstract■ Most existing models of dopamine and learning in Parkinson disease (PD) focus on simulating the role of basal ganglia dopamine in reinforcement learning. Much data argue, however, for a critical role for prefrontal cortex (PFC) dopamine in stimulus selection in attentional learning. Here, we present a new computational model that simulates performance in multicue category learning, such as the "weather prediction" task. The model addresses how PD and dopamine medications affect stimulus selection processes, which mediate reinforcement learning. In this model, PFC dopamine is key for attentional learning, whereas basal ganglia dopamine, consistent with other models, is key for reinforcement and motor learning. The model assumes that competitive dynamics among PFC neurons is the neural mechanism underlying stimulus selection with limited attentional resources, whereas competitive dynamics among striatal neurons is the neural mechanism underlying action selection. According to our model, PD is associated with decreased phasic and tonic dopamine levels in both PFC and basal ganglia. We assume that dopamine medications increase dopamine levels in both the basal ganglia and PFC, which, in turn, increase tonic dopamine levels but decrease the magnitude of phasic dopamine signaling in these brain structures. Increase of tonic dopamine levels in the simulated PFC enhances attentional shifting performance. The model provides a mechanistic account for several phenomena, including (a) medicated PD patients are more impaired at multicue probabilistic category learning than unmedicated patients and (b) medicated PD patients opt out of reversal when there are alternative and redundant cue dimensions. ■

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“…In addition, YKS improved BPSD such as hallucination, agitation, aggressiveness, and anxiety in patients with AD, [1][2][3] DLB, 4,5) PD, or PDD. 6,7) Reduced dopaminergic activity in the striatum and PFC in 6-OHDA-lesioned rats caused anxiogenic responses in the elevated plus-maze test, 49) whereas decreased DA levels in the medial PFC increased anxiety induced by social defeat stress. 50) Reduced PFC dopaminergic function or the blockade of DA receptors in the PFC impaired working memory.…”

Section: Discussionmentioning

confidence: 99%

Yokukansan, a Traditional Japanese Medicine, Enhances the L-DOPA-Induced Rotational Response in 6-Hydroxydopamine-Lesioned Rats: Possible Inhibition of COMT

Ishida

Ebihara

Tabuchi

et al. 2016

Biological & Pharmaceutical Bulletin

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The aim of the present study was to investigate the effects of the traditional Japanese medicine yokukansan (YKS) on the function of dopamine (DA) in the rat nigrostriatal system. Unilateral 6-hydroxydopamine lesions were produced in the rat nigrostriatal system. Despite a marked loss in the striatal immunoreactivity of tyrosine hydroxylase on the lesion side, striatal serotonin (5-HT) immunoreactivity was not affected. Treatment using L-3,4-dihydroxyphenylalanine (L-DOPA) in conjunction with benserazide for 15 d induced abnormal involuntary movements (AIMs) such as locomotive (rotational response), axial, forelimb, and orolingual movements in the lesioned rats. The L-DOPA-induced locomotive and axial, but not forelimb and orolingual, AIMs were significantly increased and prolonged by the pre-administration of YKS. We next investigated

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Emotional, cognitive and neurochemical alterations in a premotor stage model of Parkinson's disease

Cited by 274 publications

References 42 publications

A Guide to Neurotoxic Animal Models of Parkinson's Disease

A Guide to Neurotoxic Animal Models of Parkinson's Disease

A Neurocomputational Model of Dopamine and Prefrontal–Striatal Interactions during Multicue Category Learning by Parkinson Patients

Yokukansan, a Traditional Japanese Medicine, Enhances the L-DOPA-Induced Rotational Response in 6-Hydroxydopamine-Lesioned Rats: Possible Inhibition of COMT

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