Memory disruption in rats with nigral lesions induced by MPTP: a model for early Parkinson's disease amnesia

Cunha, Cláudio Da; Ms, Gevaerd; Ma, Vital; Miyoshi, Edmar; Andreatini, Roberto; Silveira, Ricardo dos Reis; Rn, Takahashi; Canteras, Newton S.

doi:10.1016/s0166-4328(01)00211-x

Cited by 105 publications

(57 citation statements)

References 76 publications

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“…This view has been re-evaluated following the findings that the infusion of MPTP by intranasal (i.n.) route [105][106][107] or directly into the rat SNc [108][109][110] causes a partial loss of dopamine neurons and depletion of striatal dopamine that result in olfactory and memory deficits. Corroborating clinical observations, the administration of benserazide/L-DOPA to MPTP-lesioned rats, at a dose that restores the striatal dopamine levels, fails to reverse MPTP-induced learning and memory impairment [110].…”

Section: Caffeine As a Palliative Treatment For The Non-motor Impairmmentioning

confidence: 99%

Effects of Caffeine in Parkinson's Disease: From Neuroprotection to the Management of Motor and Non-Motor Symptoms

Prediger

2010

JAD

145

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Abstract. Parkinson's disease (PD) is the second most common neurodegenerative disorder affecting approximately 1% of the population older than 60 years. Classically, PD is considered to be a motor system disease and its diagnosis is based on the presence of a set of cardinal motor signs (rigidity, bradykinesia, rest tremor) that are consequence of a pronounced death of dopaminergic neurons in the substantia nigra pars compacta. Nowadays there is considerable evidence showing that non-dopaminergic degeneration also occurs in other brain areas which seems to be responsible for the deficits in olfactory, emotional and memory functions that precede the classical motor symptoms in PD. The present review attempts to examine results reported in epidemiological, clinical and animal studies to provide a comprehensive picture of the antiparkinsonian potential of caffeine. Convergent epidemiological and pre-clinical data suggest that caffeine may confer neuroprotection against the underlying dopaminergic neuron degeneration, and influence the onset and progression of PD. The available data also suggest that caffeine can improve the motor deficits of PD and that adenosine A2A receptor antagonists such as istradefylline reduces OFF time and dyskinesia associated with standard 'dopamine replacement' treatments. Finally, recent experimental findings have indicated the potential of caffeine in the management of non-motor symptoms of PD, which do not improve with the current dopaminergic drugs. Altogether, the studies reviewed provide strong evidence that caffeine may represent a promising therapeutic tool in PD, thus being the first compound to restore both motor and non-motor early symptoms of PD together with its neuroprotective potential.

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Section: Caffeine As a Palliative Treatment For The Non-motor Impairmmentioning

confidence: 99%

Effects of Caffeine in Parkinson's Disease: From Neuroprotection to the Management of Motor and Non-Motor Symptoms

Prediger

2010

JAD

145

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“…6-OHDA damages catecholamine-producing neurons in the guinea pig cochlea d'Aldin et al 1995a;Niu and Canlon 2002). MPTP is similarly toxic to DA neurons (see Mikkelsen et al 1999;Da Cunha et al 2001;Petroske et al 2001;Sedelis et al 2001). We disrupted LOC innervation by applying MPTP to the cochlear perilymph.…”

Section: Introductionmentioning

confidence: 98%

Disruption of Lateral Olivocochlear Neurons via a Dopaminergic Neurotoxin Depresses Sound-Evoked Auditory Nerve Activity

Prell

Hälsey

Hughes

et al. 2005

JARO

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We applied the dopaminergic (DA) neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) to the guinea pig cochlear perilymph. Immunolabeling of lateral olivocochlear (LOC) neurons using antibodies against synaptophysin was reduced after the MPTP treatment. In contrast, labeling of the medial olivocochlear innervation remained intact. As after brainstem lesions of the lateral superior olive (LSO), the site of origin of the LOC neurons, the main effect of disrupting LOC innervation of the cochlea via MPTP was a depression of the amplitude of the compound action potential (CAP). CAP amplitude depression was similar to that produced by LSO lesions. Latency of the N1 component of the CAP, and distortion product otoacoustic emission amplitude and adaptation were unchanged by the MPTP treatment. This technique for selectively lesioning descending LOC efferents provides a new opportunity for examining LOC modulation of afferent activity and behavioral measures of perception.

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“…Lindner et al (24,25) procuraram em seu estudo determinar se sinais clínicos parkinsonianos poderiam ser detectados em ratos com perda de células nigroestriatais e depleção dos níveis de dopamina, e se ratos de meia-idade (12 meses) teriam mais deficit que ratos jovens (2 meses). Os animais receberam infusão estriatal bilateral de 6-OHDA e foram avaliados após três meses de lesão.…”

Section: Discussionunclassified

“…A cirurgia estereotáxica permitiu a demonstração de que a infusão de MPTP diretamente na SNc de ratos produz lesão significativa de neurônios, porém, de forma mais moderada do que a 6-OHDA (25). Os poucos estudos utilizando o MPTP geram dúvidas se esse modelo é válido para o estudo de alterações motoras associadas à DP; por outro lado, ele tem sido amplamente utilizado para estudos dos deficit cognitivos associados a essa doença (12,13,25).…”

Section: Discussionunclassified

“…Os poucos estudos utilizando o MPTP geram dúvidas se esse modelo é válido para o estudo de alterações motoras associadas à DP; por outro lado, ele tem sido amplamente utilizado para estudos dos deficit cognitivos associados a essa doença (12,13,25). Sendo assim, o modelo de lesão da via nigroestriatal com 6-OHDA é utilizado para o estudo das alterações motoras da DP e ação de drogas antiparkinsonianas, já o modelo de lesão da via nigroestriatal com MPTP tem sido utilizado mais para o estudo dos deficit cognitivos (10).…”

Section: Discussionunclassified

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Análise histomorfométrica do músculo sóleo de ratos submetidos ao modelo animal de parkinsonismo induzido pelo MPTP

et al. 2013

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Fisioter Mov. 2013 abr/jun;26(2):395-402 Loureiro APC, Niederheitmann CBH, Gomes ARS, Loureiro CC, Zotz TGG. 396 benserazida + salina; 4 -MPTP-L-DOPA (n = 6): lesão na SNc por MPTP tratados com benserazida + L-DOPA. Esses animais foram submetidos a eutanásia 35 dias após os procedimentos experimentais. Foram analisados: peso corporal, peso muscular, morfologia geral do músculo com microscopia de luz e mensuração da área de secção transversa das fibras musculares. Realizaram-se comparações com o teste t pareado entre o peso corporal inicial e final. A ANOVA post-hoc Tukey foi usada para comparações entre os grupos, sendo considerado significativo p ≤ 0,05. Resultados: Não foram encontradas diferenças estatisticamente significativas nas variáveis analisadas. Conclusão: Os dados analisados não excluem a possibilidade de alterações ocorrerem no interior dessas células, nos tipos de fibras musculares ou em longo prazo.[P]Palavras-chave: Rigidez muscular. Músculo esquelético. Doença de Parkinson.1-Metil-4-Fenil-1,2,3,6-Tetra-Hidropiridina.[B] [K]

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Memory disruption in rats with nigral lesions induced by MPTP: a model for early Parkinson's disease amnesia

Cited by 105 publications

References 76 publications

Effects of Caffeine in Parkinson's Disease: From Neuroprotection to the Management of Motor and Non-Motor Symptoms

Effects of Caffeine in Parkinson's Disease: From Neuroprotection to the Management of Motor and Non-Motor Symptoms

Disruption of Lateral Olivocochlear Neurons via a Dopaminergic Neurotoxin Depresses Sound-Evoked Auditory Nerve Activity

Análise histomorfométrica do músculo sóleo de ratos submetidos ao modelo animal de parkinsonismo induzido pelo MPTP

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