Navegando por Palavras-chave "6-hydroxydopamine"

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    Development of Bladder Dysfunction in a Rat Model of Dopaminergic Brain Lesion
    (Wiley-Blackwell, 2011-01-01) Soler, Roberto [UNIFESP]; Fuellhase, Claudius; Santos, Cesar; Andersson, Karl-Erik; Wake Forest Univ; Universidade Federal de São Paulo (UNIFESP); Ludwig Maximilians Univ Munchen
    Aims: Parkinson's disease (PD) is one of the most common neurological disorders causing lower urinary tract dysfunction. We evaluated the temporal development of bladder dysfunction in rat PD model where urodynamic changes were induced by unilateral injection of 6-hydroxydopamine (6-OHDA) into the medial forebrain bundle (MFB). Methods: Female Sprague--Dawley rats underwent a unilateral stereotaxic injection of 6-OHDA or vehicle (sham group) into the MFB. Cystometry was performed in conscious animals at 3, 14, and 28 days after the injury. Aged-matched unlesioned rats were used as healthy controls. Results: Three days after lesion 6-OHDA rats showed higher threshold (TP), maximum pressures (MP), and spontaneous activity (SA) compared to healthy controls. Sham animals exhibited higher TP. After 14 days 6-OHDA rats had also higher micturition frequency, decreased bladder capacity, micturition volume and bladder compliance (Bcom) compared to sham and healthy controls. Sham animals showed lower Bcom and higher MP and SA. After 28 days, 6-OHDA rats exhibited the same changes as those in 14 days, while sham-operated animals showed parameters similar to those in healthy controls. Conclusions: These findings suggest that 6-OHDA lesion of the MFB causes bladder dysfunction already after 3 days. A pattern of detrusor overactivity was more clearly defined 14 days after the injection and persisted for 28 days. Cystometry may be a useful tool to study the pathophysiology of bladder dysfunction in PD, and urodynamic parameters may possibly be used to evaluate the effects of therapeutic interventions. Neurourol. Urodynam. 30: 188-193, 2011. (C) 2010 Wiley-Liss, Inc.
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    Hemiparkinsonian rats rotate toward the side with the weaker dopaminergic neurotransmission
    (Elsevier B.V., 2008-06-03) Da Cunha, Claudio; Wietzikoski, Evellyn Claudia; Ferro, Marcelo Machado; Martinez, Glaucia Regina; Barbato Frazao Vital, Maria Aparecida; Hipolide, Debora [UNIFESP]; Tufik, Sergio [UNIFESP]; Canteras, Newton Sabino; Universidade Federal do Paraná (UFPR); Universidade Federal de São Paulo (UNIFESP); Universidade de São Paulo (USP)
    Rats with unilateral lesion of the substantia nigra pars compacta (SNpc) have been used as a model of Parkinson's disease. Depending on the lesion protocol and on the drug challenge, these rats rotate in opposite directions. the aim of the present study was to propose a model to explain how critical factors determine the direction of these turns. Unilateral lesion of the SNpc was induced with 6-hydroxydopamine (6-OHDA) or 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). Separate analysis showed that neither the type of neurotoxin nor the site of lesion along the nigrostriatal. pathway was able to predict the direction of the turns these rats made after they were challenged with apomorphine. However, the combination of these two factors determined the magnitude of the lesion estimated by tyrosine-hydroxylase immunohistochemistry and HPLC-ED measurement of striatal dopamine. Very small lesions did Dot cause turns, medium-size lesions caused ipsiversive turns, and large lesions caused contraversive turns. Large-size SNpc lesions resulted in an increased binding of [H-3] raclopride to D2 receptors, while medium-size lesions reduced the binding of [H-3]SCH-23390 D1 receptors in the ipsilateral striatum. These results are coherent with the model proposing that after challenged with a dopamine receptor agonist, unilaterally SNpc-lesioned rats rotate toward the side with the weaker activation of dopamine receptors. This activation is weaker on the lesioned side in animals with small SNpc lesions due to the loss of dopamine, but stronger in animals with large lesions due to dopamine receptor supersensitivity. (C) 2008 Elsevier B.V. All rights reserved.