Important role of striatal catalase in aging- and reserpine-induced oral dyskinesia

Abı́lio, Vanessa C.; Silva, Regina H.; Carvalho, Reinaldo de Amorim; Grassl, Christian; Calzavara, Mariana Bendlin; Registro, Sibele; D’Almeida, Vânia; Ribeiro, R. de A.; Frussa‐Filho, Roberto

doi:10.1016/j.neuropharm.2004.04.003

Cited by 59 publications

(27 citation statements)

References 40 publications

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“…This has been paralleled to the induction of dyskinesia in this model of the disease, in the presence of elevated DA levels (Cotzias et al , 1971 ). Finally, melatonin has been reported to improve clinical manifestation of dyskinesia associated with compromised DA function (Shamir et al , 2001 ;Abilio et al , 2004 ), but it does not exert symptomatic improvement in animals or people with PD (Papavasiliou et al , 1972 ;Shaw et al , 1973Shaw et al , , 1975Shaw , 1977 ;Willis , 2005 ). The sequelae of DART pairs symptomatic improvement with DART and dyskinesia with DA overdose.…”

Section: Bright-light Therapy Pd and Underlying Depressionmentioning

confidence: 82%

A historical justification for and retrospective analysis of the systematic application of light therapy in Parkinson’s disease

Willis¹,

Moore²,

Armstrong³

2012

Reviews in the Neurosciences

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For the past 40 years the primary purpose of therapeutics for Parkinson's disease (PD) has been to replace deficient dopamine (DA) in the nigrostriatal dopamine (NSD) system. Even in the presence of limited efficacy, abundant side effects and impoverished quality of life, the involvement of other systems in the aetiology and treatment of this disorder has been sorely neglected and the excessive use of DA replacement therapy (DART) continues on a global basis. Recent scientific work suggests that the retina plays a major role in NSD function and intimates light therapy in the management of PD. After a thorough review of historical evidence supporting this contention, a retrospective, open-label study on 129 PD patients, whereby they were monitored for a period extending for a few months to eight years, was carried out. Primary motor and non-motor symptoms were monitored using an objectified global rating scale and timed motor tests that were assessed at regular intervals for the duration of the study. Thirty-one patients with other neurological disorders (OND) served as controls to determine whether any therapeutic effects seen with light were generalizable across other conditions. Patients were classified as compliant (COM), semi-compliant (SCOM), or early quit (EQUIT; prematurely discontinued treatment). EQUIT patients showed deterioration, while the COM group improved on most parameters. The SCOM patients were not as good as the COM group. The OND group showed significant improvement in depression and insomnia, but exposure to light did not improve motor function. The total drug burden of PD patients maintained on light was less with fewer side effects than SCOM or EQUIT groups. These results confirm the value of the strategic application of light therapy with controlled doses of DART in PD and warrants further controlled investigation. That the symptomatic improvement continued as long patients remained in the program suggests that exposure to light, under a strict daily regimen, combined with controlled DART, actively slows or arrests the progressive degenerative process underlying PD.

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Section: Bright-light Therapy Pd and Underlying Depressionmentioning

confidence: 82%

A historical justification for and retrospective analysis of the systematic application of light therapy in Parkinson’s disease

Willis¹,

Moore²,

Armstrong³

2012

Reviews in the Neurosciences

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“…In fact, little and contradictory data are available concerning interstrain variability in catalase activity in other brain areas. For example, higher catalase activity has been detected in the striatum, whereas lower activity has been reported in the whole brain homogenate of SHRs compared with normotensive controls (1,19). The hypertensive response elicited by ethanol or acetaldehyde was associated with bradycardia.…”

Section: Discussionmentioning

confidence: 99%

“…Furthermore, previously reported findings on brain catalase activity in experimental models of genetic hypertension are limited and inconsistent (1,19), and there are no reports on RVLM ALDH activity in SHRs versus WKY rats. In the present study, we tested the hypothesis that enhanced ethanol oxidation to acetaldehyde by local catalase underlies, at least partly, the exaggerated pressor response elicited by intra-RVLM ethanol in SHRs.…”

mentioning

confidence: 99%

Enhanced catabolism to acetaldehyde in rostral ventrolateral medullary neurons accounts for the pressor effect of ethanol in spontaneously hypertensive rats

El‐Mas

Abdel‐Rahman

2012

American Journal of Physiology-Heart and Circulatory Physiology

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We have previously shown that ethanol microinjection into the rostral ventrolateral medulla (RVLM) elicits sympathoexcitation and hypertension in conscious spontaneously hypertensive rats (SHRs) but not in Wistar-Kyoto (WKY) rats. In this study, evidence was sought to implicate the oxidative breakdown of ethanol in this strain-dependent hypertensive action of ethanol. Biochemical experiments revealed significantly higher catalase activity and similar aldehyde dehydrogenase (ALDH) activity in the RVLM of SHRs compared with WKY rats. We also investigated the influence of pharmacological inhibition of catalase (3-aminotriazole) or ALDH (cyanamide) on the cardiovascular effects of intra-RVLM ethanol or its metabolic product acetaldehyde in conscious rats. Compared with vehicle, ethanol (10 μg/rat) elicited a significant increase in blood pressure in SHRs that lasted for the 60-min observation period but had no effect on blood pressure in WKY rats. The first oxidation product, acetaldehyde, played a critical role in ethanol-evoked hypertension because 1) catalase inhibition (3-aminotriazole treatment) virtually abolished the ethanol-evoked pressor response in SHRs, 2) intra-RVLM acetaldehyde (2 μg/rat) reproduced the strain-dependent hypertensive effect of intra-RVLM ethanol, and 3) ALDH inhibition (cyanamide treatment) uncovered a pressor response to intra-RVLM acetaldehyde in WKY rats similar to the response observed in SHRs. These findings support the hypothesis that local production of acetaldehyde, due to enhanced catalase activity, in the RVLM mediates the ethanol-evoked pressor response in SHRs.

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“…Several hypotheses have been proposed to explain the mechanism underlying dyskinesias induced by long-term APDs but none has been conclusively verified as the ultimate underlying cause of this syndrome (Abilio et al, 2004;Seeman, 2010).…”

Section: Introductionmentioning

confidence: 99%

An examination of synaptic proteins following chronic haloperidol in a rat model of tardive dyskinesia.

Kessas¹,

Creed²,

Nóbrega³

2010

Psychology & Neuroscience

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Tardive dyskinesia (TD) is a late-onset side effect mainly affecting the orofacial region of patients treated chronically with classic antipsychotic drugs such as haloperidol (HAL). The causes of TD remain unknown. We hypothesized that faulty synaptic re-organization might be related to TD-like syndromes and used the vacuous chewing movements (VCM) model in rats to investigate the expression of four synaptic proteins, synaptophysin, syntaxin, spinophilin and PSD-95, in brains of HAL-treated rats. Male Sprague-Dawley rats were treated for 14 weeks with either haloperidol decanoate (21 mg/kg once every 3 weeks, I.M) or vehicle and VCMs were monitored on a weekly basis. As expected, VCMs developed reliably and were consistently more pronounced in some rats than in others. Using immunohistochemistry in anatomically preserved brain sections as well as Western Blot analyses of whole cells or synaptosomal fractions in striatal tissue, we found no significant effect of chronic HAL on levels of these proteins. Neither did we find significant differences in the levels of the four synaptic markers when comparing rats showing High vs. Low levels of VCMs. These results suggest that structural synaptic alterations (e.g. involving increased number of synapses) may not be the underlying mechanism of oral dyskinesias induced by chronic antipsychotic drug treatment. The possibility that functional neuroplastic changes occur remains to be investigated.

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Important role of striatal catalase in aging- and reserpine-induced oral dyskinesia

Cited by 59 publications

References 40 publications

A historical justification for and retrospective analysis of the systematic application of light therapy in Parkinson’s disease

A historical justification for and retrospective analysis of the systematic application of light therapy in Parkinson’s disease

Enhanced catabolism to acetaldehyde in rostral ventrolateral medullary neurons accounts for the pressor effect of ethanol in spontaneously hypertensive rats

An examination of synaptic proteins following chronic haloperidol in a rat model of tardive dyskinesia.

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