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Advanced Neurology Stress accelerates parkinsonism in rats

it minimizes the animals’ habituation to stressors. Furthermore, a previous study showed that repeated
40
In this context, our results corroborate those of other administration of exogenous CORT causes motor
studies that explored the role of stress and CORT levels impairment, accompanied with structural and functional
48
in PD. For instance, Rudyk et al. investigated the role changes in the motor cortex of rats. Another study
53
of unpredictable stress in the protocol of PD induced by demonstrated that exogenous CORT administration
paraquat. Interestingly, they found an increase in plasma and immobilization stress independently cause motor
CORT levels. Another study using the 6-OHDA-induced impairments. Hence, the stress-induced aggravation
54
parkinsonism model combined with the restraint stress of motor symptoms in PD could be related to increased
protocol showed that elevated CORT levels aggravated CORT levels. Nonetheless, this seems unlikely in the
neuronal loss in the nigrostriatal pathway and motor present study because reserpine did not significantly
symptoms in the PD model. Our study extended these promote the increase in CORT levels induced by UMS
46
findings to the reserpine treatment model, demonstrating under our experimental conditions.
an anticipatory effect of stress on the onset of motor
symptoms using a progressive approach with repeated 5. Conclusion
application of a low dose. Chronic UMS anticipates and aggravates motor impairment
An explanation for the acceleration of motor symptoms in the animal model of progressive parkinsonism treated
due to unpredictable stress could be the exacerbation of with repeated low-dose reserpine, accompanied with
oxidative stress, as evaluated via lipid peroxidation assay. increased plasma CORT levels. Furthermore, these effects
Fernandes et al. revealed that a low dose of reserpine on motor impairment were not associated with striatal
29
(0.1 mg/kg) increased lipid peroxidation 48 h after the oxidative stress. Considering these data, additional
10 injection. It is well-established that oxidative stress research is warranted to clarify the mechanisms underlying
th
can cause motor 6,49,50 and cognitive impairments. the stress-induced exacerbation of motor symptoms in PD.
6,51
Differences in the study protocol, such as the fact that Acknowledgments
euthanasia was performed 72 h instead of 48 h after the
last reserpine injection, may explain the disagreement The authors would like to thank Claudenice Moreira dos
between our findings and those of previous studies. Santos for capable technical assistance.
29
Despite these differences, our study demonstrated that
acceleration of motor symptoms did not occur due to Funding
increased striatal lipid peroxidation. This is possibly This study was financed by Fundação de Amparo à Pesquisa
due to the small sample size of the study, which could do Estado de São Paulo – FAPESP (grant 2017/26253-3),
have masked the results. Furthermore, evaluating and by Coordenação de Aperfeiçoamento de Pessoal de
oxidative stress using other techniques could provide a Nível Superior/Brasil – CAPES (finance code 001). RHS
more comprehensive analysis. Therefore, further studies and DS are recipients of research fellowships from Conselho
are warranted to elucidate the mechanisms underlying Nacional de Desenvolvimento Científico e Tecnológico
the stress-induced acceleration of motor impairment (CNPq, grants 313631/2021-2 and 305076/2023-0).
observed in the present study.
Conflict of interest
An alternative explanation could be the involvement of
inflammatory processes in the striatum and substantia nigra The authors declare no conflicts of interest.
in animals subjected to this protocol, as neuroinflammation
is known to be a key factor in the progression of motor Author contributions
impairment in PD. 28,45 Repeated low-dose reserpine Conceptualization: Regina H. Silva, Deborah Sucheck
treatment has been shown to induce neuroinflammation in Formal analysis: Debora M. G. Cunha, Laura F. M. Olivatto,
the nigrostriatal pathway. Furthermore, although Rudyk Raphael Wuo-Silva
28
et al. found no differences in the number of Iba1-positive Investigation: Laura F. M. Olivatto, Debora M. G. Cunha,
48
cells in the SNpc of rats subjected to chronic unpredictable Leonardo B. Silva, Alvaro C. Lima, Marcela Becegato,
stress and paraquat administration, Sugama et al. Vinicius S. Bioni
52
observed an increase in the number of OX42 microglia in Methodology: Regina H. Silva, Deborah Suchecki
the SNpc and locus coeruleus in rats exposed to chronic Writing – original draft: Debora M. G. Cunha, Laura F. M.
restraint stress. Altogether, these findings suggest that the Olivatto
neuroinflammation generated during stress increases in an Writing – review & editing: Alvaro C. Lima, Marcela
animal model of PD. Becegato, Regina H. Silva

Volume 3 Issue 4 (2024) 8 doi: 10.36922/an.4037