Author/Authors :
Ahmadian, Nahid Neurosciences Research Center - Tabriz University of Medical Sciences - Tabriz, Iran , Mahmoudi, Javad Neurosciences Research Center - Tabriz University of Medical Sciences - Tabriz, Iran , Talebi, Mahnaz Neurosciences Research Center - Tabriz University of Medical Sciences - Tabriz, Iran , Sadigh-Eteghad, Saeed Neurosciences Research Center - Tabriz University of Medical Sciences - Tabriz, Iran , Molavi, Leila Pharmaceutical Biotechnology Department - Faculty of Pharmacy - Tabriz University of Medical Sciences - Tabriz, Iran , Rostrup, Egill Mental Health Centre Glostrup - University of Copenhagen - Glostrup, Denmark , Ziaee, Mojtaba Cardiovascular Research Center - Tabriz University of Medical Sciences - Tabriz, Iran
Abstract :
The present study was conducted to examine the effect of sleep deprivation (SD) on the
anti-apoptotic pathways in Parkinsonian rats.
Materials and Methods: Male Wistar rats (n = 40) were assigned to four groups (10 animals each):
sham surgery (Sham), 6-hydroxydopamine (6-OHDA)-lesioned (OH), 6-OHDA-lesioned plus grid
control (OH+GC), 6-OHDA-lesioned plus SD (OH+SD). Parkinson’s disease (PD) model was induced
by the unilateral intra-striatal infusion of 6-OHDA (10 μg/rat). SD (4 hr/day, for 14 days) was induced
using a multiple platforms water tank. On the last day of interventions, animals were subjected to
open field test for horizontal motor performance assessment. Also, brain-derived neurotrophic factor
(BDNF), Bcl-2 and Bax were assessed in the striatum of study groups.
Results: SD obscured the motor deficits of PD animals observed in open field test. BDNF level and
Bcl2/Bax ratio significantly increased in the OH group, and SD reduced their levels in the PD animals.
Conclusion: SD suppressed the anti-apoptotic compensatory responses in the striatum; therefore, it
may accelerate continual neuronal cell death in PD.
Keywords :
6-Hydroxy dopamine , Bcl-2 , BDNF , Bax Parkinson’s disease , Sleep deprivation
