Prolonged hyperoxia preconditioning attenuates behavioral symptoms of 6-hydroxydopamine-induced Parkinsonism.
OBJECTIVE
Several lines of evidences show that hyperoxia preconditioning provides neuronal protection against central nervous system ischemic damages. Common pathways including mitochondrial dysfunction, apoptosis, and caspase activation are involved in acute neurodegeneration (e.g. after cerebral ischemia) and chronic neurodegeneration (e.g. neuronal death in Parkinson's disease). The aim of the present research was to study the effect of hyperoxia preconditioning on 6-hydroxydopamine (6-OHDA)-induced Parkinsonism.


METHODS
Male Wistar rats were first subjected to either air with high oxygen concentration (>90%) or atmospheric air for prolonged (24 hours) or intermittent (six consecutive days, 4 hours each day) periods and then 6-OHDA was injected into their left striatums by stereotaxic surgery. Development and severity of the 6-OHDA-induced Parkinsonism was assessed using apomorphine-induced rotational test, elevated body swing test, and rotarod test within 2-5 weeks after the surgery.


RESULTS
Significant data obtained in rats treated with prolonged hyperoxia, but not the intermittent hyperoxia. In these rats, the number of apomorphine-induced rotations was ∼60% lower than that in control and sham groups. Rats belonging to the prolonged hyperoxia group also showed considerably better motor performance and learning pattern in rotarod test. These results were confirmed by the data obtained in the elevated body swing test.


CONCLUSIONS
Our findings show that the prolonged hyperoxia preconditioning attenuates the behavioral symptoms of 6-OHDA-induced Parkinsonism. Considering the well-known correlation between dopaminergic neuronal death in the substantia nigra and the behavioral symptoms of 6-OHDA-induced Parkinsonism, it could be speculated that the prolonged hyperoxia preconditioning induces the mechanisms that provide dopaminergic neuroprotection against Parkinsonism-induced toxins.
Physiological Research Center, Kashan University of Medical Sciences, Kashan, Iran.
Gholam Ali
GA
Hamidi
Ayda
A
Faraji
Hassan Azhdari
HA
Zarmehri
Hashem
H
Haghdoost-Yazdi
D000818:Animals; D001522:Behavior, Animal / Q000502:physiology; D001526:Behavioral Symptoms / Q000139:chemically induced / Q000503:physiopathology / Q000517:prevention & control*; D018496:Hyperoxia / Q000378:metabolism*; D019194:Ischemic Preconditioning; D008297:Male; D016627:Oxidopamine / Q000633:toxicity*; D020734:Parkinsonian Disorders / Q000139:chemically induced / Q000503:physiopathology / Q000517:prevention & control*; D011597:Psychomotor Performance / Q000502:physiology*; D051381:Rats; D017208:Rats, Wistar; D013997:Time Factors
D016627:Oxidopamine