Anti-TH monoclonal antibody, clone 2C6

Exercise exerts helpful effects in Parkinson's disease. In this study, the 6-hydroxydopamine (6-OHDA) injection was used to investigate the effect of exercise on apomorphine-induced rotation and neurorestoration. Rats (n = 32) were divided into four groups: (1) Saline+Noexercise (Sham); (2) 6-OHDA+Noexercise (6-OHDA); (3) Saline+Exercise (S+EXE), and (4) 6-OHDA+Exercise (6-OHDA+EXE). The rats were administered 8 mu g 6-OHDA by injection into the right medial forebrain bundle. After 2 weeks, the exercise group was run (14 consecutive days, 30 min per day). One month after the surgery, following the injection of apomorphine, the 6-OHDA group displayed a significant increase in rotation and the 6-OHDA+EXE group showed a significant reduction of rotational asymmetry (P < 0.001). 6-OHDA injection reduced the mRNA and protein expression of the AMP-activated protein kinase, brain-derived neurotropic factor, and tyrosine hydroxylase in relation to the Sham group and exercise increased these levels. Expression of the silent information regulator 2 homolog 1 and peroxisome proliferator-activated receptor gamma coactivator 1-alpha was unexpectedly enhanced in the 6-OHDA groups in relation to the Sham group. These findings suggest that the 6-OHDA injection increased the neurodegeneration and mitochondrial and behavioral dysfunctions and the treadmill running attenuated these disorders in the ipsilateral striatum of the 6-OHDA+EXE group.

MPTP produces oxidative stress, damages niagrostriatal dopaminergic neurons and develops Parkinsonism in rodents. Due to paucity of information, the thyroidal status in brain regions and peripheral tissues during different post-treatment days in MPTP-induced mice had been executed in the present study. MPTP depleted tyrosine hydroxylase protein expressions that signify the dopaminergic neuronal damage in substantia nigra. MPTP elevated ROS formation differentially in brain regions (cerebral cortex, hippocampus, substantia nigra) with maximal elevation at hippocampus. The changes in thyroid hormone (T-4 and T-3) levels indicate that brain regions might combat the adverse situation by keeping the levels of thyroid hormones either unchanged or in the elevated conditions in the latter phases (day-3 and day-7), apart from the depletion of thyroid hormones in certain brain regions (T-4 in SN and hippocampus, T-3 in hippocampus) as the immediate (day-1) effects after MPTP treatment. MPTP caused alterations of cellular morphology, RNA:Protein ratio and TPO protein expression, concomitantly depleted TPO mRNA expression and elevated TSH levels in the thyroid gland. Although T-4 levels changed differentially, T-3 levels remained unaltered in thyroid gland throughout the post-treatment days. Results have been discussed mentioning the putative role of T4 and TSH in apoptosis and/or proliferation/differentiation of thyrocytes. In blood, T-4 levels remained unchanged while the changes in T-3 and TSH levels did not signify the clinical feature of hypo/hyperthyroidism of animals. In the pituitary, both T-4 and T-3 levels remained elevated where TSH differentially altered (elevated followed by depletion) during post-treatment days. Notably, T-4, T-3 and TSH levels did not alter in hypothalamus except initial (day-1) depletion of the T-4 level. Therefore, the feedback control mechanism of hypothalamo-pituitary-blood-thyroid-axis failed to occur after MPTP treatment. Overall, MPTP altered thyroidal status in the brain and peripheral tissues while both events might occur in isolation as well.