|| Checking for direct PDF access through Ovid
Regulated endocrine-specific protein, 18 kDa (RESP18) was first cloned in 1994. Its function in the brain especially in neurodegenerative diseases remains unclear. In this study, RESP18 knockout (KO) and littermate wild-type (WT) mice were comprehensively analyzed. The dopaminergic toxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) was applied to generate subchronic Parkinson's disease model. We found that KO mice displayed a reduction in locomotor activity and motor coordination under physiological conditions. Five and six days after MPTP administration, the behavioral impairments were detected in MPTP-treated WT mice, whereas such impairments were not detected in MPTP-treated KO mice. The depletion of tyrosine hydroxylase-positive nerve fibers in the striatum was similar between MPTP-treated KO mice and WT littermates. Furthermore, the striatal level of α-synuclein protein was increased by treatment with MPTP in WT mice, but not in KO mice. The loss of dopaminergic neurons was markedly alleviated, and the activation of glial cells was inhibited in the substantia nigra of KO mice challenged with MPTP. These results suggested that RESP18 deficiency might protect dopaminergic neurons against MPTP toxicity.RESP18 KO mice displayed a reduction in locomotor activity and motor coordination.The behavioral impairments were detected in MPTP-treated WT mice, but not in KO mice.The loss of DA neurons was markedly alleviated in the SN of MPTP-treated KO mice.The activation of glial cells was inhibited in the SN of MPTP-treated KO mice.RESP18 deficiency protects DA neurons against MPTP toxicity.