University of Southern California, Department of Cell and Neurobiology, Keck School of Medicine of the University of Southern California, Los Angeles, CA 90033, USA.
Pharmacol Biochem Behav. 2010 Jun;95(4):466-72. doi: 10.1016/j.pbb.2010.03.009. Epub 2010 Mar 27.
Sex differences in Parkinson's disease (PD) have been reported in humans and rodent models, with a higher incidence in men and increased severity in male rodents. The current study examined sex differences and the effects of gonadal steroid hormones in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-lesioned mouse model of PD. Male (n=51) and female (n=50) mice were gonadectomized and received physiologic replacement with testosterone or estrogen (Experiment 1), or no hormones (Experiment 2). Two weeks later, mice received either MPTP (10 mg/kg per day for 5 days) or saline. Higher doses killed female mice. Mice were tested one week after MPTP for motor performance using rotarod, pole and gait tests. In hormone-treated mice, males significantly outperformed females in all three tests (p<0.05). Compared with females, males had a greater overall rotarod performance (ORP: 1317.1+/-98.3 vs. 988.1+/-95.6), descended a pole faster (7.1+/-0.6 vs. 9.6+/-0.7s), and had longer stride lengths (hindlimb 7.3+/-0.1 vs. 6.8+/-0.1cm). By contrast, ovariectomized female mice receiving saline outperformed castrated males on the rotarod (1296.6+/-83.3 vs. 811.2+/-113.7, p<0.05) and descended a pole faster (9.7+/-2.0 vs. 15.6+/-1.9s, p<0.05). MPTP significantly impaired ORP (p<0.05) in hormone-treated males (703.7+/-65.5) and females (432.8+/-88.6, p<0.05). After MPTP, stride length was selectively decreased in males (hindlimb 6.6+/-0.1 cm, p<0.05), and pole test performance was unimpaired in either sex. After gonadectomy, MPTP did not decrease motor performance in males (p>0.05) but significantly reduced ORP in females (975.9+/-110.3 vs. saline females, p<0.05). Our results show that small, chronic doses of MPTP produce subtle, sexually-dimorphic impairments in motor performance, but without a loss of tyrosine hydroxylase-positive neurons in the substantia nigra. In gonadectomized mice, this sex difference is reversed.
帕金森病(PD)在人类和啮齿动物模型中存在性别差异,男性发病率较高,雄性啮齿动物病情更严重。本研究探讨了 1-甲基-4-苯基-1,2,3,6-四氢吡啶(MPTP)诱导的 PD 啮齿动物模型中的性别差异和性腺类固醇激素的作用。雄性(n=51)和雌性(n=50)小鼠去势并接受生理替代睾酮或雌激素(实验 1)或不接受激素(实验 2)。两周后,小鼠接受 MPTP(每天 10mg/kg,连续 5 天)或生理盐水。高剂量会杀死雌性小鼠。MPTP 后一周,用旋转棒、杆和步态测试评估小鼠的运动表现。在激素处理的小鼠中,雄性在所有三个测试中的表现均显著优于雌性(p<0.05)。与雌性相比,雄性的整体旋转棒表现更好(ORP:1317.1+/-98.3 比 988.1+/-95.6),下杆速度更快(7.1+/-0.6 比 9.6+/-0.7s),步幅更长(后肢 7.3+/-0.1 比 6.8+/-0.1cm)。相比之下,接受生理盐水的去卵巢雌性小鼠在旋转棒上的表现优于去势雄性(1296.6+/-83.3 比 811.2+/-113.7,p<0.05),下杆速度更快(9.7+/-2.0 比 15.6+/-1.9s,p<0.05)。MPTP 显著损害了雄性(p<0.05,703.7+/-65.5)和雌性(p<0.05,432.8+/-88.6)激素处理的小鼠的 ORP。在接受 MPTP 后,雄性(后肢 6.6+/-0.1cm,p<0.05)和雌性(后肢 6.6+/-0.1cm,p<0.05)的步幅长度选择性降低,但两性的杆测试表现均未受损。去势后,MPTP 并未降低雄性的运动表现(p>0.05),但显著降低了雌性的 ORP(975.9+/-110.3 比生理盐水雌性,p<0.05)。我们的结果表明,小剂量、慢性 MPTP 可引起运动表现的微妙、性别二态性损伤,但黑质内酪氨酸羟化酶阳性神经元无丢失。在去势的小鼠中,这种性别差异被逆转。