Szczypka M S, Mandel R J, Donahue B A, Snyder R O, Leff S E, Palmiter R D
Howard Hughes Medical Institute, Department of Biochemistry, University of Washington, Seattle 98195, USA.
Neuron. 1999 Jan;22(1):167-78. doi: 10.1016/s0896-6273(00)80688-1.
Dopamine-deficient mice (DA-/- ), lacking tyrosine hydroxylase (TH) in dopaminergic neurons, become hypoactive and aphagic and die by 4 weeks of age. They are rescued by daily treatment with L-3,4-dihydroxyphenylalanine (L-DOPA); each dose restores dopamine (DA) and feeding for less than 24 hr. Recombinant adeno-associated viruses expressing human TH or GTP cyclohydrolase 1 (GTPCH1) were injected into the striatum of DA-/- mice. Bilateral coinjection of both viruses restored feeding behavior for several months. However, locomotor activity and coordination were partially improved. A virus expressing only TH was less effective, and one expressing GTPCH1 alone was ineffective. TH immunoreactivity and DA were detected in the ventral striatum and adjacent posterior regions of rescued mice, suggesting that these regions mediate a critical DA-dependent aspect of feeding behavior.
多巴胺缺乏小鼠(DA-/-)在多巴胺能神经元中缺乏酪氨酸羟化酶(TH),变得活动减退、摄食减少,并在4周龄时死亡。每天用L-3,4-二羟基苯丙氨酸(L-DOPA)治疗可挽救它们;每次给药可恢复多巴胺(DA)水平并使摄食恢复不到24小时。将表达人TH或GTP环水解酶1(GTPCH1)的重组腺相关病毒注射到DA-/-小鼠的纹状体中。两种病毒双侧共注射可使摄食行为恢复数月。然而,运动活动和协调性仅得到部分改善。仅表达TH的病毒效果较差,单独表达GTPCH1的病毒则无效。在获救小鼠的腹侧纹状体和相邻的后部区域检测到TH免疫反应性和DA,这表明这些区域介导了摄食行为中关键的DA依赖性方面。