L-DOPA Plays a role as a neurotransmitter regulating blood pressure in the lower brain stem, and endogenously evoked L-DOPA is a casual factor for glutamate release and resultant delayed neuronal cell death by transient ischemia in rats

[I]L多巴在压力感受性反射中的作用：[1](1)电解损毁右侧孤束核，选择性地使同侧延髓尾侧腹外侧腹外侧区L多巴的组织含量减少45%。(2)反复、持续地间歇刺激右主动脉降压神经，引起L多巴的释放、低血压和心动过缓。急性损毁同侧孤束核可抑制L-多巴酚丁酸的释放。[2]在分离的孤束核单细胞神经元上，L多巴0.1~1 mM使HVA钙电流增加，最大作用超过对照电流的50%。此作用可被竞争性的L-多巴阻断剂L-多巴甲酯阻断。[II]L-多巴作为脑缺血迟发性神经细胞死亡的偶然因素的鉴定：四支血管阻断造成的短暂性脑缺血10min使大鼠纹状体微透析过程中细胞外L-多巴、多巴胺和谷氨酸含量增加，并导致神经细胞死亡。在缺血前10min，纹状体内灌流竞争性多巴受体拮抗剂L-多巴转运体环己酯，呈浓度依赖性地减少谷氨酸释放而不改变多巴胺的释放，并保护神经元免于细胞死亡。[III]L多巴转运体：(1)在非洲爪哇卵母细胞中，注射兔肠上皮多聚酶A+核糖核酸，观察到L-[14C]多巴转运体具有高亲和力的转运活性。这种摄取部分依赖于Na+，但不依赖于Cl-。L-酪氨酸、-苯丙氨酸、-亮氨酸和E-赖氨酸抑制这种转运活性。联合注射反义cRNA和与兔rBAT互补的寡核苷酸几乎完全抑制卵母细胞对L-[14C]DOPA的摄取。因此，rBAT负责L-[14C]DOPA的摄取活性。

[I] Function of L-DOPA in baroreceptor reflex:[1] (1) Electrolytic lesions of the right nucleus tractus solitarii selectively decrease by 45 % the tissue content of L-DOPA in the dissected ipsilateral caudal ventrolateral medulla.(2) Intermittent stimulation of the right aortic depressor nerve repetitively and constantly causes L-DOPA release, hypotension and bradycardia.(3) Baroreceptor activation selectively evokes L-DOPA. This L-DOPA release is suppressed by acute lesion in the ipsilateral nucleus tractus solitarii.[2] In a single cell neuron isolated from nucleus tractus solitarii, L-DOPA 0.1 to 1 mM augments HVA Ca2+ current with the maximal effect of 50 % over the control current. The effect is blocked by L-DOPA methyl ester, a competitive L-DOPA antagonist.[II] Identification of L-DOPA as a casual factor for delayed neuronal cell death induced by brain ischemia: Ten-min transient ischemia due to four vessel occlusion increases extracellular L-DOPA, dopamine and glutamate during rat striatal microdialysis, and elicits neuronal cell death. Intrastriatal perfusion of 10-100 nM L-DOPA cyclohexyl ester, a competitive DOPA antagonist, 10 min before ischemia, concentration-dependently decreases glutamate release without modification of dopamine release by ischemia, and protects neurons from cell death.[III] L-DOPA transporter:(1) In Xenopus laevis oocytes, injected with polyA+ RNA from rabbit intestinal epithelium, the transport activity for L-[14C]DOPA with a high affinity is observed. This uptake was partially Na+-dependent but Cl- -independent. L-Tyrosine, -phenylalanine, -leucine and E〜lysine inhibit this transport activity. Coinjection of an antisence cRNA, as well as oligonucleotide complementary to rabbit rBAT cDNA almost completely inhibited the uptake of L-[14C]DOPA in the oocytes. rBAT is thus responsible for the L-[14C]DOPA uptake activity.