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]左旋多巴在压力感受器反射中的作用：[1]（1）电毁损右侧孤束核，选择性地使同侧延髓尾侧腹外侧区左旋多巴组织含量减少45%。(2)反复和持续地间歇刺激右主动脉减压神经会导致左旋多巴释放、低血压和心动过缓。(3)压力感受器激活选择性地唤起左旋多巴。这种左旋多巴的释放受到同侧孤束核急性损伤的抑制。[2]在从孤束核分离的单细胞神经元中，L-DOPA 0.1至1 mM增强HVA Ca 2+电流，最大效应为对照电流的50%。该作用被竞争性左旋多巴拮抗剂左旋多巴甲酯阻断。[II]L-DOPA作为脑缺血诱导的迟发性神经元细胞死亡的偶然因素的鉴定：由于四血管闭塞导致的10分钟短暂缺血增加了大鼠纹状体微透析期间细胞外L-DOPA、多巴胺和谷氨酸，并诱发神经元细胞死亡。在缺血前10分钟，纹状体内灌注10-100 nM L-DOPA环己酯（一种竞争性DOPA拮抗剂），浓度依赖性地减少谷氨酸释放，而不改变缺血引起的多巴胺释放，并保护神经元免于细胞死亡。[III]左旋多巴转运蛋白：（1）在非洲爪蟾卵母细胞中，注射兔肠上皮细胞的polyA+ RNA后，可观察到高亲和力的左旋多巴转运活性。这种吸收部分依赖于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。共注射反义cRNA以及与兔rBAT cDNA互补的寡核苷酸几乎完全抑制卵母细胞对L-[14 C]DOPA的摄取。因此，rBAT负责L-[14 C]DOPA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.