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

[1]左旋多巴在压力受体反射中的作用：(1)右侧孤束核的电解损伤选择性地减少了同侧侧侧脊髓尾侧腹外侧左旋多巴的组织含量，减少了45%。(2)反复、持续地间歇性刺激右主动脉降压神经，引起左旋多巴释放、低血压、心动过缓。(3)压力感受器激活选择性地唤起左旋多巴。这种左旋多巴释放被同侧孤束核的急性损伤所抑制在孤立束核分离的单个细胞神经元中，0.1 ~ 1 mM的左旋多巴增加HVA Ca2+电流，最大效果比对照电流高50%。这种作用被左旋多巴甲酯（一种竞争性左旋多巴拮抗剂）阻断。[II]确定左旋多巴是脑缺血引起的延迟性神经元细胞死亡的一个偶然因素：四支血管闭塞导致的10分钟短暂性缺血在大鼠纹状体微透析期间增加细胞外左旋多巴、多巴胺和谷氨酸，并引起神经元细胞死亡。缺血前10 min灌注10 ~ 100 nM竞争性多巴拮抗剂L-DOPA环己基酯，可浓度依赖性地降低谷氨酸释放，而不改变缺血后多巴胺的释放，保护神经元免于细胞死亡。[III] L-DOPA转运体：(1)将兔肠上皮的polyA+ RNA注入非洲爪蟾卵母细胞，观察其对高亲和力的L-[14C]DOPA的转运活性。这种摄取部分依赖Na+，但不依赖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。共注射一种反义rna，以及与兔rBAT cDNA互补的寡核苷酸，几乎完全抑制了卵母细胞对L-[14C]DOPA的摄取。因此rBAT负责L-[14C]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.