Casini G, Rickman D W, Sternini C, Brecha N C
Department of Neurobiology, Brain Research Institute, CURE Digestive Diseases Research Center, UCLA School of Medicine, Los Angeles, California 90095, USA.
J Comp Neurol. 1997 Dec 22;389(3):496-507.
Tachykinin (TK) peptides influence neuronal activity in the inner retina of mammals. The aim of this investigation was to determine the cellular localization of the neurokinin 1 receptor (NK1), whose preferred ligand is the TK peptide substance P (SP), in the rat retina. These studies used a polyclonal antiserum directed to the C-terminus of rat NK1. The majority of NK1-immunoreactive (IR) cells were located in the proximal inner nuclear layer (INL), and very rarely they were found in the distal INL. Some small and large NK1-IR somata were present in the ganglion cell layer. NK1-IR processes were densely distributed across the inner plexiform layer (IPL) with a maximum density over lamina 2 of the IPL. Immunoreactive processes also crossed the INL and ramified in the outer plexiform layer where they formed a sparse meshwork. NK1-IR processes were rarely observed in the optic nerve fiber layer. Double-label immunofluorescence studies with different histochemical markers for bipolar cells indicated that NK1 immunoreactivity was not present in bipolar cells. Together, these observations indicate that NK1 immunoreactivity is predominantly expressed by amacrine, displaced amacrine, interplexiform, and some ganglion cells. Double-label immunofluorescence experiments were also performed to characterize NK1-containing amacrine cells. Sixty-one percent of the gamma-aminobutyric acid (GABA)-IR cells, 71% of the large tyrosine hydroxylase (TH)-IR cells, and 100% of the small TH-IR cells contained NK1 immunoreactivity. In addition, most (91%) of the NK1-IR cells had GABA immunoreactivity. In contrast, vasoactive intestinal polypeptide-, TK-, choline acetyltransferase-, and parvalbumin-IR amacrine tells did not express NK1 immunoreactivity. Overall, the present findings suggest that SP acts directly upon several cell populations, including GABA-containing amacrine cells and ganglion cells, to influence visual information processing in the inner retina.
速激肽(TK)肽影响哺乳动物视网膜内层的神经元活动。本研究的目的是确定神经激肽1受体(NK1)在大鼠视网膜中的细胞定位,其首选配体是TK肽P物质(SP)。这些研究使用了针对大鼠NK1 C末端的多克隆抗血清。大多数NK1免疫反应性(IR)细胞位于近端内核层(INL),在远端INL中很少发现。神经节细胞层中有一些大小不一的NK1-IR胞体。NK1-IR突起密集分布在内网状层(IPL),在IPL的第2层密度最高。免疫反应性突起也穿过INL并在外网状层分支,在那里形成稀疏的网络。在视神经纤维层中很少观察到NK1-IR突起。用不同的双极细胞组织化学标记进行的双标记免疫荧光研究表明,双极细胞中不存在NK1免疫反应性。总之,这些观察结果表明,NK1免疫反应性主要由无长突细胞、移位无长突细胞、网间细胞和一些神经节细胞表达。还进行了双标记免疫荧光实验以表征含NK1的无长突细胞。61%的γ-氨基丁酸(GABA)-IR细胞、71%的大型酪氨酸羟化酶(TH)-IR细胞和100%的小型TH-IR细胞含有NK1免疫反应性。此外,大多数(91%)的NK1-IR细胞具有GABA免疫反应性。相比之下,血管活性肠肽、TK、胆碱乙酰转移酶和小白蛋白-IR无长突细胞不表达NK1免疫反应性。总体而言,目前的研究结果表明,SP直接作用于包括含GABA的无长突细胞和神经节细胞在内的多个细胞群体,以影响视网膜内层的视觉信息处理。