Yamamoto T, Staines W A, Dewar K, Geiger J D, Daddona P E, Nagy J I
Department of Anatomy, University of Ottawa, Ont., Canada.
Brain Res. 1988 Nov 22;474(1):112-24. doi: 10.1016/0006-8993(88)90674-9.
Immunohistochemical, neuroanatomical and lesion methods were used to investigate the projections of adenosine deaminase immunoreactive (ADA-IR) neurons in the striatum (caudate/putamen) and hypothalamus to the substantia nigra (SN). Striatal ADA-IR neurons were distributed within two zones; anteriorly in the medial and ventromedial extreme of the head and body of the striatum, and posteriorly in the tail of the striatum. The posterior hypothalamus contained ADA-positive neurons which were confined to the tuberomammillary nucleus (TM). The SN was devoid of ADA-positive neurons, but contained two distinct types of ADA-IR fiber terminations. One type was confined to bands located at the ventrolateral and dorsomedial borders of the pars reticulata and consisted of fine puncta. The other type was distributed throughout the SN and consisted of long, beaded fibers. Injections of the retrograde tracer Fluoro-gold (FG) into the SN gave rise to FG-labelling of significant numbers of ADA-IR neurons in both the striatum and TM. Medial SN injections preferentially labelled ADA-IR neurons in the anterior striatum and lateral SN injections labelled posterior ADA-IR striatal neurons. Kainic acid lesions of the anterior medial striatum selectively abolished the punctate ADA-IR band in the medial SN and left the long, ADA-IR nigral fibers in an apparently hypertrophied state. Despite depletion of ADA-IR neurons in the striatum by kainic acid, ADA activity increased significantly at striatal lesion sites. The results suggest that the SN receives two topographically segregated fine terminal fields from striatal ADA-IR neurons, and a substantial innervation from ADA-IR neurons in the TM as well. These findings add to the heterogeneous chemical composition of nigral afferents and are discussed in the context of adenosine neuromodulatory mechanisms in the striatonigral system.
采用免疫组织化学、神经解剖学和损伤方法，研究纹状体（尾状核/壳核）和下丘脑内腺苷脱氨酶免疫反应性（ADA-IR）神经元向黑质（SN）的投射。纹状体ADA-IR神经元分布在两个区域；前部位于纹状体头部和体部的内侧和腹内侧极端，后部位于纹状体尾部。下丘脑后部含有ADA阳性神经元，这些神经元局限于乳头体核（TM）。黑质不含ADA阳性神经元，但含有两种不同类型的ADA-IR纤维终末。一种类型局限于位于网状部腹外侧和背内侧边界的带，由细点状结构组成。另一种类型分布于整个黑质，由长的、串珠状纤维组成。向黑质注射逆行示踪剂荧光金（FG），导致纹状体和TM中大量ADA-IR神经元出现FG标记。黑质内侧注射优先标记前部纹状体中的ADA-IR神经元，黑质外侧注射标记后部纹状体ADA-IR神经元。前内侧纹状体的 kainic 酸损伤选择性地消除了黑质内侧的点状ADA-IR带，并使长的、ADA-IR黑质纤维处于明显肥大状态。尽管 kainic 酸使纹状体中的ADA-IR神经元减少，但纹状体损伤部位的ADA活性显著增加。结果表明，黑质接受来自纹状体ADA-IR神经元的两个拓扑学上分离的精细终末场，以及来自TM中ADA-IR神经元的大量神经支配。这些发现增加了黑质传入纤维的异质性化学成分，并在纹状体黑质系统中的腺苷神经调节机制背景下进行了讨论。
