Xue Y D, Wong P T, Leong S K
Department of Pharmacology, Faculty of Medicine, National University of Singapore.
Acta Neuropathol. 1997 Dec;94(6):572-82. doi: 10.1007/s004010050752.
Glutamate-, aspartate-, N-methyl-D-aspartate receptor (NMDAR1 and 2 subunits)-, and nitric oxide synthase (NOS)-immunoreactive neurons were studied in the arcuate nucleus (AN) of mice treated neonatally with monosodium glutamate (MSG) which is known to cause extensive neuronal loss in this hypothalamic nucleus. It was found that intensely stained glutamate- and aspartate-immunoreactive neurons present in the AN of control mice were completely absent in the MSG-lesioned AN as well as the ventromedial nucleus lateral to the AN. Similarly, NMDAR1-immunoreactive neurons were mostly absent in the MSG-lesioned AN but remained intact in the ventromedial nucleus. There was also a substantial loss of NMDAR2 immunoreactivity within the AN. In contrast, NOS-immunoreactive neurons in the AN survived the neonatal glutamate treatment, although they appeared to be less intensely stained.
对新生期用谷氨酸单钠（MSG）处理的小鼠弓状核（AN）中谷氨酸、天冬氨酸、N-甲基-D-天冬氨酸受体（NMDAR1和2亚基）以及一氧化氮合酶（NOS）免疫反应性神经元进行了研究，已知MSG会导致该下丘脑核团广泛的神经元丢失。结果发现，对照小鼠AN中强烈染色的谷氨酸和天冬氨酸免疫反应性神经元在MSG损伤的AN以及AN外侧的腹内侧核中完全缺失。同样，NMDAR1免疫反应性神经元在MSG损伤的AN中大多缺失，但在腹内侧核中保持完整。AN内NMDAR2免疫反应性也有大量丢失。相比之下，AN中的NOS免疫反应性神经元在新生期谷氨酸处理后存活下来，尽管它们的染色似乎不太强烈。
