Effects of excitatory amino acid lesions upon neurokinin B and acetylcholine neurons in the nucleus basalis of the rat.
Effects of excitatory amino acid lesions upon neurokinin B and acetylcholine neurons in the nucleus basalis of the rat.
复制标题
兴奋性氨基酸损伤对大鼠基底核神经激肽 B 和乙酰胆碱神经元的影响。
DOI：
10.1016/0006-8993(95)00187-u
复制
发表时间：
1995
期刊：
影响因子：
2.9
通讯作者：
Mobley,SL
中科院分区：
文献类型：
--
作者：
Wenk,GL;Rance,NE;Mobley,SL
基底大细胞核（NBM）含有投射到新皮质的胆碱能神经元，并受到含兴奋性氨基酸的终末的密集神经支配。兴奋性输入平衡的功能障碍或NBM细胞对谷氨酸敏感性的改变可能是选择性衰老的基础。一些大的NBM神经元含有神经激肽B（NKB）mRNA。本研究探讨了α-2-氨基-3-羟基-5-甲基-异恶唑-4-丙酸（AMPA）或N-甲基-d-天冬氨酸（NMDA）是否不同地破坏含NKB、NKB受体或胆碱能NBM细胞，以及这种脆弱性是否会因衰老而改变。注射AMPA或NMDA显着降低新皮层ChAT活性，与对照水平相比，在所有三个年龄组，病变和年龄组之间没有相互作用。原位杂交组织化学和NKB受体的研究结果表明，NBM中含有NKB的神经元，以及它们支配的神经元，在年轻或老年大鼠中不容易受到NMDA或AMPA的影响。虽然NKB mRNA阳性细胞弥漫分布在整个基底前脑，只有一小部分的大NBM细胞含有NKB mRNA。结果表明，NKB不广泛共定位与乙酰胆碱在大鼠基底前脑和NBM NKB神经元不直接支配胆碱能细胞。
The nucleus basalis magnocellularis (NBM) contains cholinergic neurons that project to the neocortex and is densely innervated by excitatory amino acid-containing terminals. A dysfunction in the balance of excitatory inputs or an alteration in the sensitivity of NBM cells to glutamate may underlie the selective vulnerability to aging. Some large NBM neurons contain neurokinin B (NKB) mRNA. The present study investigated whether α-2-amino-3-hydroxy-5-methyl-isoxazole-4-propionic acid (AMPA) or N-methyl-d-aspartate (NMDA) differentially destroy NKB-containing, NKB-receptive, or cholinergic NBM cells, and whether this vulnerability is altered by aging. Injections of AMPA or NMDA significantly decreased neocortical ChAT activity, as compared to control levels, across all three age groups, with no interaction between lesion and age group. The results of in situ hybridization histochemistry and NKB receptor studies suggest that NKB-containing neurons in the NBM, and the neurons they innervate, are not vulnerable to NMDA or AMPA in either young or old rats. While NKB mRNA-positive cells were diffusely distributed throughout the basal forebrain, only a small proportion of the large NBM cells contained NKB mRNA. The results suggest that NKB does not extensively colocalize with acetylcholine within the basal forebrain of rats and that NBM NKB neurons do not directly innervate cholinergic cells.