HABENULA AND THALAMUS CELL TRANSPLANTS MEDIATE DIFFERENT SPECIFIC PATTERNS OF INNERVATION IN THE INTERPEDUNCULAR NUCLEUS
HABENULA AND THALAMUS CELL TRANSPLANTS MEDIATE DIFFERENT SPECIFIC PATTERNS OF INNERVATION IN THE INTERPEDUNCULAR NUCLEUS
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DOI：
10.1523/jneurosci.12-08-03272.1992
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发表时间：
1992-08-01
影响因子：
5.3
通讯作者：
HAUN, F
中科院分区：
文献类型：
--
作者：
ECKENRODE, TC;MURRAY, M;HAUN, F
使用对P物质（SP）和胆碱乙酰转移酶（ChAT）有免疫反应的胚胎细胞悬浮移植物，对脚间核（IPN）特定的肽能和胆碱能区域的神经支配进行了研究。在新生和成年宿主大鼠中，首先通过双侧缰核脚间束（FR）损伤，使IPN失去来自内侧缰核的正常SP和胆碱能输入。在成年宿主中，将胚胎缰核细胞移植物置于去神经的IPN附近，介导了局限于缰核靶向亚核的SP染色正常模式的恢复，以及IPN内固有SP细胞染色强度的增加。ChAT染色没有恢复。将缰核移植物植入新生宿主后，出现了类似的SP染色模式，但此外，胆碱能亚核的正常ChAT染色有部分恢复，而正常肽能亚核出现异常ChAT染色。将胚胎丘脑细胞作为对照移植物植入成年宿主，在IPN中产生了一种令人惊讶的ChAT染色模式，与将缰核移植物植入新生宿主时所见相同；因此，成年IPN能够支持由异常胆碱能来源介导的神经再支配，而对其正常的缰核胆碱能传入纤维无反应。这种结果模式意味着IPN对缰核SP和胆碱能神经支配的调节，以及成熟的正常胆碱能传入纤维与其靶标之间的某种相互作用，当这些传入来源异常时这种相互作用缺失。
Innervation of specific peptidergic and cholinergic compartments of the interpeduncular nucleus (IPN) was investigated using embryonic cell suspension transplants immunoreactive for substance P (SP) and ChAT. In both neonatal and adult host rats, the IPN was first denervated of its normal SP and cholinergic input from the medial habenula by bilateral lesions of the fasciculi retroflexi (FR). In adult hosts, transplants of embryonic habenular cells placed near the denervated IPN mediated a return of the normal pattern of SP staining restricted to habenula-target subnuclei, plus an increase in staining intensity of SP cells intrinsic to the IPN. There was no recovery of ChAT staining. A similar pattern of SP staining resulted following habenular transplants into neonatal hosts, but in addition there was a partial recovery of normal ChAT staining in cholinergic subnuclei and anomalous ChAT staining in normally peptidergic subnuclei. Control transplants of embryonic thalamus cells placed into adult hosts produced a surprising pattern of ChAT staining in the IPN identical to that seen with habenula transplants placed into neonatal hosts; the adult IPN was thus able to support reinnervation mediated by an aberrant cholinergic source while being refractory to its normal habenular cholinergic afferents. This pattern of results implies regulation by the IPN of habenular SP and cholinergic innervation, and some interaction between the maturing normal cholinergic afferents and their targets that is missing when these afferent sources are abnormal.